A History of Ultraviolet Photobiology For Humans

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A History of Ultraviolet Photobiology for Humans, Animals and

Microorganisms¶
Article in Photochemistry and Photobiology · January 2003

DOI: 10.1562/0031-8655(2002)076<0561:AHOUPF>2.0.CO;2 · Source: PubMed
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Photochemistry and Photobiology, 2002, 76(6): 561–579
Invited Review
A History of Ultraviolet Photobiology for Humans,

Animals and Microorganisms{
Philip E. Hockberger*
Department of Physiology, The Feinberg School of Medicine, Northwestern University, Chicago, IL
Received 12 June 2002; accepted 20 September 2002
INTRODUCTION improvements in instrumentation and careful experimentation.

This is followed by a more detailed discussion of the evidence
Ancient civilizations understood that sunlight provides visibility,
linking sunlight and UV radiation with physiological and
warmth, health and vitality. Their understanding of how sunlight
pathological changes in humans, nonhuman animals and micro-
provides these life-sustaining influences was immersed in mythol-
organisms. Each group has its own unique narrative relating it to
ogy and cultural traditions. Offspring, dissatisfied with the
UV radiation. A recurring theme is that UV radiation has both
intellectual power of their ancestors’ explanations, sought new
beneficial and harmful effects depending upon the type of
mythologies in their search for a better understanding of the
organism, wavelength region (UVA, UVB or UVC) and irradiation
cosmos and their relationship with it.
dose (intensity 3 duration).
Starting in the late 17th century, a new mythology arose in
Europe that was based on scientific principles and provided the
basis for a more reliable understanding of the relationship between THE DISCOVERY OF UV RADIATION,
humans and sunlight. By the start of the 19th century, the ITS PROPERTIES AND RELATIONSHIP
application of these principles led to the realization that sunlight is WITH SUNLIGHT
not a single stimulus but, rather, a collection of stimuli of different The discovery of UV radiation and its properties was a gradual
wavelengths (e.g. infrared, visible, ultraviolet). This realization process that spanned three centuries and involved scientists from
inspired additional studies aimed at determining whether different many countries (21–24). In 1614, Sala made a seminal observation.
wavelengths might be responsible for the different effects of He noticed that sunlight turned silver nitrate crystals black. In
sunlight. As this review documents, indeed they are. 1777, Scheele found that paper soaked in silver chloride solution
This review focuses primarily on studies before 1920 that were darkened when exposed to sunlight. When he directed sunlight
involved in the discovery of UV radiation, its properties and its through a prism onto the paper, the violet end of the spectrum was
influences on living organisms. After 1920, the number of UV- more effective than the reddish end.
related publications grew rapidly, reaching at least 275 for the In 1801, Ritter made the hallmark observation. He noticed that
years 1920–1927 alone (1). Between 1960 and 2001, there are invisible rays just beyond the violet end of the spectrum were even
37 466 publications on the subject ‘‘ultraviolet radiation’’ listed in more effective at darkening silver chloride–soaked paper. He called
PUBMED, a U.S. government-supported computer database of them ‘‘deoxidizing rays’’ to emphasize their chemical reactivity
health-related research. Due to the extent of the literature, this and to distinguish them from the ‘‘heat rays’’ at the other end of the
review covers only the most important studies between 1920 and visible spectrum. Over time, the simpler term ‘‘chemical rays’’ was
2001. The selection of these studies was made solely by the author, adopted to describe these invisible rays along with the adjacent
and any omissions and shortcomings are his responsibility. There violet-blue rays. The terms chemical and heat rays remained
are a number of excellent reviews on UV photobiology written popular throughout the 19th century, but they were eventually
between 1920 and 2001, and these should be consulted for more dropped in favor of the more restrictive terms ultraviolet and
in-depth analyses (cf. [1–20]). infrared radiation, respectively.
We begin with the discovery of UV radiation, its properties and Initial studies of the chemical rays focused on their ability to
relationship with sunlight. These discoveries were unveiled stimulate chemical reactions. In 1809, Gay Lussac and Thénard
through a series of serendipitous observations coupled with demonstrated that concentrated sunlight was capable of converting
a mixture of hydrogen and chlorine gases into hydrochloric acid. In
{Posted on the web site on 1 October 2002. 1815, Planché noted that chemical rays darkened many kinds of
*To whom correspondence should be addressed at: Department of metallic salts. Between 1826 and 1837, Niépce and Daguerre found
Physiology, M211, The Feinberg School of Medicine, Northwestern that silver iodide was especially light-sensitive, and they used this
University, 303 East Chicago Avenue, Chicago, IL 60611, USA. Fax: discovery as the basis for their early work in photography. In 1842,
312-503-5101; e-mail: p-hockberger@northwestern.edu
Abbreviations: BCE, before common era; CE, common era; CNS, central Becquerel and Draper independently showed that when sunlight
nervous system; Hg, mercury. was passed through a prism onto a daguerreotype plate (a gelatin
Ó 2002 American Society for Photobiology 0031-8655/01 $5.0010.00 emulsion containing silver iodide), wavelengths between 340 and
561
562 P. E. Hockberger
400 nm induced a photochemical reaction. This was the first blackened metal to absorb radiation, but each device differed as to
indication of the spectral extent of UV radiation. how the radiation was quantified. The thermopile used a stack of
During the 19th century, physicists made several important tightly packed metal plates to amplify the photoelectric signal. The
theoretical and empirical contributions that helped to clarify the radiometer measured light intensity by the number of revolutions
properties of UV radiation. In 1802, Wollaston expanded on induced over time, and the bolometer measured a decrease in
Newton’s earlier observation that sunlight was composed of electrical resistance upon absorption of radiation. Each provided
different colors by showing that sunlight possesses discrete bands an effective means of measuring radiation throughout the UV–
of light rather than a continuous spectrum. In 1814, Fraunhofer visible–infrared spectrum.
mapped over 500 bands of sunlight, later called ‘‘Fraunhofer Early in the 20th century, new discoveries in photochemistry
lines,’’ some of which are within the UV region. In 1859, Kirchoff and photophysics improved both theoretical and empirical under-
and Bunsen invented the spectroscope and demonstrated that standings of the behavior of electromagnetic radiation. In 1900,
different atoms absorb and emit different wavelengths of light. Planck theorized that radiation is composed of tiny packets of
They speculated that the gaps in the solar spectrum are the result of energy called ‘‘quanta.’’ In 1905, Einstein theorized that Planck’s
selective absorption by atoms in the Earth’s atmosphere. quanta were massless particles of energy (named ‘‘photons’’ in
A major breakthrough in photophysics came in 1865 when 1928 by Lewis) that are released from atoms and molecules upon
Maxwell proposed a theory that light and sound are part of a lar- absorption of light. In 1913, Bohr proposed that electrons absorb
ger spectrum of energy with wave-like properties. He called them the light energy and reemit it at wavelengths that correspond to the
‘‘electromagnetic waves’’ because he believed that they were electron’s energy. In 1926, Schrödinger developed a theory of
generated by the interaction of electric and magnetic fields. In wave mechanics that treated electrons as waves rather than par-
1882, Maxwell’s theory was confirmed by Hertz who developed ticles. These theories provided a new conceptual framework for
a means for measuring microwaves, the first empirical evidence for studies of radiation.
radiation beyond the UV–visible–infrared spectrum. His results About the same time, experimentalists were devising new ways
reinforced the belief that electromagnetic radiation travels in waves to measure the extent of UV radiation. In 1903, Schumann used
at discrete frequencies (or wavelengths). a carbon spark discharge lamp and fluorite prism placed in
The development of artificial lighting provided another source of a vacuum chamber (called a ‘‘vacuum spectrograph’’) to detect the
UV radiation, although this was not appreciated at first. In 1808, emission of hydrogen at 120 nm. In 1906–1908, Lyman used the
Davy invented the ‘‘open’’ arc lamp using charcoal electrodes vacuum spectrograph to detect emission of helium at 50 nm. He
attached to a large Voltaic battery. Unfortunately, the charcoal also demonstrated that oxygen, but not nitrogen, absorbs radiation
electrodes deteriorated in the process. In 1843, Foucault tried between 127 and 176 nm. In 1920, Millikan used a high-intensity
carbon electrodes that were more stable, but the arc was dim. In nickel spark lamp in a vacuum spectrograph to measure the
1876–1877, Jablochkov and Brush bolstered the power of carbon emission of hydrogen at 20 nm. He also detected the emission of
electrodes using the Gramme dynamo and generated the first useful weak X-rays indicating that there was no natural cut-off between
electric arc lamps. In 1898, Bremer introduced fluoride salts into UV and X-rays.
the carbon electrodes that further enhanced their brightness. In Atmospheric scientists helped to establish the relationship
1850, Stokes used aluminum electrodes to produce a ‘‘closed’’ arc between sunlight and UV radiation. In 1902, Langley showed that
lamp in a quartz tube that emitted UV rays to 185 nm. In 1835, the Earth’s atmosphere reduces UV radiation by approximately 40
Wheatstone invented the mercury (Hg) vapor lamp, which was per cent. Based on Lyman’s results, Miethe and Lehman proposed
brighter than previous arc lamps, but it was prone to flicker and in 1909 that oxygen in the upper atmosphere absorbs most of the
deterioration. It would take the contributions of many inventors UV radiation. They determined that the lower limit reaching the
over the next 66 years before Cooper-Hewitt would produce the Earth’s surface was between 291.21 and 291.55 nm. In 1921, Fabry
first commercially viable Hg vapor lamp. and Buisson measured the spectral composition of sunlight and the
In 1802, Davy showed that artificial light was produced by absorption characteristics of ozone. They surmised that ozone in
passing electrical current through a platinum wire. Although simpler the upper atmosphere is responsible for filtering most of the solar
than the open arc lamp, it was not as bright. Nevertheless, in 1820, UV radiation. In 1919, Dorno demonstrated that the intensity of
De La Rue turned Davy’s observation into the first incandescent UV radiation penetrating the atmosphere varies throughout the day
light bulb. In 1879, Swan enhanced the brightness by using a thin (greatest when directly overhead) and with the seasons of the year
carbon filament instead of platinum wire. The same year, Edison (greatest in summer).
patented an incandescent lamp based on a thin cotton filament By 1920, the existence of UV radiation, its properties and
encased in a partly evacuated tube. His lamp burned brighter and relationship with sunlight was well established. The potential for
longer (50 h) than any other incandescent lamp, and it soon replaced commercial and industrial applications shifted the focus to
arc lamps as the most popular form of artificial lighting. In 1906, development of new sources (fluorescent lamps, photoflash lamps,
Coolidge invented the tungsten light bulb. Tungsten is more stroboscopes, lasers, advanced photon source) and better devices
malleable than other metals, allowing it to be coiled; with more for measuring it (filters, detectors, spectrometers). Research on the
wire, it burned brighter and longer than other incandescent bulbs. interaction of UV radiation with atoms, molecules, solutions and
Tungsten also emits a broader spectrum than carbon-based the atmosphere continued. An example of the latter is the work of
filaments, yielding a whiter (and more UV-intensive) light. Molina, Rowland and Crutzen, who have studied the destructive
Another significant development in photophysics was the effect of industrial pollutants on the ozone layer. There was also
invention of devices for quantifying radiation. In 1829, Nobili increasing interest in understanding the effects of UV radiation on
invented the thermopile, and it was improved in 1852 by Melloni. living organisms, especially humans. The connection between
In 1876, Crookes invented the rotating vane radiometer, and in sunlight and UV radiation raised the possibility that many of the
1878 Langley invented the bolometer. All three inventions used effects of sunlight that had been observed over the centuries might
Photochemistry and Photobiology, 2002, 76(6) 563
be due to these invisible rays. As revealed in the following therapeutic influence. By the 18th century, reports began to appear
sections, there is ample evidence supporting such a connection. in the medical literature indicating that sunlight ameliorated
(Note on terminology: During the 20th century, the study of UV different skin diseases. In 1735, Fiennius (cited in 31) described
radiation led to the development of different terminologies. a case in which he cured a cancerous growth on a patient’s lip
Physicists developed a terminology based on the physical using a sunbath. In 1774, Faure (cited in 30) reported that he
properties of UV radiation. They adopted the term ‘‘near UV’’ to successfully treated skin ulcers with sunlight, and in 1776 LePeyre
refer to solar UV that reaches the Earth’s surface, i.e. 290–400 nm. and LeConte (cited in 28) found that sunlight concentrated through
They used the term ‘‘vacuum UV’’ for the region that required a lens accelerated wound healing and destroyed tumors.
a vacuum to measure it, i.e. below 180 nm. They used the term ‘‘far There were also reports that sunlight had beneficial effects on
UV’’ for the region between the near and vacuum UV regions, i.e. internal maladies. In 1782, Harris (cited in 31) used irradiated
180–290 nm. Biologists developed a different terminology that mollusk shells to improve a case of rickets (fragile bones). In 1815,
emphasized the effects of solar UV on living organisms. They used Loebel (32) used facial irradiation to heal a case of amaurosis
the term ‘‘UVC’’ to refer to the solar region that was absorbed by (partial blindness caused by disease of the optic nerve), and in
the ozone layer in the Earth’s upper atmosphere, i.e. below 290 nm, 1845, Bonnet (33) reported that sunlight could be used to treat
and therefore had no biological effect. The term ‘‘UVA’’ was used tuberculosis arthritis (bacterial infection of the joints). In 1879,
for the region 320–400 nm that penetrated window glass and had Martin (34) used stripes of blue and white light to treat progressive
physiological effects on organisms. The term ‘‘UVB’’ was applied degeneration of the optic nerve.
to the region between the UVC and UVA, i.e. 290–320 nm, and Additional observations indicated that sunlight was capable of
this region was believed to be responsible for the deleterious altering basic human physiology. In 1843, Scharling (35) measured
effects of sunlight on living organisms.) reduced production of CO2 in subjects at night, and in 1866 von
Pettenkofer and Voit (36) reported that serum bicarbonate levels
HUMANS, SUNLIGHT AND UV RADIATION were lower at night. In 1850, Berthold (37) found that hair
production was greater in the daytime, and in 1888 Feré (38) noted
Human fascination with sunlight undoubtedly began before the that breathing and pulse rate were reduced under red light. These
dawn of civilization (25–30). Our hominid ancestors must have results were supported by similar data from animal studies (see
recognized its importance for vision and warmth and, eventually, below), but it would be well into the 20th century before the notion
agriculture. Given the sun’s importance and our ancestors’ of daily (circadian) rhythms would take hold.
primitive understanding of the cosmos, it is not surprising that Probably the most remarkable claim during this period was the
they worshiped the sun. Hieroglyphic-, cuneiform- and alphabet- positive influence of sunlight on mental health. This idea can be
based writings indicate that the sun was revered as a god by the traced back to Hippocrates (cited in 39) who recognized that
Egyptians, Assyrians, Persians and Babylonians between 3000 and depression was more common in the winter months in Greece
500 BCE. Archaeological and anthropological evidence suggests when there was less sunlight. In 1806, Pinel (39) identified two
that the sun was also deified by other ancient civilizations types of seasonal depression, one occurring in winter and another
including the Druids, Aztecs, Incas and American Indians. Even in summer. By 1845, his student Esquirol (39) documented several
the ancient Greeks, who were the first to write about the cases of both types of depression. In 1876, Ponza (40) reported that
importance of sunlight in human health, worshiped the sun god light therapy was beneficial for treating patients with mental
Helios. illness. In particular, he found that violet-blue light was useful for
Around 400 BCE, two events of scientific importance occurred reducing mania, whereas red light improved depression. During the
in Greece. The Ionian philosopher Anaxagoras was put on trial for 20th century, phototherapy would be rediscovered several times
promoting the idea that the sun is a big fiery rock, rather than as an effective means for treating seasonal affective disorders
a deity, and the Athenian physician Hippocrates prescribed (41–43).
heliotherapy (sunbathing) for both medical and psychological One of the earliest indications that sunlight might have
purposes. These events initiated a change, albeit a slow one, in detrimental effects involved cases of smallpox. It had been known
human understanding of the relationship between sunlight and for centuries that sunlight aggravated smallpox, although the origin
living organisms. of this connection is unknown. By the time the son of Edward I of
The practice of heliotherapy continued throughout the Greco- England (1239–1307 CE) contracted the disease, it was standard
Roman era, and it appears in the writings of Herodotus (5th century practice to cover patients and windows with scarlet sheets and
BCE), Cicero and Celsus (second century BCE), Vitruvius (first blankets (29). This remedy was widely known and documented
century BCE), Pliny the Elder (23–79 CE), Galen (130–200 CE), as far away as China and Japan during the Middle Ages. Never-
Antyllus (third century CE) and Oribasius (325–400 CE). After the theless, there was virtually no scientific assessment of its effective-
fall of the Roman Empire, the practice apparently fell into oblivion. ness until the 19th century.
It reappeared during the Early Middle Ages, documented by the In 1832, Picton (44) was the first to document the detrimental
Persian scholar and physician Avicenna (980–1037 CE). Sunbath- effects of sunlight on patients with smallpox. He reported that
ing for medical and cosmetic purposes has continued to the present soldiers confined to dungeons during a smallpox epidemic con-
time due to a pervasive cross-cultural belief in the healing power of tracted the disease but recovered without suppuration or scarring.
sunlight. As outlined in the following section, early scientific In 1848, Piorry (45) recommended keeping patients with the dis-
studies supported and reinforced this belief. ease in darkened rooms until the disease passed. In 1867, Black
(46) found that exclusion of sunlight slowed the development of
The health-promoting influence of sunlight
the pustules of smallpox and prevented pit formation. By 1871,
Although heliotherapy has been practiced for at least 2400 years, Waters (47) and Barlow (48) independently confirmed the posi-
there was very little objective evidence supporting its purported tive results of light deprivation on patients with smallpox under
controlled conditions. They noted that the treatment was more hand was not caused by the heat rays of the sun because covering
effective if started early in the disease before eruptions. In 1898, the opposite hand with a black cloth prevented the response even
Chatiniére (49) used similar red light therapy to treat measles. though the air temperature under the cloth was 6–88F warmer.
Despite the widespread success of red light therapy, there was no Furthermore, he found that illumination of the hand of a Negro
agreement as to how it worked. In 1893, Finsen (50) speculated failed to elicit sunburn even though the temperature of the Negro’s
that the chemical rays were detrimental to smallpox patients, skin increased by the same amount as his own.
although he provided no evidence for this or offered any Home was clearly puzzled by his results. He mentioned that he
explanation as to how such rays might aggravate the disease. had experienced a severe burn on the back of his legs 40 years
Four years later, he showed that chemical rays had the opposite earlier during a voyage to the West Indies. This occurred despite
effect in the treatment of lupus vulgaris (cutaneous tuberculosis). In the fact that he was wearing a thin pair of linen trousers. He stated
this case, he demonstrated that the chemical rays from sunlight or ‘‘I could not image how it happened, always suspecting it to be the
an arc lamp had antibacterial actions (see section below on effect of the bites of insects; but I never satisfied myself upon that
microorganisms) and that, under appropriate conditions, it cured subject.’’ Armed with his new results, he surmised that both burns
the disease. For this accomplishment, he was awarded the 1903 were caused by the sun but not by the heat rays. He reasoned that
Nobel Prize in Physiology or Medicine and endowed with financial black skin somehow provided a protective shield against sunburn.
support for the Finsen Light Institute in Copenhagen. When he asked Sir Humphrey Davy for his interpretation of the
results, Davy concluded that the radiant heat of sunlight was
absorbed by black skin and converted into ‘‘sensible’’ heat. There
Diagnostic uses of light
was no indication as to what Davy meant by sensible, but this was
The prospect of using light for diagnostic purposes was initiated by likely an attempt to bring Home’s results in line with the
Richardson in 1868 (cited in 51). Using various light sources, most conventional wisdom.
notably a magnesium arc lamp, he showed that light was Evidence that UV rays could be harmful to people came initially
transmitted through the more lucent structures of living and dead from scientists working with arc lamps. In 1843, Fizeau and
bodies. Absorption of light by internal structures allowed him to Foucault (57) reported problems with their eyes after experiment-
view the obscure outlines of bones of the hand and foot and ing with a carbon arc lamp, and they suspected that it was caused
structures within the cheeks, neck, chest and abdomen. Even by the chemical rays. In 1859, Charcot (58) noted that arc lamps
pulsations within blood vessels were visible although the vessels caused skin burns, and he too believed it was due to the chemical
themselves were indistinct. In an extremely emaciated young rays. In 1889, Maklakoff (59) reported that welders experienced
subject, the beating of the heart was faintly discernable although irritation of the eyes and skin within a few hours of exposure to
the motions of the heart valves were not. He also made similar high-intensity welding arcs. He noted a progression of effects
observations of structures in a frog, chick and carp. In 1870, including acute flu-like symptoms, erythema, pain and delayed
Nicholson (51) succeeded in viewing internal organs of the human pigmentation.
body using a calcium lamp. In 1889, Widmark (60,61) published his landmark studies
In 1898, Gebhard (52) used an arc lamp and daguerreotype plate confirming that UV rays from arc lamps were responsible for skin
to show that light can penetrate the human body. He placed the burns. He showed that burns were induced by the chemical rays of
plate in the palm of his hand and shielded it from light with plaster a carbon arc lamp transmitted through a prism and filtered through
of Paris. When the back of his hand was exposed to the lamp, the water to remove the heat rays. Furthermore, burns were avoided if
plate darkened demonstrating that light had passed completely the lamplight was filtered through window glass, indicating that
through his hand. In 1901, Darbois (53) demonstrated that a piece rays below 320 nm were the primary culprits. These results were
of photographic paper, placed between two glass slides and extended in 1891 by Hammer (62), who found distinct differences
inserted into the mouth and then irradiated with an arc lamp between sunburn caused by chemical and heat rays. He showed
through the cheek, became blackened after 1 min. The previous that heat rays caused redness of the skin that appeared quickly and
year, Kime (54) showed that sunlight was capable of producing an disappeared shortly after exposure (within minutes). Chemical
image on a photographic plate after passing completely through the rays, on the other hand, caused redness that appeared several hours
thorax. Despite these successes, the discovery of X-rays by later, was persistent, and was followed by desquamation (loss of
Röntgen in 1895 and its incredible resolution shifted attention skin) and eventually increased pigmentation. These results were
away from light as a diagnostic tool. It would reappear in the late confirmed by Hausser and Vahle (63) in 1927, and they produced
20th century, however, with the invention of optical coherence the first detailed action spectra for erythema and pigmentation.
tomography (55). Other investigators documented changes in skin attributed to the
chemical rays of sunlight. In 1885, Unna (64) found that sun-
exposed skin was thicker and displayed enhanced keratinization. In
The dark side of sunlight and arc lamps
1890–1892, Berliner (65) and Wolters (66) declared that chemical
Despite numerous observations on the growth-promoting and rays were responsible for sunburn, xeroderma pigmentosum and
healing effects of sunlight, the underlying physiology was poorly Hutchinson’s summer eruptions. By 1894, Unna (67) was con-
understood. For centuries, conventional wisdom assumed that the vinced that UV and, possibly, the violet-blue rays of sunlight
warmth of sunlight simply accelerated the natural growth and were responsible for increased skin thickness, pigmentation and
healing powers of the body. Negative effects, like sunburn skin cancer in sailors. In 1896, Dubreuilh (68) reported that people
(erythema) and blindness caused by sungazing (solar retinopathy), with outdoor (rural) occupations were more prone to skin cancer
were believed to be due to excessive exposure to the sun’s heat. In than those with indoor (urban) occupations.
1821, Home (56) was the first person in the modern era to openly There were also reports of people who were unusually
question this assumption. He argued that sunburn to the back of his susceptible to sunburn. In 1886, Veiel (69) reported a case of
a woman who became sunburned through a window glass. Because Wright (92) recommended using concentrated sunlight or artificial
she was protected by a red veil, Veiel concluded that it was caused light to treat trachoma and corneal ulcers.
by the sun’s chemical rays. In 1898, Anderson (70) reported that Although the above studies focused on the therapeutic effects of
two patients exhibiting seasonal sunburn (hydroa aestivale) light therapy, other investigators studied the body’s natural
possessed an unusual porphyrin-like pigment in their urine. adaptive responses to sunlight. In 1901, Ehrmann (93) reported
Ehrman (71) suggested that this pigment was hematoporphyrin, that skin tanning arises from local stimulation of melanin pro-
although Günther (72) noted that not all patients with porphy- duction inside specialized skin cells (melanoblasts). In 1916,
rinuria were light-sensitive. In 1913, Meyer-Betz (73) confirmed the Jüngling (94) showed that melanin production was enhanced by
photosensitizing properties of hematoporphyrin by administering it light rays longer than 330 nm, whereas sunburn was induced by
to himself. rays below 330 nm. In 1920, With (95) argued that skin thickening
helps protect against the damaging effects of UV rays, and Rollier
(83) reported that heliotherapy for surgical tuberculosis was more
effective in tanned people. These results were interpreted as
The safety of arc lamps and sunbathing is debated
evidence that the body is endowed with natural mechanisms for
By the start of the 20th century, additional reports questioned the regulating the amount of light exposure.
safety of arc lamps and the healthiness of sunbathing. Moeller (74) Rollier also noted that heliotherapy was accompanied by
demonstrated that continuous exposure of skin to an arc lamp increased lymphocyte production (lymphocytosis) suggesting
caused a sequence of changes that included vasodialation, swelling a potential beneficial effect of sunlight on the immune system.
of the extracellular space, hyperplasia of the epidermis and an This observation was consistent with evidence obtained by
abnormal horning process. Hyde (75) described similarities in the Wickline (96) and Chamberlain and Vedder (97) between 1908
damaging action of UV rays, X-rays and radium exposure on skin, and 1911 that showed that lymphocytosis developed gradually
and he presented epidemiological data suggesting that sunlight over many months for Americans living in the Philippines. In
causes skin cancer. 1919, Taylor (98) reported that 25 of 38 adults at a summer retreat
In 1916, Burge (76) argued that glass blower’s cataracts, caused in Massachusetts (USA) displayed an increase in lymphocyte
by arc lamps, are due to absorption of UV rays by the lens proteins production. Although these studies did not control for other
leading to their precipitation. The same year, Verhoeff and Bell environmental variables (e.g. climate and lifestyle changes),
(77) showed that cataracts are caused by an indirect process Aschenheim (99) demonstrated that exposure of infants to direct
initiated by the heat rays of the arc lamp. They found that sunlight, for as little as 1 h, resulted in lymphocytosis. There was
absorption of heat caused damage to the ciliary body leading to also compelling evidence from animal studies that supported these
malformation of the lens. In 1920, Van der Hoeve (78) showed that claims (see below).
absorption of UV rays had the same effect, i.e. damage to the By 1920, the overriding consensus was that sunlight had
ciliary epithelial cells, interfering with the nutrition of the lens. By a positive influence on health. According to Laurens (1), ‘‘at one
1922, Schanz (79,80) argued that both infrared and UV rays are time there was considerable argument as to whether ultra violet
responsible for the cataracts of glass workers. radiation could act directly on deep seated organs, and there are
Despite these observations, many health professionals, especi- still some who believe that this is the case. The only reasonable
ally those working at the Finsen Light Institute, continued to extol conclusion, however, is that following ultra violet irradiation some
the virtues of heliotherapy as long as protective eyewear was used. photochemical substance formed in the skin is carried by the blood
Their advice was bolstered by a growing list of diseases that could stream to these various organs, there bringing about the observed
be treated with heliotherapy including verrucose tuberculides, changes.’’ He continued ‘‘the sun bath by dilating the capillaries
lupus erythematosus, alopcia areata, acne vulgaris and naevus activates the circulation and may induce a continuous tonic action
vascularis planus (50). In addition, investigators from outside of on the sensory nerve terminals in the skin, thus restoring tone to
the Finsen Institute obtained positive results with light therapy. muscles and promoting physiologic processes throughout the body.
Schouli (81) and Festner (cited in 82) used red light to reduce the This is the probable explanation of the increased metabolism of the
severity and duration of scarlet fever and skin inflammation body, of the improvement in general health and of the increased
(erysipelas). Bernhard (cited in 83) and Rollier (83) used Alpine resistance to disease.’’
sunbaths to heal wounds and surgical (extrapulmonary) tubercu- The possibility that sunlight and its associated UV rays might be
losis. Hasselbalch and Jacobaus (84) used a carbon arc lamp to harmful to humans did not take hold until later in the 20th century.
treat cardiac afflictions, and Huldschinsky (85) used sunbaths and This change in attitude was influenced by four main factors. First,
UV rays from an Hg arc lamp to treat rickets. By 1924, Hess experimental studies using animals and microorganisms provided
(86,87) and Steenbock (88) and their colleagues had independently compelling evidence of the damaging effects of UV rays, as
shown that sunlight cured rickets by inducing vitamin D described in the following sections. Second, evidence emerged that
production in the skin. other kinds of radiation (e.g. X-rays, gamma rays) had deleterious
Light was also used successfully to treat diseases of the eye. effects on living organisms fostering the belief that all forms of
Nesnamov (cited in 89) used sunlight through a collecting lens to radiation are harmful. Third, governmental agencies were
treat corneal ulcers. Nicolas (90) used sunlight to treat conjunctival established with the responsibility of supporting health-related
tuberculosis and an Hg arc lamp to treat scrofula and tuberculosis research, and they took a proactive role in funding investigations
of the outer eye. Schanz (80) confirmed Nicolas’s results and added that studied the pathological effects of UV radiation. Fourth,
eyelid eczema to the list of eye diseases treatable with light. Duke- additional epidemiological data indicated a correlation between
Elder (91) showed that UV rays were effective for treating skin cancers and excessive exposure to sunlight. The collective
tubercular and inflammatory eye conditions involving the con- influence of these four factors eventually shifted the opinion of the
junctiva, cornea, iris, ciliary body, choroids and retina. By 1923, scientific community and the public. By the end of the 20th
century, exposure to direct summer sunlight for extended periods enhanced motor activity during illumination. In 1875, Von Platen
was considered a health risk. (112) found that illumination of the frog retina stimulated oxygen
uptake, CO2 production and increased metabolism. The same year,
ANIMALS, SUNLIGHT AND UV RADIATION Pott (113) showed that an individual mouse produced more CO2
under green or yellow light than under violet, red or sunlight. It
Physiological effects
also produced less CO2 at night.
Experimental investigation of the influence of sunlight on animals In 1879, van Pesch (114) found that pea beetles exposed to light
began in the early 19th century. As with the human studies, the consumed more oxygen than those in the dark. Two years later,
earliest observations indicated that sunlight exerted a positive Fubini (115) reported that frogs illuminated after lungectomies
influence on animal health including enhanced growth, develop- generated less CO2 than normal frogs, indicating that the effect was
ment, respiration and metabolism. In addition, there were not just a local skin response. The same year, Moleschott and
physiological studies of the effect of light on contractile tissues, Fubini (116) reviewed the literature and concluded that violet-blue
skin pigmentation, immune response and biological rhythms. light enhanced CO2 production in amphibians, birds and mammals.
There was much interest in whether these effects were mediated They surmised that blinded animals produced less CO2 during
directly through the skin or indirectly through the central nervous illumination and that both the respiratory rate and tissue respiration
system (CNS) via the eyes. There was only occasional mention of were affected. In 1885, Moleschott (117) reported that light-
phototoxic or photophobic responses, although this possibility was induced CO2 production in frogs was mediated locally through the
vigorously investigated during the 20th century. skin as well as through the visual system. By 1887, Fubini and
Growth and development. In 1824, Edwards (100) reported that Spallitta (118) showed that all colors were effective at increasing
sunlight enhanced the rate of development of frog eggs. Twenty- CO2 production, though not to the same degree.
six years later, Higginbothom (101) showed that development of Vision and CNS involvement in light responses. In 1883,
frog and salamander eggs progressed normally in the dark as long Lubbock (119) showed that ants are able to see UV rays, and in
as temperature was controlled. In 1858, Beclard (102) found effects 1914 Van Herwerden (120) found that Daphnia (water fleas)
of light that were not as easy to explain. He noted that eggs of the responded to rays shorter than 334 nm. In 1924, von Frisch (121)
common house fly, Musca, developed faster under violet-blue light demonstrated that bees can perceive rays at 300 nm, and Lutz (122)
compared with green, yellow, red or white light; furthermore, confirmed that bees, wasps and fruit flies see UV rays. In 1924–
green light inhibited their development. In 1874, Schnetzler (103) 1925, Schiemenz (123) and Wolff (124) provided evidence that
found that green light also hindered the development of frog eggs. fish can see the 365 and 340 nm lines of an Hg arc lamp. Recent
In 1878, Yung (104) reported that violet-blue light increased evidence indicates that some birds are also capable of UV vision
development and metabolism of frog, turtle and snail eggs, (125) and that insects (126) and fish (127) are endowed with the
whereas red and green light hindered them. In 1880, Schenk (105) ability to perceive UV polarized light.
found that tadpoles obtained from eggs incubated under red light In 1922, Shoji (128) measured the extent of UV absorption by
were more motile than those obtained from eggs incubated under the cornea in 11 different kinds of animals (including man) and
blue light. showed that it absorbs UV rays shorter than 300 nm. He found the
In addition to studies of egg development, there were reports on average peak absorption of the lens was 366 nm and that
the effect of light on the growth of animals. In 1871, Pöey (106) substantial UV rays were transmitted to the retina in some animals.
reported that General Pleasanton had performed experiments Mayer and Dworski (129,130) used UV rays from a Hg vapor lamp
showing that piglets grew faster under violet light compared with to treat experimentally induced corneal tuberculosis in rabbits and
white light. In 1874, Hammond (107) noted that a 20 day old cat guinea pigs. Under virtually identical conditions, they found the
kept in the dark for 10 days weighed less than its littermate even treatment effective in the rabbits but not in the guinea pigs,
though it had weighed more initially. After 5 days in normal indicating species differences in the effectiveness of the treatment.
lighting, the light-deprived cat weighed the same as its littermate. Although the importance of the retina in vision and its
In 1900, Borissow (108) found that dogs and rabbits grown in light anatomical connection to the CNS were well known by the 19th
weighed more at the end of a month than those grown in dim light. century, the visual transduction process was not understood. In
In 1924, however, Degkwitz (109) was unable to show any effect 1866, Schutze (cited in 31) demonstrated that vertebrate eyes
of light on the growth of puppies so long as their diet and exercise possess two kinds of photoreceptors: rods for dim vision and cones
were carefully controlled. for color vision. In 1877, Boll (131,132) and Kühne (133,134)
In general, the above studies indicated that light had a stimula- independently published their classical studies on visual purple
tory effect on growth and development, although it depended upon (rhodopsin), the photoreceptor pigment of rods, and established
the color of the light. The most consistent stimulatory effects were that it was involved in the detection of light. Sixty years later,
obtained with violet-blue light, although the quality of the filters Hosoya (135) showed that rhodopsin absorbs UV as well as visible
(usually liquids) and the intensities of the light were not addressed. rays. Although UV rays are substantially absorbed by the cornea
Nevertheless, additional studies demonstrated other positive effects and lens, recent evidence indicates that they can affect mate choice,
of chemical (UV and violet-blue) rays on living organisms, as communication, foraging for food and circadian rhythms (136; also
described below. see Indirect Effects [Photosensitization], below).
Respiration and metabolism. In 1858, Beclard (102) noted that Several investigators studied the influence of light on blinded
violet-blue light enhanced CO2 production in adult frogs but not in animals. In 1876, Fubini (137) showed that blinded frogs put on
the birds or mammals he tested. In 1870, Selmi and Piacentini more weight than normal frogs when both were raised under
(110) reported that yellow light enhanced CO2 production in a dog, identical lighting conditions. Both groups displayed accelerated
hen and turtle. In 1872, Chassanowitz (111) confirmed Beclard’s weight gains when light exposure was discontinued. In 1878, Bert
results using frogs and further showed that it was not due simply to (138) confirmed Fubini’s results, and in 1879 Wedensky (139)
demonstrated that blinded frogs oriented their heads towards the dark. In 1874, Pouchet (162) found similar results with other types of
light source so that both halves of their body received equivalent fish raised in darkness. He also noticed that fish with cataracts
exposure. Upon decapitation, he showed that frogs experienced (clouded corneas) were darker than their peers, suggesting
heightened spinal reflexes on the side facing the light. In 1888, involvement of the eyes in the production of pigmentation. In
Wedensky (140) reported that Golowin had discovered that light 1875, Bert (163) confirmed Brücke’s observations on chameleons,
and heat enhance spinal reflexes in the frog. but he proposed that it was caused by a local effect on the skin rather
In 1883, Graber (141) showed that blinded salamaders and than mediated through the eyes (i.e. CNS). Bert (163) and Hoppe-
naturally blind ringworms avoided UV and violet-blue light, and Seyler (164) both showed that chameleons are more responsive to
he suggested that the response was mediated through the skin. In blue light than red or yellow light, indicating that changes in
1890, Dubois (142) confirmed that blinded salamanders displayed pigmentation were unlikely to be due to changes in skin temperature.
an aversion to shorter wavelengths of light, and, in 1895, Finsen Immune system. The effect of light on the immune system was
(50) extended the results to frogs, earthworms, woodlice, beetles first reported by Kondratieff (165), who showed that violet and
and flies. Around the same time, Loeb (143) and Hesse (144) white light enhanced recovery of sepsis-induced infection in
reported that planarians (flatworms) move away from intense rabbits. Furthermore, he found that light increased the severity of
visible light, and Parker and Burnett (145) showed that even sepsis-induced cramps as well as caused an increase in body
blinded planarians are negatively phototaxic. Agreeing with temperature. When sepsis was severe, he noticed that violet and
Graber, they believed that the response was mediated through white light paradoxically decreased the animal’s body temperature.
the skin. As with humans, sunlight stimulates lymphocytosis in animals.
Contractile tissues. Several studies showed that light stimulated In 1908, Polito (166) detected lymphocytosis in rabbits exposed to
the motility of contractile tissues. Between 1844 and 1859, Arnold direct sunlight for as little as 15 min. In 1921, Clark (167) found
(146), Reinhardt (147) and Brown-Sequard (148) observed that similar results with rabbits whose ears were shaved and irradiated
artificial light induced contraction of the iris muscle in the with an iron arc lamp for 1 h. She showed that there was an initial
extracted eyes of eels and frogs. Brown-Sequard further demon- transient drop in lymphocytes within the first few hours after
strated that it was due to a direct effect of light on the pupillary irradiation, followed by an increase that reached a maximum 5
sphincter muscle. In 1892, Steinach (149) extended these results to days after exposure, followed by recovery by the ninth day.
fish and amphibians by showing contraction of the papillary Although all wavelengths between 230 and 750 nm induced the
muscle in response to light in isolated eyes even after carefully initial transient decrease, the subsequent increase was obtained
removing the optic and oculomotor nerves. only with rays between 230 and 320 nm. Whole blood irradiated
In 1857, Marmé and Moleschott (150) found that communica- outside the body and reintroduced showed no such effect. She
tion across the frog neuromusclular junction was enhanced by proposed that UV rays produced a ‘‘cutaneous reflex’’ that
light. In 1879, Uskoff (151) noticed that spontaneous ciliary stimulated lymphocyte-producing organs via the blood stream.
movement of isolated frog epithelial cells was momentarily Some investigators speculated that lymphocytosis helps to
stopped when illumination of the cells was changed from violet- explain both the positive and negative effects of heliotherapy in
blue to red light but not by red light alone. In 1905, Dreyer and humans. In 1919, Murphy and Strum (168) demonstrated that mice
Jansen (152) reported that UV rays caused capillary stasis in the with lymphocytosis show a high degree of immunity to certain
frog’s web, tongue and mesentery. In 1924, Campbell and Hill transplantable tumors as well as enhanced resistance to bacterial
(153) obtained similar results using mesenteries of the frog and infection. Around the same time, Levy (169,170) and Gassul (171)
mouse. reported that UV irradiation of mice between 10 min and 56 h
Other studies demonstrated wavelength-dependent responses in caused progressive engorgement of internal organs (especially the
excitable cells. In 1919, Adler (154) showed that UV, but not spleen) with blood. Clark (167) suggested that this may explain the
visible, rays stimulated smooth muscle contraction in the frog, lung hemorrhaging that was frequently seen after heliotherapy for
rabbit and guinea pig. In 1954, Giese and Furshpan (155) showed tuberculosis.
that low-intensity UV rays increased the frequency of discharge of Biological rhythms. The first evidence of biological rhythms
the stretch receptor of a crayfish muscle, whereas high-intensity originated with the study of plants. In 1729, De Mairan (cited in
UV rays decreased it. In 1957, Pierce and Giese (156) found that 172) showed that leaves display periodic movements even in
high-intensity UV rays reduced the amplitude of action potentials complete darkness that corresponded to day–night cycles. Further
in the axons of frogs and crabs, but irradiation with blue light studies by many investigators confirmed and extended these
immediately afterwards reversed the effect (photoreactivation). In results, as reviewed by Bunning (173). The earliest evidence of
1971, Fork (157) used violet-blue and green laser light to stimulate light-dark cycles in animals was provided by Kiesel (174) in 1894.
action potentials in slug neurons without causing permanent He described cyclical changes in arthropod pigmentation that
damage to the cells. Recently, Yuste and colleagues (158) have persisted in the dark. Thirty years later, Marcovitch (175) found
achieved the same result in mammalian neurons using an infrared that the sexual development of aphids is dependent upon the length
laser and two-photon absorption in the violet-blue region. of daylight.
Skin pigmentation. It is well known that chameleons become Between 1926 and 1932, Bremer (176) showed that pupation in
darker when exposed to direct sunlight. In 1852, Brücke (159) insects is dependent upon light–dark cycles, Beiling (177)
showed that this was the result of pigment cells moving to the demonstrated that the activity of bees is dependent upon the time
surface, and he surmised that the response was mediated through the of day, and Bisonette (178) showed that the breeding behavior of
visual system. Shortly thereafter, Wittich (160) reported that frog ferrets is dependent upon the length of daylight. Rowan (179)
skin became lighter in sunlight, the opposite of chameleons. In 1858, reported that increased daylight enhances gonad development in
DuBois-Reymond (161) found that the skin of the electric catfish, the migratory junco bird. These results and others led Bunning
like frog skin, became brighter in sunlight and turned black in the (180), in 1936, to propose the concept of an endogenous biological
clock in animals modulated by daily cycles of light and dark. In Chronic low-dose solar-simulated UV radiation can cause both
1959, Halberg (cited in 181) coined the term ‘‘circadian rhythms’’ local and systemic immunosuppression (197,198). This has been
to describe these cycles. shown using either UVA or UVB rays. Suppression of the immune
Until recently, most scientists believed that circadian rhythms in system may permit the outgrowth of UV-induced skin tumors.
mammals were modulated only by visible rays. In 1987, Brainard Reproductive system damage. In 1928, Altenburg (199) dem-
and colleagues (182) demonstrated that UVA rays suppressed the onstrated that UV rays cause mutations in fruit flies if the rays
nocturnal production of melatonin in mice, and in 1994 (183) they reach the reproductive organs. One can only wonder whether other
showed that UVA rays altered murine neuroendocrine and insects that are equally unprotected from sunlight and UV radiation
circadian rhythms. In 1995, Amir and Robinson (184) showed are susceptible to similar damage and whether solar-induced
that UVA rays are capable of inducing phase shifts in the mutations contribute to evolutionary changes.
expression of a transcription factor (Fos) in the hypothalamus of Skin cancer. In 1928, Findlay (200) reported that skin tumors
the rat. Very recently, Berson, Yau and colleagues (185,186) have developed in depilated albino mice exposed for 8 months to UV
demonstrated that rat retinal ganglion cells are photosensitive, due rays from a quartz Hg vapor lamp. Exposure of mice to the
to the photosensitive pigment melanopsin that absorbs throughout combination of UV rays and coal tar produced skin tumors in only
the UV and visible spectrum, and that these cells are responsible 3 months. In 1934, Roffo (201) demonstrated that skin cancer
for setting the circadian clock. could be induced in rats by exposure to either sunlight or Hg arc
Cultured cells. During the past decade, several groups have lamps. In 1936, Funding et al. (202) found that 290–320 nm
shown that irradiation of cultured cells with UV rays activates (UVB) was the region of sunlight most responsible for inducing
genes that influence cell division and immune responses. The tumors in experimental animals. These results coincided with
activatable genes include plasminogen activator (187), interleukin- Latarjet’s (203) proposal that changes in atmospheric ozone levels
1 (188), c-fos (189), small proline-rich proteins (190), growth could increase the risk of skin cancer.
arrest and damage-inducible proteins (191), multi-drug resistance In 1941, Blum and associates (204,205) reported that skin cancer
one gene (192) and p53 (193). Many of the UVC-inducible genes could be reproducibly induced in the ears of mice exposed to UV
are activated by a transcription factor complex involving either AP- rays from arc lamps. A single exposure was insufficient, and cancer
1, NFkB or p53 protein (194). In some cases, UVB and UVA rays developed over time in a predictable fashion. Total irradiation dose
induced similar responses. It remains unclear, though, whether was important but not the exposure interval (reciprocity held).
these responses reflect physiological responses to UV rays or Only wavelengths below 320 nm worked. Unlike humans, dermal
pathological effects due to cell injury. tumors in mice were common. The authors speculated that this
could be due to the greater UV penetration of mouse skin. In 1943,
Bain and Rusch (206) showed that UV rays are more effective in
Pathological effects
producing tumors in mice when given at low intensities over long
The possibility that sunlight and artificial sources of UV radiation periods rather than at high intensities over short periods.
might be harmful to nonhuman animals did not arise in force until In 1975, Freeman (207) irradiated mice with a monochrometer at
the 20th century. Nevertheless, there were isolated reports in the intervals between 290 and 320 nm and produced the first action
previous century of inhibitory effects of light. As mentioned above, spectrum for skin cancer. Using daily dosages equivalent to the
Beclard (102), Schnetzler (103) and Yung (104) noticed that green threshold dose for erythema production in untanned human skin,
light inhibited the growth and development of both vertebrate and he found that the peak carcinogenic response occurred at 310 nm.
invertebrate eggs, although the spectroscopic properties of the His results supported the hypothesis that the carcinogenic
filters were not described. Graber (140), Loeb (143), Hesse (144) effectiveness of UV rays is proportional to the erythema effec-
and Finsen (50) reported that various vertebrate and invertebrate tiveness. He speculated that the two effects may have a common or
animals avoided UV and violet-blue light if the intensity was too similar site of action.
high. In 1882, Marshall (195) noticed that the motile larvae of In 1976, Zigman and colleagues (208) showed that longer
sponges accumulated on the side of the tank with less light, and 3 wavelength UV rays from a ‘‘black light’’ are capable of inducing
years later Ultzmann (196) found that isolated sperm survived for skin cancer in mice, a result confirmed by Strickland (209), who
48 h if protected from cold and light. also noted that UVA rays were far more carcinogenic when
Early in the 20th century, the debate in the literature over the combined with UVB. In 1993, Setlow et al. (210) reported that
healthiness of heliotherapy and arc lamps provided the motivation UVA and violet light (420 nm) from high-intensity lamps are
for testing these ideas using animal models. The following studies capable of inducing cutaneous malignant melanoma in fish. In
are examples of pathological responses in animals that were induced 1994, De Gruijl and van der Leun (211) calculated that skin cancer
by exposure to UV rays. In most cases, the investigators employed in hairless mice and humans occurs over a broad region of the solar
high-intensity artificial lights (arc lamps, fluorescent lamps, lasers) spectrum with peaks at 300 and 380 nm, the shorter wavelength
whose spectral emissions were enriched in UV rays. In these cases, region approximately 1000-fold more effective.
the relevance of the results to sunlight is often unclear. The possibility that sunlight can cause mutations in skin cells
Circulatory and immune system damage. Campbell and Hill leading to skin cancer has been supported by studies of tumor
(153) reported that UV rays from either a carbon arc lamp or a Hg biopsies in humans and animals. Brash and colleagues (212,213)
vapor lamp projected through a lens onto frog or mouse mesentery found mutations in the p53 gene in nonmelanoma tumors in
caused localized stasis in capillaries independent of temperature humans, and De Gruijl and associates reported similar mutations in
changes. Similar results were obtained with visible light if the mouse skin irradiated with UVB rays (214). Quantitative studies
tissue was bathed in eosin or hematoporphyrin. The latter induced suggest that this mutation is present in approximately 50% of
the formation of thrombii and localized leukocytosis, whereas UV human basal cell carcinomas and 15% of squamous cell
rays alone induced only leukocytosis. carcinomas (212,215). The incidence of tumors with p53 mutations
is much higher in mice exposed to UVB rays, but approximately Giese (156). The absorbance of UV radiation by nerve cells
the same in mice exposed to UVA rays (216). Because the p53 differed from the action spectrum of the response (i.e. wavelength
gene controls cell cycle regulation, a loss of function mutation in dependence). The absorption peak was between 240 and 270 nm,
this gene could be an early event in the initiation of nonmelanoma whereas the peak of the action spectrum was around 310 nm. This
skin cancers. disparity led Booth and his associates to suggest that thiamin may
Damage to cultured cells. Several investigators have noted that be involved in the response. Lüttgau’s results indicated that UV
illumination of cells through a microscope caused deleterious rays induce a decrease in membrane sodium permeability,
effects. In 1879, Uskoff (151) noted that isolated white blood cells consistent with the possibility of membrane injury. Chalazonitis
displayed greater outgrowth of processes during microscopic (239) showed that the photodynamic action of dyes on nerve cells
examination with red light compared with violet-blue light. In resembled the effect of UV radiation alone, suggesting a common
1915, Lewis and Lewis (217) found that the mitochondria of mechanism.
embryonic chick cells degenerate after 15 min of microscopic Blindness. In 1916, Verhoeff and Bell (77) studied the effect of
observation. They also noted that the mitochondria-specific dye UV rays (below 305 nm) from an Hg arc lamp on the eyes of
Janus green was toxic even in the absence of light. In 1916, rabbits. They found dose-dependent effects on the conjunctiva,
Macklin (218) reported that cultures of embryonic chick heart cornea, iris and lens. At low doses, there was a slight conjunctival
degenerate quickly when illuminated through a microscope using hyperemia but no effect on the other ocular tissues. At medium
daylight, tungsten globe or a Welsbach burner. Degeneration was doses, haziness of the cornea developed. At high doses, there was
exacerbated in the presence of dyes (gentian violet, Janus green), edema and purulent exudation in the cornea and iris. Upon
a result reported previously by Churchland and Russell (219) using microscopic examination, the lens capsular epithelium was
cultured frog pericardial cells. As described in Indirect Effects swollen, and there was a ring of densely packed cells surrounding
(Photosensitization) (below), the result with the dyes probably the exposed region. Some changes emerged 24–48 h after
involved the generation of toxic photoproducts due to the irradiation including shedding of the corneal epithelial cells and
interaction of light with the dyes. leukocyte infiltration of the damaged areas. There was evidence of
Macklin (218) and Kite (220) showed that placing a filter repair after 3–10 days, and by 5 weeks all tissues exhibited marked
between the light source and condensor reduces phototoxicity in recovery. There was no noticeable damage to the retina even with
cultured plant and animal cells. The filter consisted of a glass very intense exposures.
vessel filled with a solution of dye (copper sulphate or copper In 1976, Ham et al. (240) exposed the retinae of monkeys to
acetate) that restricted transmission to wavelengths between 450 high-intensity laser lines from eight monochromatic sources
and 670 nm (actually 280–670; see ref. 221). In 1922, Goodrich between 442 and 1064 nm. The violet-blue lines, but not the
and Scott (222) found that illumination of embryonic chick heart others, caused histological damage similar to that found in retinae
cells with a tungsten–halogen lamp was not harmful if the intensity from patients who gazed voluntarily at the sun for 1 h before
was kept below 280 foot-candles. In 1958, Frederic (223) showed submitting to enucleation for malignant melanoma. Because light
that 90 foot-candles was damaging to cells when using violet-blue transmission through the lens peaks at 470 nm, they argued that
light (436 and 511 nm) but not green, yellow or red light (556, 571 solar blindness is most likely caused by the shorter wavelengths of
and 625 nm). In the presence of Janus green, he noted that even 4 sunlight with possible thermal enhancement induced at longer
foot-candles was toxic. Curiously, these authors failed to cite the wavelengths. Over the next two decades, many investigators would
substantial literature on the toxic effects of light and dyes on other lend support to their hypothesis that violet-blue light is the primary
tissues and organisms. It is unclear whether they were unaware of cause of solar retinopathy (241).
this literature or whether they felt that it was so well known that it Indirect effects (Photosensitization). There are reports in the
did not need to be cited. literature describing enhanced light sensitivity in ancient Egyptian
Between 1932 and 1934, Kemp and Juul (224) and Mayer and and Indian cultures caused by injestion of certain fruits and
Schreiber (225) reported that UV rays retard division of cultured vegetables. There were, apparently, even attempts to treat various
mammalian cells. In 1944, Carlson and Hollaender (226) used medical conditions using diet and light (242). Nevertheless, the first
grasshopper neuroblasts to show that the effects of UV rays on cell scientific reports for such a relationship were noted by Dammann
division depend upon the cell cycle. Early prophase was the most (243) in 1883 and by Wedding (244) in 1887. They reported that
sensitive period, resulting in slower division. In 1974, Wang et al. animals that ate buckwheat in the sunlight developed bubble-
(227) reported that UVA rays killed cultured mammalian cells, forming rashes on their skin only in areas lacking pigmentation.
although they suspected that it was due to toxic photoproducts Wedding hypothesized that sunlight caused a chemical reaction
induced in the culture medium. Between 1978 and 1980, Parshad, with the buckwheat as it traversed the cutaneous blood vessels in
Sanford and colleagues (228,229) determined that UVA and violet- nonpigmented areas. This caused quite a stir and even the famous
blue light had a lethal effect on cultured mammalian cells even scientist Virchow expressed reservations about this interpretation
when irradiated in saline. They provided direct evidence of single- (244). Over time, additional experiments supported Wedding’s
strand DNA breaks and indirect evidence that production of idea, and eventually the scientific community embraced it.
hydrogen peroxide was involved. Peak and Peak (230) confirmed The first kind of supporting evidence came from an unlikely
these results and demonstrated that DNA–protein crosslinking also source. Raab (245) found that Paramecia stained with the
occurs. fluorescent dye acridine red were killed when exposed to visible
Damage to excitable cells. Between 1931 and 1957, many light. He also showed that animals treated with eosin and exposed
investigators demonstrated that exposure to UV rays decreases the to visible light suffered from edema and necrosis in the irradiated
excitability of neurons including Audait (231), Hutton-Rudolph area. While investigating the cause of the toxicity, he found that
(232), Lüthy (233), Booth et al. (234), Boyarsky (235), von Muralt neither the light nor the dye was toxic when given alone.
and Stämpfli (236), Gasteiger (237), Lüttgau (238) and Pierce and Furthermore, the dye was nontoxic if exposed to light separately
and then applied. He concluded that it was the combination of dye searched for it; others fled from it; some grew in it; others were
and light that was responsible for the effect. damaged by it. None lived exclusively in the dark. In 1875,
Between 1900 and 1910, von Tappeiner (Raub’s mentor), Lessona (257) observed that marine pteropods and heteropods
Jodlbauer and their colleagues went on to show that this toxic effect avoided sunlight and only approached the ocean surface at night. In
(which they called ‘‘photodynamic sensitization’’) could be pro- 1879, Engelmann (258,259) obtained results that supported
duced using any fluorescent dye and any wavelength (UV or visible) Schmarda’s observations. He showed that the amoeba Pelomyxa
that excited the dye. This led von Tappeiner (246) to propose that it became immotile upon illumination, whereas the photosynthetic
was the emitted light that was responsible for the toxicity. alga Euglena was attracted to light.
In 1932, Blum (3) reviewed the results of 121 papers related to About this time, Downes and Blunt (cited in 260) made one of
this topic, and he concluded that it was not the light but rather some the most influential discoveries in all of photobiology. They
chemical toxin produced by the interaction of light with the dyes. noticed that direct sunlight inhibited the growth of microorganisms
This effect, he pointed out, was clearly distinct from the direct in test tubes containing Pasteur solution. Illumination for several
effect of UV rays on cells. Photodynamic actions required a dye hours resulted in test tubes free of bacteria for several months (if
or some other chemical to interact with the light, and the response the tube was subsequently sealed with a sterile cotton plug).
was dependent upon the presence of oxygen. The latter was Additional tests revealed that the bactericidal action was dependent
demonstrated by Straub (247), who hypothesized that the photo- upon the intensity, duration and wavelength of sunlight (violet-blue
dynamic effect was due to direct oxidation of cellular con- being the most effective), as well as on the availability of oxygen.
stituents. Blum (3) surmised that cellular damage was an indirect Over the next 20 years, their results were confirmed and extended
effect caused by photooxidation of the dye, resulting in the by numerous investigators who employed various types of bacteria,
generation of a toxic by-product, probably a peroxide. He also growth media and light sources.
ventured that the photosensitivity of range animals feeding on In 1878, Tyndall (260) was the first to confirm Downes and
either buckwheat or St. John’s wort was due to the same kind of Blunt’s observations, but he suggested that it might be due to
photochemical reaction. suppression of bacterial growth rather than a killing action. In
In 1910, Hausmann (248) sensitized mice to visible rays by 1882, Jamieson (260) agreed that sunlight had a bactericidal effect,
injecting them with hematoporphyrin, a natural blood-borne but that it was most likely due to temperature elevation of the
molecule that absorbs violet-blue light. He noticed lympocytosis medium rather than a direct effect on the bacteria. In 1885,
especially near the surface muscles and speculated that damage to Duclaux (260) and Arloing (260) demonstrated that sunlight had
the blood vessels was the primary cause of the sensitization. In a direct killing effect on pure cultures of Tyrothrix scaber and
1919, Adler (249) showed that visible light stimulated skeletal Bacillus anthracis, respectively. Duclaux noted different sensitiv-
muscle if the muscle was sensitized with eosin. In 1928, Earle ities to light between strains. In 1887, Roux (260) confirmed that
(250,251) found that illumination of cultured mammalian cells oxygen was required for the bactericidal effect of sunlight on B.
(fibroblasts and white blood cells) through a microscope was toxic anthracis and its spores. In 1888, Gaillard (260) found that
if red blood cells were present. He presumed that the red blood sunlight was damaging to many kinds of bacteria and spores but
cells produced a toxic by-product when exposed to light. In 1937, not to molds or yeast. He agreed that the rate of destruction was
Büngeler (252) showed that photoactive compounds, which were dependent upon the intensity of sunlight, the composition of the
not inherently carcinogenic, could enhance the carcinogenicity of medium and the presence of oxygen.
light. In 1890, Janowski (260) showed that direct sunlight killed
Based upon Raub’s observations, von Tappeiner (253) predicted Bacillus typhosus in either liquid or gelatin medium. In addition,
that the interaction of light with chemicals could be a useful tool in the effectiveness of sunlight was dependent upon the initial
medicine. To test this idea, von Tappeiner and Jesionek (254) used concentration of bacteria and independent of any effect on the
topical eosin and light exposure to treat human skin tumors. medium. Koch (261) reported that sunlight killed the tubercle
Although they reported some success, it would take most of the 20th bacillus. In 1891, Tizzoni and Cattani (262) found that exposing
century to verify the utility of ‘‘photodynamic therapies’’ (255). the tetanus bacillus to 1 month of sunlight eliminated its lethal
effect when injected into rabbits. This result was obtained only
MICROORGANISMS, SUNLIGHT when the irradiation occurred in the presence of air (oxygen).
AND UV RADIATION Dandrieu (263) showed that sunlight had a sterilizing effect on
water, and he recommended using artificial light as a means of
Microorganisms are single-celled animals that range in size from sterilizing drinking water. In 1887, Klebs (264) noted in his
100 lm to less than 1 lm in diameter. Their existence and role as ‘‘General Pathology’’ textbook that bacteria and other micro-
mediators of infectious diseases were established during the 19th organisms grew best when shielded from light, especially sunlight.
century. Improvements in microscopy allowed scientists to He recommended having bushes removed from pastures suspected
visualize their morphology and behavior as well as to investigate of harboring anthrax because bushes shield the bacillus from
the conditions under which they propagated. It was during this sunlight.
period that scientists discovered the influence of light on these tiny In 1892, Geisler (260) used a prism and heliostat to show that
creatures. Unlike the narratives for humans and nonhuman animals sunlight and electric lamps were lethal to Bacillus typhosus. Using
described above, the damaging effect of sunlight (and UV rays) on quartz test tubes, he demonstrated that UV rays were the most
microorganisms was noticed early on. lethal, although longer wavelengths were damaging at higher
intensities. Buchner (260) developed a very sensitive assay for cell
Pathological responses
death that allowed him to detect the killing action of direct sunlight
In 1845, Schmarda (256) reported that microorganisms found in in as little as 10 min. He ruled out any contribution of infrared rays
stagnant water displayed different responses to light. Some by exposing the cultures through 0.5 m of water. This led him to
speculate that sunlight has a natural sterilizing effect on rivers, anthracis so that, unlike the original bacilli, it was able to obtain
streams and lakes. nitrogen from ammonium salts or amino acids as well as grow in
Between 1893 and 1895, Ward (260) performed a remarkable sugar-containing media. This was the first demonstration of the
series of experiments demonstrating superb technical skill and mutagenic effects of UV rays.
ingenuity. Using improved versions of Buchner’s assay and In 1917, Browning and Russ (283) found no germicidal effect of
Geisler’s apparatus, he showed that violet-blue and near UV a tungsten arc lamp with emission lines longer than 300 nm,
(UVA) rays were the most damaging part of sunlight on bacteria. although no intensity measurements were reported. Bovie and
He also noted that pigmented fungi were resistant, consistent with Hughes (284) found that a sublethal dose of UV rays at 280 nm
the notion that pigments serve as protective filters. Finsen (50) inhibited cell division of Paramecia. They noticed that upon
showed that sunlight concentrated by a lens and passed through the removal of the irradiation, cell division was often accelerated.
ear of a white rabbit was capable of bactericidal action. In 1896, Henri (285) found that egg albumin absorbs rays in the UV region
Westbrook (265,266) showed that the bactericidal effect of leading him to suggest that the bactericidal effect of sunlight is
sunlight was greatest at the surface of cultures, whereas bacterial proportional to protoplasmic absorption. Burge (286), however,
growth was facilitated deeper in the medium due to elevated killed bacteria with UV rays, extracted their enzymes and found
temperature and decreased oxygen availability. that the proteolytic enzymes were unharmed.
In 1893, Richardson (267) showed that sunlight had a sterilizing In 1923, Bayne-Jones and van der Lingen (287) demonstrated
effect on human urine and that irradiation of urine in the presence of that the absorption spectrum of a bacterial emulsion correlated with
oxygen resulted in the generation of hydrogen peroxide. D’Arcy and the wavelength-dependence of the bactericidal action between 185
Hardy (268) showed that UVA and violet-blue rays from a high- and 350 nm. They found no bactericidal action at wavelengths
intensity electric arc lamp stimulated production of an oxidizing longer than 350 nm even at 408C or pH 4.6, conditions that
substance in water, possibly ozone. This, they suggested, might accelerated killing at shorter wavelengths. Coblentz and Fulton
explain the bactericidal action reported by Ward. In 1927, Bedford (288) calculated the total energy needed to kill a single bacterium
(269) showed that UV light stimulated hydrogen peroxide pro- was 19 pW from an Hg arc lamp emitting at 170–280 nm. They
duction in culture medium. This led him to suggest that the demonstrated that continuous and intermittent exposures were
destructive action of UV light on bacteria is caused by the interaction equally effective (reciprocity). Wykoff (289,290) reported that the
of light with photosensitizers in the medium resulting in hydrogen energy required to kill bacteria with X-rays was 100 times less than
peroxide production leading to irreparable damage to the bacteria. that required with even the most potent UV rays (i.e. 265 nm). He
Between 1900 and 1904, Bie (270,271) used a carbon arc lamp calculated that only one in four million absorbed UV photons is
and liquid filters to confirm that violet-blue and UV rays were capable of causing cell death.
lethal to bacteria. He also noted that oxygen was not required for In 1929, Gates (291–293) measured an action spectrum for the
the UV effect (272). In 1901, Strebel (273) showed that UV rays bactericidal effect induced by an Hg arc lamp. The action spectrum
from cadmium and aluminum arc lamps were more powerful than corresponded to the absorption spectrum of nucleic acids with
sunlight for killing bacteria. Bang (274,275) reported that Bacillus a peak response at 265 nm. He proposed that the bactericidal effect
prodigiosus exhibited different sensitivities to UV rays from metal was caused by UV-induced damage to nucleic acids. He also
arc lamps. He recorded lethality with 340–360 (UVA) and 200– noticed that cell division was more sensitive to UV rays than to cell
300 nm (UVC 1 UVB), although the latter region was more growth. In 1945, Tatum and Beadle (294) used Hg arc lamps to
effective, and lethality increased at warmer temperatures. In 1903, induce mutations in Neurospora, supporting a direct effect of UV
Barnard and Morgan (276) used a prism and several types of arc rays on nucleic acids.
lamps to confirm that the greatest bactericidal action occurred at In 1943, Hollaender (295) reported that E. coli were killed with
emission lines between 226 and 328 nm (UVC 1 UVB). light of 350–490 nm (UVA 1 violet-blue), but it required 10 000–
Between 1904 and 1905, Hertel (260) performed the first 100 000 times more incident energy than at 265 nm (UVC). The
rigorous quantitative assessment of the effects of light on response at longer wavelengths was also different in that it
microorganisms. Using a thermopile and galvanometer, he displayed a threshold, temperature coefficient (Q10) of 2 and
demonstrated that UV rays from an arc lamp are several orders caused retarded growth and other sublethal effects. Jagger and
of magnitude more lethal than visible rays. The order of potency colleagues (296) confirmed Hollaender’s observation that UVA
was UVC . UVB . UVA . visible rays. He also observed some rays inhibited bacterial growth as well as cell division in the
interesting cellular behaviors in response to UV rays including absence of exogenous sensitizing agents. Webb and Bhorjee (297)
avoidance, strange locomotory behaviors (circular, screwing and demonstrated that UVA and violet light as low as 5 kJ/m2
rotatory motions), cell contractions and death. completely inhibited the induction of an enzyme in Escherichia
Between 1906 and 1907, Thiele and Wolf (277,278) used carbon coli (b-galactosidase).
and Hg arc lamps to confirm Bie’s observation that the bactericidal Webb (15) reviewed the literature showing that UVA rays cause
action of UVB and UVC wavelengths did not require oxygen, lethal and mutagenic effects in microorganisms even in the absence
whereas killing by UVA–visible rays did. They also noted that of exogenous photosensitizers. Unlike UVB effects, UVA effects
lethality to the longer wavelengths was more pronounced at higher are oxygen-dependent. In 1980, D’Aoust and colleagues (298)
temperatures (30–408C). In 1910, Cernovodeanu and Henri showed that flavins are endogenous photosensitizers that underly
(279,280) argued that the UV action of arc lamps on bacteria the damaging effect of visible light in bacteria. Hartman (299)
was independent of temperature. In 1914, Henri and Moycho (281) reported that irradiation of E. coli with UV rays (300–400 nm)
determined that 280 nm was the most lethal emission line of the arc induced hydrogen peroxide production, a process that probably
lamps, and they calculated that an emission energy of 2 3 105 erg/ involves flavins (300).
cm2 was needed to kill the bacteria. Henri and Henri (282) showed In 1960, Beukers and Berends (301) demonstrated that
that sublethal doses of UV radiation modified the metabolism of B. irradiation of frozen solutions of thymine with UVC resulted in
the formation of thymine dimers, and this eventually led to the (323) showed that purple bacteria, which are normally attracted to
discovery that dimers could be formed between adjacent light, are negatively phototaxic if the intensity is too high. In 1959,
pyrimidines (302). Hanawalt and Setlow (303) showed that DNA Clayton (324) reported that phototaxis of purple bacteria occurs in
synthesis rate in bacteria recovers after UV exposure. In 1964, the absence of oxygen and carbon dioxide.
Setlow and Carrier (304) and Pettijohn and Hanawalt (305) In 1955, Zalokar (325) found increased photocarotenogenesis
independently found that DNA is spontaneously repaired in in Neurospora (fungus) exposed to violet-blue light. Curry and
bacteria after UV exposure. This eventually led to the notion of Gruen (326) demonstrated positive phototropism to violet-blue
nucleotide excision repair (306). light using Phycomyces (fungus). In 1960, Delbrück and
In 1949, Kelner (307) found that the survival of bacteria exposed Shropshire (327) showed that the action spectrum for phototro-
to UV rays is higher if they are illuminated with visible light pism in Phycomyces corresponded to the absorption spectrum of
immediately afterwards (called ‘‘photoreactivation’’). This led to flavinoids. Sargent and Briggs (328) demonstrated that violet-blue
the discovery of the enzyme photolyase, a flavin-based enzyme light altered the circadian rhythm of Neurospora. Diehn (329)
activated by violet-blue light that repairs pyrimidine dimers (308). confirmed Curry and Gruen’s observation using Euglena. In
Studies of DNA repair mechanisms in bacteria have contributed to 1979, Bialcyzyk (330) reported that motile cells of Physarum
unraveling the basis of certain human disease including xeroderma (slime mold) avoided violet-blue light. Recently, Selbach and
pigmentosum and Cockayne syndrome (309,310). There is also Kuhlmann (331) found that Chlamydodon (a ciliated bacterium)
emerging evidence that binding of transcription factors to the is capable of sensing the direction of light and that it is likely
promoter regions of genes can inhibit repair and create hotspots for mediated by a photoreceptor excited by UVA and violet-blue
UV photoproducts (311,312). rays.
Most studies of UVA and violet-blue light responses have
implicated carotenoids and flavins as molecular photoreceptors. In
Physiological responses
1935–1937, Castle (332) and Bünning (333) proposed that
The physiological response of microorganisms to light was first carotenes were involved in phototropism in the fruiting bodies of
noticed by Schmarda (mentioned above), but the first rigorous Phycomyces and Pilobolus (fungi) and in the coleoptiles of the
studies were performed by Engelmann. In 1879, he found that plant Avena. In 1950, Galston (334) proposed the alternative
Euglena was attracted to light (i.e. positively phototaxic) and that ‘‘flavin hypothesis’’ in which riboflavin acts as a photosensitizing
the light sensitivity resided at the base of its flagellum (258,259). In agent in the photooxidation and stimulation of the growth hormone
1883, he demonstrated that phototaxis of other protozoans toward (auxin) indole acetic acid. Forty years later, Galland (335) reported
Euglena was due to light-induced production of oxygen in the that flavins are still regarded as the most common photoreceptors
latter (313). In 1888, he showed that photosynthetic (purple) in blue light responses, although carotenoids and pterins have been
bacteria congregated in the near infrared region of the spectrum, implicated in some cases.
i.e. 800–900 nm (314). He inferred that this was a region of One of the more controversial discoveries is the observation that
absorption by a pigment with properties similar to chlorophyll (he cells produce, transmit and perceive ultraweak electromagnetic
called it ‘‘bacteriochlorophyll’’) that was important for the radiation (also called ultraweak photon emission, low-level
photosynthetic growth of the bacteria. bioluminescence and bioelectromagnetism). The controversy was
In 1888, Loeb (315) proposed that phototaxis of Euglena is due instigated in 1923 by Gurwitsch (336), who reported that dividing
to differential stimulation of their pigmented eyespots (stigma), Paramecia emit weak UV rays (luminescence) that are capable of
rather than direct activation of the flagellum. In 1911, Mast (316) stimulating cell division in other Paramecia. His results were
reported experiments indicating that phototaxis involves both the supported by Alpatov and Nastjukova (337), who showed that the
eyespots and the flagellum. In his model, flagellar motion causes low intensity output from a broadband xenon arc lamp (visible and
the bacterium to rotate; rotation, in turn, causes alternating UV rays) increases the rate of cell division of Paramecia, whereas
exposure of a photoreceptor adjacent to each eyespot (which high intensities reduce it. Hollaender and Claus (338,339),
periodically shades the photoreceptors) producing a succession of however, were unable to obtain a mitogenic effect in bacteria
on–off responses. The latter allows alignment of the axis of the with either UV or visible light. Using sensitive detection
bacterium to the light. In 1915, Buder (317) determined that techniques, Popp (340) and others have measured spontaneous
Euglena oriented toward a light source in the direction of the light emission of low-intensity electromagnetic radiation (visible and
rays, rather than to the light-intensity gradient. Brucker (318) UV) from many types of plant and animal cells including
observed that the threshold for phototaxis in Euglena was raised by mammalian cells. The significance of these emissions, typically
light adaptation. Links (cited in 319) proposed a model for 10–100 photons per second, is still under investigation.
bacterial phototaxis which hypothesized that light-induced eleva-
tion of intracellular ATP activates the flagellar motor.
In 1902, Beijerinck (320) reported that chromogenic bacteria are
CONCLUSIONS
attracted to light. Pieper (319) found that blue-green algae were The discovery of UV radiation and its effects on living organisms
attracted to light greater than 575 nm but were negatively was a gradual process that involved contributions from chemists,
phototaxic to light below 500 nm. Between 500 and 575 nm, he physicists and biologists. When it became clear that UV radiation
found that the reaction was positive in dim light and negative in is a component of sunlight, there was much interest in whether it
bright light. In 1919, Metzner (321) showed that nonphotosynthetic might be responsible for some of the effects of sunlight on living
spirilla became phototactic when impregnated with the photo- organisms. The cumulative evidence to date indicates that UV
senstizing dye eosin. In 1948, Manten (322) proposed that radiation has both beneficial and harmful effects depending upon
phototaxis in purple bacteria results from the sudden decrease in the type of organism, wavelength region (UVA, UVB or UVC) and
the rate of photosynthesis upon leaving the light. In 1956, Schlegel irradiation dose (intensity 3 duration).
The biological data so far are consistent with the following Solar and Ultraviolet Radiation, Vol. 55. World Health Organization,
general statements. First, high doses of either UVC, UVB or UVA United Kingdom.
19. Black, H. S., F. R. de Gruijl, P. D. Forbes, J. E. Cleaver, H. N.
radiation are harmful to all living organisms in the following order:
Ananthaswamy, E. C. deFabo, S. E. Ullrich and R. M. Tyrell (1997)
UVC . UVB . UVA. In the case of UVC and UVB, the cause is Photocarcinogenesis: an overview. J. Photochem. Photobiol. B 40,
direct damage to nucleic acids and proteins that can lead to genetic 29–47.
mutation or cell death. The mechanism underlying UVA damage is 20. Hanawalt, P. C. (2001) Controlling the efficiency of excision repair.
less well understood, but it probably involves the generation of Mutat. Res. 485, 3–13.
21. Burne, D. (1992) Light. Dorling Kindersley, London.
reactive oxygen molecules that can damage many different
22. Luckiesch, M. (1920) Artificial Light, Its Influence on Civilization.
components of cells including nucleic acids and proteins. Second, Century, New York.
low doses of UVA radiation can induce physiological responses in 23. Pincussion, L. (1930) Photobiologie. Thieme, Leipzig.
organisms probably by activating specific genes. The mechanism 24. Houston, R. A. (1938) A Treatise on Light, 7th ed. (Edited by
underlying gene activation is unclear, and it is uncertain whether Longmans). Green. New York.
25. Mead, R. (1748) A Treatise Concerning the Influence of the Sun and
low doses of UVC and UVB radiation can induce similar
Moon Upon Human Bodies, and the Diseases Thereby Produced
responses. Third, many of the physiological and pathological (English translation by T. Stack). Brindley, London.
effects of UVA radiation can be obtained with violet-blue light. 26. Raum, J. (1889) Der gegenwärtige Stand unserer Kenntnisse über den
This is most likley due to a common photochemical transduction Einfluss des Lichtes auf Bacterien und auf den thierischen
process involving flavinoids and carotenoids. Organismus. Z. Hyg. Infektionskr. 6, 312–368.
27. Freund, L. (1904) Elements of General Radio-Therapy for Practi-
tioners (English translation by G. H. Lancashire). Rebman, New
Acknowledgements—I wish to thank Fred Urbach, Thomas Coohill and York.
an anonymous reviewer for their critical reading of the manuscript as 28. Rollier, A. (1923) Heliotherapy. Oxford Medical Publishers, London.
well as helpful comments and suggestions. I am grateful to the following 29. Goodman, H. (1926) The Basis of Light Therapy. Medical Lay Press,
individuals for their assistance in finding many of the references: Ron New York.
Simms and Ramune Kubilius (Galter Health Sciences Library, Northwest- 30. Russell, E. H. and W. K. Russell (1927) Ultraviolet Radiation and
ern University), Stephen Greenberg (National Library of Medicine), Re-
Actinotherapy. William Wood, New York.
becca Woolbert (John Crerar Library, University of Chicago), Rich
31. Giese, A. C. (1964) Historical introduction. In Photophysiology, Vol.
McGowan (Library of the Health Sciences, University of Illinois at
1 (Edited by A. C. Giese), pp. 1–18. Academic Press, New York.
Chicago) and Michelle Carver (Center for Research Libraries, Chicago).
32. Loebel, L. (1815) Wichitige Ansichten über die Berücksichtigung der
I also wish to thank Dennis Valenzeno for his encouragement, advice
Insolation in mehreren Uebelseynsformen, vorzüglich in der Amaur-
and suggestions regarding the scope and content of this review.
ose und über die Realisirung der Idee eines Sonnenbades. J. der pract.
Heilkunde 40, 56–85.
REFERENCES 33. Bonnet, A. (1845) Traite des Maladies des Articulations. Bailliere,
Paris.
1. Laurens, H. (1928) The physiological effects of radiation. Physiol. 34. Martin, E. (1879) De l’emploi de la lumiere bleue conjuguee avec
Rev. 8, 1–91. la lumiere blanche dans le traitement des maladies chroniques de
2. Duggar, B. M. (1936) Effects of radiation on bacteria. In Biological la retine et du nerf optique des bains de lumiere et des verres
Effects of Radiation (Edited by B. M. Duggar), pp. 1119–1149. bichromiques. Gaz. Hopitaux. 52, 115.
McGraw-Hill Co., New York. 35. Scharling, E. A. (1843) Versuche über die Quantität der, von einem
3. Blum, H. F. (1932) Photodynamic action. Physiol. Rev. 12, 23–55. Menschen in 24 Stunden ausgeathmeten, Kohlensäure. Ann. Chem.
4. Blum, H. F. (1945) The physiological effects of sunlight on man. Pharm. 45, 214–242.
Physiol. Rev. 25, 483–530. 36. von Pettenkofer, M. and K. Voit (1866) Über die Kohlensäureaus-
5. Blum, H. F. (1959) Carcinogenesis by Ultraviolet Light. Princeton
scheidung und Sauerstoffaufnahme während des Wachens und
University Press, Princeton, NJ.
Schlafens beim Menschen. Ber. Münchner Akad., Nov. 10 issue.
6. Hollaender, A. (1946) Effects of ultraviolet radiation. Annu. Rev.
37. Berthold, A. A. (1850) Beobachtung über das quantitative Verhältniss
Physiol. 8, 1–16.
der Nagel- und Haarbildung beim Menschen. Arch. Anat. Physiol.
7. Hollaender, A. (1955–1956) Radiation Biology, Vol. 1–3 (Edited by
A. Hollaender). McGraw-Hill, New York. Wiss. Med. January 3 issue, 158–166.
8. Giese, A. C. (1947) Radiations and cell division. Q. Rev. Biol. 22, 38. Fere, C. (1888) Degenerescence et Criminalite; Essai Physiologique.
253–282. Bailliere, Paris.
9. Giese, A. C. (1950) Action of ultraviolet radiation on protoplasm. 39. Wehr, T. A. and N. E. Rosenthal (1989) Seasonality and affective
Physiol. Rev. 30, 431–458. illness. Am. J. Psychiatry 146, 829–839.
10. Giese, A. C. (1964) Studies on ultraviolet radiation action upon 40. Ponza, G. (1876) De l’influence de la lumiere coloree dans le
animal cells. In Photophysiology, Vol. 2 (Edited by A. C. Giese), pp. traitement de la folie. Ann. Med. Psychol., Ser. 5, 15, 20.
203–245. Academic Press, New York. 41. Hasselbalch, K. A. (1905) Die Wirkungen des chemischen Lichtbades
11. Jagger, J. (1967) Introduction to Research in Ultraviolet Photo- auf Respiration und Blutdruck. Skand. Arch. Physiol. 17, 431–472.
biology. Prentice-Hall, Englewood Cliffs, NJ. 42. Siebeck, R. (1946) Gedenktage: Dr. Helmut Marx. Dtsch. Med.
12. Jagger, J. (1983) Physiological effects of near-ultraviolet radiation on Wochenschr. 71, 322.
bacteria. Photochem. Photobiol. Rev. 7, 1–75. 43. Lewy, A. J., H. E. Kern, N. E. Rosenthal and T. A. Wehr (1982)
13. Setlow, R. B. and J. K. Setlow (1972) Effects of radiation on Bright artificial light treatment of a manic-depressive patient with
polynucleotides. Annu. Rev. Biophys. Bioeng. 1, 293–346. a seasonal mood cycle. Am. J. Psychiatry 139, 1496–1498.
14. Urbach, F. and P. D. Forbes (1976) Cutaneous photobiology: past, 44. Picton, J. M. W. (1832) Traitement de la variole par l’exclusion de la
present and future. J. Investig. Dermatol. 67, 209–224. lumiere. Arch. Gen. Med. 30, 406–407.
15. Webb, R. B. (1977) Lethal and mutagenic effects of near-ultraviolet 45. Piorry, P. A. (1848) Traite de Medecine Practique et de Pathologie
radiation. Photochem. Photobiol. Rev. 2, 169–261. Iatrique ou Medicale, Vol. 7, p. 495. Bailliere, Paris.
16. Senger, H. (1982) The effect of blue light on plants and micro- 46. Black, C. (1867) How to prevent pitting on the face by small-pox in
organisms. Photochem. Photobiol. 35, 911–920. persons unprotected by vaccination. The Lancet July 29 issue, 792–
17. Ananthaswamy, H. N. and W. E. Pierceall (1990) Molecular 793.
mechanisms of ultraviolet radiation carcinogensis. Photochem. Photo- 47. Waters, J. H. (1871) Action of light in small-pox. The Lancet Feb. 4
biol. 52, 1119–1136. issue, 151–152.
18. IARC (International Agency for Research on Cancer) (1992) IARC 48. Barlow, W. H. (1871) On the exclusion of light in the treatment of
Monographs on the Evaluation of Carcinogenic Risks to Humans: small-pox. The Lancet July 1 issue, 9–10.
49. Chatiniére, M. (1898) Contagiosite de la Rougeole Sa Phototherapie. 79. Schanz, F. (1922) Phototherapy in eye diseases. Munch. Med.
Presse Med. No. 75, Septembre 10 issue, 78–79. Wochenschr. 69, 1341–1342.
50. Finsen, N. R. (1901) Phototherapy (English translation by J. H. 80. Schanz, F. (1922) Die physikalischen Vorgänge bei der optischen
Sequeira). Edward Arnold Press, London. Sensibilisation und beim Sehakt. Munch. Med. Wochenschr. 69,
51. Anonymous (1872) Dr. Richardson’s researches on the transmis- 215–216.
sion of light through animal structures. The Lancet Oct. 26 issue, 81. Schouli, E. (1899) Die Lichttherapie (Phototherapie) bei Scarlatina. Z.
p. 617. diät. phys. Ther. 3, 612.
52. Gebhard, W. (1898) Die Heilkraft des Lichtes, p. 131. Grieben, 82. Bie, V. (1901) Behandlung von Masern und Scharlach mit
Leipzig. Ausschl. der sog. Chem. Lichtstrahlen. Mitt. Finsens Med. Lysinst.
53. Darbois, P. (1901) Traitement du lupus vulgaire. Thesis, Paris. 2, 146.
54. Kime, J. W. and P. Hortatler (1900) Light as a remedial agent. Med. 83. Rollier, A. (1923) Heliotherapy. Oxford Medical, London.
Rec. (NY) 58, 572–574. 84. Hasselbach, K. A. and H. Jacobaus (1907) Ueber die Behandlung von
55. Huang, D., E. A. Swanson, C. P. Lin, J. S. Schuman, W. G. Stinson, Angina pectoris mit starken Kohlenbogenlichtbäden. Berl. Klin.
W. Chang, M. R. Hee, T. Flotte, K. Gregory, C. A. Puliafito and J. G. Wochenschr. 44, 1247–1252.
Fujimoto (1991) Optical coherence tomography. Science 254, 1178– 85. Huldschinsky, K. (1919) Heilung von Rachitis durch künstliche
1181. Höhensonne. Dtsch. Med. Wochenschr. 45, 712–713.
56. Home, E. (1821) On the black rete mucosum of the Negro, being 86. Hess, A. F. (1924) Experiments on the action of light in relation to
a defence against the scorching effect of the sun’s rays. Philos. Trans. rickets. Trans. Am. Pediatr. Soc. 36, 57.
R. Soc. Lond. B Biol. Sci. (part 1), 1–6. 87. Hess, A. F. (1923–1924) The role of ultraviolet rays in rickets. Atl.
57. Fizeau and Foucault (1843) Observations concernant l’action des Med. J. 27, 467–469.
rayons rouges sur les plaques dagueeriennes. C. R. Hebd. Seances 88. Steenbock, H. (1924) The induction of growth promotive and
Acad. Sci. 23, 679–682. calcifying properties in a ration by exposure to light. Science 60,
58. Charcot, P. (1859) Erytheme produit par l’action de la lumiere 224–225.
electrique. C. R. Seances Soc. Biol. Fil. 5, 63–65. 89. Dworetsky, A. (1902) Die Entwickelung und der gegenwärtige Stand
59. Maklakoff (1889) L’influence de la lumiere voltaique sur les der Lichttherapie in Russland. Z. diät. phys. Ther. 5, 235–250.
teguments du corps humain (l’insolation electrique). Arch. Ophtalmol. 90. Nicolas, F. (1922) A report of three cases of tuberculosis of the
9, 97–113. conjunctiva. Arch. Ophthalmol. 51, 379–383.
60. Widmark, E. J. (1889) Über den Einfluss des Lichtes auf die Haut. 91. Duke-Elder, W. S. (1926) The therapeutic action of ultra-violet light
Hygiea 3, 1–23. upon the eyes. Br. Med. J. 1, 891–895.
61. Widmark, J. (1889) De l’influence de la lumiere sur la peau. Biol. 92. Wright, J. W. (1923) Solarization in trachoma. Am. J. Ophthalmol. 6,
Fören. Forhandl. Verhandlungen Biolog. Vereins 1, 9–13 and 131– 279–280.
93. Ehrmann, S. (1901) Erfahrungen über die therapeutische Wirkung
134.
der Elektricität und der X-Strahlen. Wien. med. Wochenschr. 30,
62. Hammer, F. (1891) Über den Einfluss des Lichtes auf die Haut.
1418–1419.
Ferdinand Enke, Stuttgart.
94. Jüngling, O. (1916) Vergleichende Untersuchungen über dir Wirkung
63. Hausser, K. W. and W. Vahle (1927) Sonnenbrand und Sonnen-
des Sonnenlichtes und des Lichtes der Quecksilber-Quarzlampe
bräunung. In Zellteilung und Strahlung, Vol. 6 (Edited by T. Reiter
(‘‘künstliche Höhensonne’’) auf die Haut. Strahlentherapie 7, 413–438.
and D. Gabor), pp. 101–120. Springer, Berlin.
95. With, C. (1920) Studies on the effect of light on vitiligo. Br. J.
64. Unna, P. (1885) Ueber das Pigment der menschlichen Haut.
Dermatol. 32, 145–155.
Monatsschr. prakt. Dermatol. 4, 277–294.
96. Wickline, W. A. (1908) The effects of tropical climate on the white
65. Berliner, C. (1890) Ueber Hutchinsons Sommererprurigo und
race. Mil. Surgeon 23, 282–289.
Sommereruption. Monatsschr. prakt. Dermatol. 11, 449, 480. 97. Chamberlain, W. P. and E. B. Vedder (1911) A study of Arneth’s
66. Wolters, M. (1892) Beitrag zur Kenntniss der Sclerodermie. Arch. nuclear classification of the neutrophiles in healthy and adult males,
Dermatol. Syphilol. 24, 695–738 and 943–981. and the influence thereon of race, complexion and tropical residence.
67. Unna, P. (1894) Carcinom der Seemanshaut. In Lehrbuch der Philipp. J. Sci. 6, 405–419.
speciellen pathologischen, Vol. 6 (Edited by J. Orth, H. Steinbrügge, 98. Taylor, H. D. (1919) Effect of exposure to the sun on the circulating
P. G. Unna and R. Greeff), p. 719. August Hirschwald, Berlin. lymphocytes in man. J. Exp. Med. 29, 41–51.
68. Dubreuilh, W. (1896) Des Hyperkeratoses circonscriptes. Ann. 99. Aschenheim, E. (1913) Der Einfluss der Sonnenstrahlen auf die
Dermatol. Syphiligr. 7, 1158–1204. leukocytäre. Blutzusammensetzung. Z. Kinderheilkd. 9, 87–98.
69. Veiel, T. (1887) Ueber einen Fall von Eczema solare. Arch. Dermatol. 100. Edwards, W. F. (1824) De l’influence des agens physiques sur la vie,
Syphilol. 19, 1113–1116. Vol. 16, pp. 12, 13, 396. Crochard, Paris.
70. Anderson, T. M. (1898) Hydroa aestivale in two brothers complicated 101. Higginbothom, J. (1850) Influence of physical agents on the
with the presence of haematoporphyrin in the urine. Br. J. Dermatol. development of the tadpole of the Triton and the frog. Philos. Trans.
10, 1–4. R. Soc. Lond. B Biol. Sci. 140, 431–436.
71. Ehrmann, S. (1909) Weitere Untersuchungen über Lichtwirkung bei 102. Beclard, J. (1858) Note relative a l’influence de la lumiere sur les
Hydroa aestivalis (Bazin), Summereruption (nach Hutchinson). Arch. animaux. C. R. Hebd. Seances Acad. Sci. 46, 441–443.
Dermatol. Syphilol. 97, 75–86. 103. Schnetzler, M. J.-B. (1874) De l’influence de la lumiere sur le
72. Günther, H. (1912) Die Haematoporphyrie. Dtsch. Arch. Klin. Med. developpement des larves des grenouilles. Bibl. Univ. Arch. Sci. Phys.
105, 89–146. Nat. 51, 247–258.
73. Meyer-Betz, F. (1913) Untersuchungen über die biologische (photo- 104. Yung, E. (1878) De l’influence des differentes couleurs du spectre sur
dynamische) Wirkung des Hämatoporphyrins und anderer Derivate le developpement des animaux. C. R. Hebd. Seances Acad. Sci. 87,
des Blut- und Gallenfarbstoffs. Dtsch. Arch. Klin. Med. 112, 476–503. 998–1000.
74. Moeller, M. (1900) Der Einfluss des Lichtes auf die Haut in gesunden 105. Schenk, S. (1880) Zur Lehre über den Einfluss der Farbe auf das
und krankhaften Zustande. E. Nägele, Stuttgart. Entwickelungsleben der Thiere. In Mittheilungen aus dem Embry-
75. Hyde, J. N. (1906) On the influence of light in the production of ologischen Institute der K.K. Universitat in Wien, Vol. 1, pp. 265–
cancer of the skin. Am. J. Med. Sci. 131, 1–22. 277. University of Wien, Wien.
76. Burge, W. E. (1916) The mode of action of ultra-violet radiation in 106. Pöey, A. (1871) Influence de la lumiere violette sur la croissance de la
injurying living cells with special reference to those constituting the vigne, des cochons et des taureaux. C. R. Hebd. Seances Acad. Sci.
eye. Am. J. Physiol. 39, 335–344. 73, 1236–1238.
77. Verhoeff, F. H. and L. Bell (1916) The pathological effects of radiant 107. Hammond, W. A. (1874) Some points relevant to the sanitary
energy upon the eye. Proc. Am. Acad. Arts Sci. 51, 629–818. influence of light. The Saniarian. 1, 58–63.
78. van der Hoeve, J. (1920) Eye lesions produced by light rich in 108. Borissow, P. (1902) Zur Lehre von der Wirkung des Lichtes und der
ultraviolet rays. Senile cataract, senile degeneration of macula. Am. J. Dunkelheit auf den thierischen Organismus. Z. diät. phys. Ther. 5,
Ophthalmol. 3, 178–194. 337–338.
109. Degkwitz, R. (1924) Über Einflüsse der Ernährung und der Umwelt 136. Hunt, D. M., S. E. Wilkie, J. K. Bowmaker and S. Poopalasundaram
auf wach sende Tiere. Z. Kinderheilkd. 37, 27–97. (2001) Vision in the ultraviolet. Cell. Mol. Life Sci. 58, 1583–1598.
110. Selmi, A. and G. Piacentini (1870) Dell influenza del raggi colorati 137. Fubini, S. (1876) Ueber den Einfluss des Lichtes auf das
sulla respiratione. Rend. Ist. Lomb. Sci. Lett. Milan 3, 51–56. Körpergewicht der Thiere. Untersuchungen zur Naturlehre des
111. Chassanowitz, J. (1872) Ueber den Einfluss des Lichtes auf die Menschen und der Thiere 11, 488–503.
Kohlensäureausscheidung im thierischen Organismus. Inaugural- 138. Bert, P. (1878) Influence de la lumiere sur les etres vivants. L’Abeille
dissertation. Königsberg. Med. 7, 981–990.
112. Von Platen, O. (1875) Ueber den Einfluss des Auges auf den 139. Wedensky, N. (1879) Ueber die Wirkung des Lichtes auf die
thierischen Stoffwechsel. Pfluegers Arch. 11, 272–290. Erregbarkeit der Haut bei Fröschen. Bull. Acad. Imperiale Sci. St.
113. Pott, R. (1875) Vergleichende Untersuchungen über die Mengenver- Petersbourg, p. 349.
hältnisse der durch Respiration und Perspiration ausgescheidenen 140. Wedensky, N. (1888) Das Tagebuch der III. Versammlung der
Kohlensäure bei verscheidenen Thierspecies in gleichen Zeiträumen, Gesellschaft rüssischer Aerzte. December 31 issue, no. 2.
nebst einigen Versuchen über Kohlensäureausscheidung desselben 141. Graber, V. (1883) Fundamentalversuche über die Helligkeits- und
Thieres unter verschiedenen physiologischen Bedingungen. Habil- Farbenempfindlichkeit augenloser und geblendeter Thiere. Sitzungs-
itationsschrift, Jena. ber. Math-Nat. Kl. kaiser. Akad. Wiss. 87, 201–236.
114. Van Pesch, F. J. (1879) Eenige verschijnselen bij de ademhaling van 142. Dubois, R. (1890) Sur la perception des radiations lumineuses par la
kleine kevers. Mandblad Naturwet. 9, 116–120. peau, chez les protees aveugles des grottes de la Carniole. C. R. Hebd.
115. Fubini, S. (1881) Ueber den Einfluss des Lichtes auf die Kohlensäure- Seances Acad. Sci. 110, 358–361.
Ausscheidung bei den Batrachiern nach Wegnahme der Lungen. 143. Loeb, J. (1893) Ueber künstliche Umwandlung positiv heliotropischer
Untersuchungen Nat. Menschen Thiere 12, 100–111. Thiere in negativ heliotropische und umgekehrt. Pfluegers Arch. 54,
116. Moleschott, J. and S. Fubini (1881) Ueber den Einfluss gemischten 81–107.
und farbigen Lichtes auf die Ausscheidung der Kohlensäure bei 144. Hesse, R. (1897) Untersuchungen über die Organe der Lichtempfind-
Thieren. Untersuchungen Nat. Menschen Thiere 12, 266–428. lichung bei neiderer Thieren: II. Die Augen der Plathelminthen,
117. Moleschott, J. (1885) Ueber den Einfluss des Lichtes auf die Menge insoderheit der tricladen Tubellarien. Z. Wiss. Zool. 62, 527–
der vom Thierkörper ausgeschieden Kohlsäure. Wien. Med. Wo- 582.
chenschr. 35, 1081, 1109, 1137. 145. Parker, G. H. and F. L. Burnett (1901) The reactions of Planarians,
118. Fubini, S. and F. Spallitta (1887) Influenza della luce monochromatica with and without eyes, to light. Am. J. Physiol. 4, 373–385.
sulla espurgazione di acido carbonico. Arch. Sci. Med. (Torino) 11, 146. Arnold, F. (1844–1951) Handbuch der Anatomie des Menschen, mit
315–333. besonderer Rücksicht auf Physiologie und praktische Medicin, Vol.
119. Lubbock, J. (1883) Observations on ants, bees and wasps—part X. II. Emmerling, Freiburg.
With a description of a new genus of honey ant. Zool. J. Linn. Soc. 17, 147. Reinhardt (1843) Det Kongelige danske Videnskabernen Selskabs.
41–52.
Isis (edited by L. Oken). 12, 732–734.
120. Van Herwerden, M. A. (1914) Ueber die Perzeptionsfähigkeit des
148. Brown-Sequard, C. E. (1859) Recherches de experimentales sur
Daphnienauges für untraviolette Strahlen. Biol. Zentbl. 34, 213–216.
l’influence excitatrice de la lumiere, du froid et du la chaleur sur l’iris,
121. Von Frisch, K. (1924) Sinnesphysiologie und ‘‘Sprache’’ der Bienen.
dans les cinq classes d’animaux vertebres. J. Physiol. Homme Anim 2,
Naturwissenschaften 12, 981–987.
281–294, 451–460.
122. Lutz, F. E. (1924) Apparently non-selective characters and combina-
149. Steinach, E. (1892) Untersuchungen zur vergleichenden Physiologie
tions of characters including a study of ultraviolet in relation to
der Iris. Pfluegers Arch. 52, 495–525.
the flower-visiting habits of insects. Ann. N. Y. Acad. Sci. 29,
150. Marmé, W. and J. Moleschott (1857) Ueber den Einfluss des Lichtes
181–283.
123. Schiemenz, F. (1924) Über den Farbensinn der Fische Z. Vgl. Physiol. auf die Reizbarkeit der Nerven. Untersuchungen Nat. Menschen
1, 175–220. Thiere 1, 15–51.
124. Wolff, H. (1925) Das Farbenunterscheidungsvermögen der Ellritze. Z. 151. Uskoff, N. (1879) Einfluss von farbingem Lichte auf das Protoplasm
Vgl. Physiol. 3, 279–329. des Tierkörpers. Centralbl. Med. Wiss. 25, 449–450.
125. Pearn, S. M., A. T. Bennett and I. C. Cuthill (2001) Ultraviolet vision, 152. Dreyer, G. and H. Jansen (1905) Über den Einfluss des Lichtes auf
fluorescence and mate choice in a parrot, the budgerigar Melopsittacus tierisches Gewebe. Mitt. Finsens Med. Lysinst. 9, 180–191.
undulatus. Proc. R. Soc. Lond. B 268, 2273–2279. 153. Campbell, A. and L. Hill (1924) The effects of light upon leucocytes
126. Wehner, R. (1989) Neurobiology of polarization vision. Trends and blood-vessels in the mesentery of the living animal. Br. J. Exp.
Neurosci. 12, 353–359. Pathol. 5, 317–327.
127. Hawryshyn, C. W. (2000) Ultraviolet polarization vision in fishes: 154. Adler, L. (1919) Über Lichtwirkungen auf überlebende glattmuske-
possible mechanisms for coding e-vector. Philos. Trans. R. Soc. Lond. lige Organe. Arch. Exp. Pathol. Pharmakol. 85, 152–177.
B Biol. Sci. 355, 1187–1190. 155. Giese, A. C. and E. J. Furshpan (1954) Ultraviolet excitation of
128. Shoji, Y. (1922) Untersuchung uber die Absorption der ultravioletten a stretch receptor. J. Cell. Comp. Physiol. 44, 191–201.
Strahlen durch die Augenmedian. Mitt. Med. Fak. Kais. Univ. Tokyo 156. Pierce, S. and A. C. Giese (1957) Photoreversal of ultraviolet injury to
29, 61–129. frog and crab nerves. J. Cell. Comp. Physiol. 49, 303–317.
129. Mayer, E. and M. Dworski (1924) Studies with ultraviolet light. I. The 157. Fork, R. L. (1971) Laser stimulation of nerve cells in aplysia. Science
effect of quartz-mercury-vapor irradiations (Alpine quartz-light) on 171, 907–908.
experimental tuberculosis of the cornea in rabbits. Am. Rev. Tuberc. 158. Hirase, H., V. Nikolenko, J. H. Goldberg and R. Yuste (2002)
10, 146–156. Multiphoton stimulation of neurons. J. Neurobiol. 51, 7–247.
130. Mayer, E. and M. Dworski (1924) Studies with ultraviolet light. II. 159. Brücke, E. (1852) Ueber die Zunge der Chamäleons. Sitzungsber.
The action of quartz-mercury-vapor irradiation on inhalation tuber- Math-Nat. Kl. kaiser. Akad. Wiss. 8, 65–70.
culosis in primarily infected and sensitized guinea pigs. Am. Rev. 160. Wittich, V. (1854) Die grüne Farbe der Haut unserer Frösche, ihre
Tuberc. 10, 157–165. physiologischen und pathologischen Veränderungen. Arch. Anat.
131. Boll, F. (1877) Sull’anatomia e Fisiologia della Retina. pp. 1–24. Physiol. Wiss. Med. 41–59.
Roma. 161. DuBois-Reymond, E. (1858) Ueber lebend nach Berlin gelangte
132. Boll, F. (1877) Zur Anatomie und Physiologie der Retina. Centralbl. Zitterwelse aus West-Afrika. Untersuchungen Nat. Menschen Thiere
Med. Wiss. 15, 230–233. 5, 109–136.
133. Kühne, W. (1878) On the photochemistry of the retina and on visual 162. Pouchet, M. G. (1874) Ueber die Wechselbeziehung zwischen der
purple (English translation by Michael Foster). McMillan, London. Netzhaut and der Hautfarbe einiger Thiere. Medizinische Jährbucher
134. Kühne, W. (1878) Ueber die Farbstoffe der Vogelretina. Centralbl. (Wien), 42–44.
Med. Wiss. 16, 1–2. 163. Bert, P. (1875) Des changements de couleur du cameleon. Gaz. Hebd.
135. Hoyosa, Y. (1937) Veranderung der Absorption und der Farbe des Med. Chir. 12, 731.
Sehpurpurs durch Bestrahlung im sichtbaren und ultavioletten 164. Hoppe-Seyler, F. (1881) Physiologische Chemie, p. 25. Hirschwald,
Spektralgebiet. Jap. J. Med. Sci. III. Biophys. 4, 49–52. Berlin.
165. Kondratieff (1880) Einige Versuche über den Verlauf der bei Thieren 191. Fornace, A. J. (1992) Mammalian genes induced by radiation;
künstlich erzeugten Sepsis unter dem Einfluss verschiedenartiger activation of genes associated with growth control. Annu. Rev. Genet.
Belichtung. Inaugural-Dissertation, St. Petersburg. 26, 507–526.
166. Polito, G. (1908) L’influenza dei raggi solari sul sangue. Gazz. Int. 192. Uchiumi, T., K. Kohno, H. Tanimura, K.-I. Matsuo, S. Sato, Y.
Med. Chir. 11, 329–331. Uchida and M. Kuwano (1993) Enhanced expression of the human
167. Clark, J. H. (1921) The action of light on the leucocyte count. Am. J. multidrug resistance one gene in response to UV light irradiation. Cell
Hyg. 1, 39–62. Growth Differ. 4, 147–157.
168. Murphy, J. B. and E. Strum (1919) The lymphocytes in natural and 193. Liu, M., K. R. Dhanwada, D. F. Birt, S. Hecht and J. C. Pelling (1994)
induced resistance to transplanted tumors in mice. J. Exp. Med. 29, Increase in p53 protein half-life in mouse keratinocytes following UV-
25–40. B irradiation. Carcinogenesis 15, 1089–1092.
169. Levy, M. (1916) Über anatomische Veränderungen an der Milz der 194. Tyrrell, R. M. (1996) Activation of mammalian gene expression by
Mansnach Bestrahlung mit ultraviolet Licht. Strahlentherapie 7, 602– the UV component of sunlight–-from models to reality. Bioessays 18,
609. 139–148.
170. Levy, M. (1916) Der Einfluss ultravioletter Strahlen auf die inneren 195. Marshall, A. M. (1882) Die Ontogenie von Reniera filigrand O. Schm.
Organe der Maus. Strahlentherapie 9, 618–623. Z. Wiss. Zool. 37, 221–246.
171. Gassul, R. (1920) Experimentelle Studien über die biologische 196. Ultzmann, R. (1885) Ueber Potentia generandi und Potentia coeundi.
Wirkung des Quecksilber-Quarzlichtes (‘‘künstliche Hohensonne’’) Wien. Klin. 11, 1–32.
auf die inneren Organe. Strahlentherapie 9, 232–238. 197. Kripke, M. L. (1984) Immunologic unresponsiveness induced by UV
172. Anonymous (1729) Observation botanique. Histoire de l’Academie radiation. Immunol. Rev. 80, 87–102.
Royale des Sciences. Avec les Memoires de Mathematique et de 198. Halliday, G. M., R. Bestak, K. S. Yuen, L. L. Cavanagh and R. St. C.
Physique, pour la meme Annee, p. 35–36. Panckoucke, Paris. Barnetson (1998) UVA-induced immunosuppression. Mutat. Res.
173. Bunning, E. (1960) Opening address: biological clocks. Cold Spring 422, 139–145.
Harbor Symp. Quant. Biol. 25, 1–9. 199. Altenburg, E. (1928) The limit of radiation frequency effective in
174. Kiesel, A. (1894) Untersuchungen zur Physiologie des facettierten producing mutations. Am. Nat. 62, 540–545.
Auges. Sitzungsber. Math-Naturwiss. Kl. kaiser. Akad. Wiss. 103, 97– 200. Findlay, G. M. (1928) Ultra-violet light and skin cancer. The Lancet
139. Nov. 24 issue, 1070–1073.
175. Marcovitch, S. (1924) The migration of Aphididae and the appearance 201. Roffo, A. H. (1934) Cancer et soleil. Bull. Assoc. Fr. Etud. Cancer 23,
of sexual forms as affected by the relative length of the daily light 590–616.
exposure. J. Agric. Res. 27, 513–522. 202. Funding, G., O. M. Henriques and E. Rekling (1936) Über Licht-
176. Bremer, H. (1926) Über die tageszeitliche Konstanz im Schlüpfter- kanzer. In Internationaler Kongress für Lichtforschung 3rd ed., pp.
mine der Imagines einiger Insekten. Z. Wiss. Insektenbiol. 21, 209– 166–168. International Congress on Light, Wiesbaden.
216. 203. Latarjet, R. (1935) Influence de l’ozone atmospherique sur l’activite
177. Beiling, L. (1929) Über das Zeitgedächtnis der Bienen. Z. Vgl. biologique du rayonnement solaire. Rev. Opt. Theor. Instrum. 14,
Physiol. 9, 259–338. 398–411.
178. Bisonette, T. H. (1932) Studies on the sexual cycle in birds. VI. 204. Blum, H. F., J. S. Kirby-Smith and H. G. Grady (1941) Quantitative
Effects of white, green, and red lights of equal luminous intensity on
induction of tumors in mice with ultraviolet radiation. J. Natl. Cancer
the testis activity of the European starling (Sturnus vulgaris). Physiol.
Inst. 2, 259–268.
Zool. 5, 92–123.
205. Kirby-Smith, J. S., H. F. Blum and H. G. Grady (1941) Penetration of
179. Rowan, W. (1926) On photoperiodism, reproductive periodicity, and
ultraviolet radiation into skin, as a factor in carcinogenesis. J. Natl.
the annual migration of birds and certain fishes. Proc. Boston Soc.
Cancer Inst. 2, 403–412.
Nat. Hist. 38, 147–189.
206. Bain, J. A. and H. P. Rusch (1943) Carcinogenesis and ultraviolet
180. Bunning, E. (1936) Die endogene Tagesrhythmik als Grundlage der
radiation of wavelength 2800–3400A. Cancer Res. 3, 425–430.
photoperiodischen Reaktion. Ber. Dtsch. Bot. Ges. 54, 590–607.
207. Freeman, R. G. (1975) Data on the action spectrum for ultraviolet
181. Aschoff, J. (1965) Circadian rhythms in man. Science 148, 1427–1432.
182. Benschoff, H. M., G. C. Brainard, M. D. Rollag and G. R. Lynch carcinogenesis. J. Natl. Cancer Inst. 55, 1119–1121.
208. Zigman, S., E. Fowler and A. L. Kraus (1976) Black light induction of
(1987) Suppression of pineal melatonin in Peromyscus leucopus by
different monochromatic wavelengths of visible and near-ultraviolet skin tumors in mice. J. Investig. Dermatol. 67, 723–725.
light (UV-A). Brain Res. 420, 397–402. 209. Strickland, P. T. (1986) Photocarcinogenesis by near-ultraviolet
183. Brainard, G. C., F. M. Barker, R. J. Hoffman, M. H. Stetson, J. P. (UVA) radiation in sencar mice. J. Investig. Dermatol. 87, 272–275.
Hanifin, P. L. Podolin and M. D. Rollag (1994) Ultraviolet regulation 210. Setlow, R., E. Grist, K. Thompson and A. D. Woodhead (1993)
of neuroendocrine and circadian physiology in rodents. Vision Res. Wavelengths effective in induction of malignant melanoma. Proc.
34, 1521–1533. Natl. Acad. Sci. USA 90, 6666–6670.
184. Amir, S. and B. Robinson (1995) Ultraviolet light entrains rodent 211. De Gruijl, F. R. and J. C. Van der Leun (1994) Estimate of the
suprachiasmatic nucleus pacemaker. Neuroscience 69, 1005–1011. wavelength dependency of ultraviolet carcinogenesis in humans and
185. Hattar, S., H.-W. Liao, M. Takao, and D. M. Berson and K.-W. Yau its relevance to the risk assessment of a stratospheric ozone depletion.
(2002) Melanopsin-containing retinal galglion cells: architecture, Health Phys. 67, 320–325.
projections, and intrinsic photosensitivity. Science 295, 1065–1070. 212. Brash, D. E., J. A. Rudolph, J. A. Simon, A. Lin, G. J. McKenna, H.
186. Berson, D. M., F. A. Dunn and M. Takao (2002) Phototransduction P. Baden, A. J. Halperin and J. Ponten (1991) A role for sunlight in
by retinal ganglion cells that set the circadian clock. Science 295, skin cancer: UV-induced p53 mutations in squamous cell carcinoma.
1070–1073. Proc. Natl. Acad. Sci. USA 88, 10124–10128.
187. Mishkin, R. and R. Ben-Ishai (1982) Induction of plasminogen 213. Ziegler, A., D. J. Leffell, S. Kunala, H. W. Sharma, M. Gailani, J. A.
activator by UV light in normal and xeroderma pigmentosum Simon, A. J. Halperin, H. P. Baden, P. E. Shapiro, A. E. Bale and D.
fibroblasts. Proc. Natl. Acad. Sci. USA 78, 6236–6240. E. Brash (1993) Mutation hotspots due to sunlight in the p53 gene of
188. Kupper, T. S., A. O. Chua, P. Flood, J. McGuire and U. Gubler (1987) nonmelanoma skin cancers. Proc. Natl. Acad. Sci. USA 90, 4216–
Interleukin one gene expression in cultured human keratinocytes is 4220.
augmented by ultraviolet radiation. J. Clin. Investig. 80, 430–436. 214. Berg, R. J., H. J. Van Kranen, H. G. Rebel, A. De Vries, W. A. Van
189. Büscher, M., H. J. Rahmsdorf, M. Litfin, and M. Karin and P. Vloten, C. F. Van Kreijl, J. Van Der Leun and F. R. De Gruijl (1996)
Herrlich (1988) Activation of the c-fos gene by UV and phorbol ester: Early p53 alterations in mouse skin carcinogenesis by UVB radiation:
different signal transduction pathways converge to the same enhancer immunohistochemical detection of mutant p53 protein in clusters of
element. Oncogene 3, 301–311. preneoplastic epidermal cells. Proc. Natl. Acad. Sci. USA 93, 274–
190. Kartasova, T. and P. van de Putte (1988) Isolation, charcterization, 278.
and UV-stimulated expression of two families of genes encoding 215. Moles, J.-P., C. Moyret, B. Guillot, P. Jeanteur, J.-J. Guilhou, C.
polypeptides of related structure in human epidermal keratinocytes. Theillet and N. Basset-Seguin (1993) p53 gene mutations in human
Mol. Cell. Biol. 8, 2195–2203. epithelial skin cancers. Oncogene 8, 583–588.
216. Van Kranen, H. J., A. De Laat, J. Van De Ven, P. W. Wester, A. De 242. Ackroyd, R., C. Kelty, N. Brown and M. Reed (2001) The history of
Vries, R. J. W. Berg, and C. F. Van Kreijl and F. R. De Gruijl (1997) photodetection and photodynamic therapy. Photochem. Photobiol. 74,
Low incidence of p53 mutations in UVA (365-nm)-induced skin 656–669.
tumors on hairless mice. Cancer Res. 57, 1238–1240. 243. Dammann, C. (1883) Gesundheitspflege der landwirthschaftlichen
217. Lewis, M. R. and W. H. Lewis (1915) Mitochondria (and other Haussäugethiere, pp. 411–414. Parey, Berlin.
cytoplasmic structures) in tissue cultures. Am. J. Anat. 17, 339–401. 244. Wedding, M. (1887) Einfluss des Lichtes auf die Haut der Thiere. Z.
218. Macklin, C. C. (1916) Binucleate cells in tissue cultures. Contrib. Ethnol. (part 2) 19, 67–69.
Embryol. 13, 69–106. 245. Raab, O. (1900) Über die Wirkung fluorescirender Stoffe auf
219. Churchland, J. W. and D. G. Russell (1914) The effect of genetian Infusorien Z. Zool. 39, 524–546.
violet on protozoa and on growing adult tissue. Proc. Soc. Exp. Biol. 246. Von Tappeiner, H. (1909) Die photodynamische Erscheinung
Med. 11, 120–124. (Sensibilisierung durch fluoreszierenden Stoffe). Ergeb. Physiol. 8,
220. Kite, G. L. (1913) Studies on the physical properties of protoplasm. 698–741.
Am. J. Physiol. 32, 146–164. 247. Straub, W. (1904) Ueber chemische Vorgänge bei der Einwirkung
221. Withrow, R. B. and A. P. Withrow (1956) Generation, control, and von Licht auf fluoreszierende Substanzen (Eosin und Chinin) und die
measurement of visible and near-visible radiant energy. In Radiation Bedeutung dieser Vorgänge für die Giftwirkung. Munch. Med.
Biology, Vol. 3 (Edited by A. Hollaender), pp. 125–258. McGraw- Wochenschr. 51, 1093–1096.
Hill, New York. 248. Hausmann, W. (1910) Die Sensibilisierende Wirkung des Hämato-
222. Goodrich, H. B. and J. A. Scott (1922) The effect of light on tissue pophyrins. Biochem. Z. 30, 276–316.
cultures. Anat. Rec. 24, 315–318. 249. Adler, L. (1919) Über Lichtwirkungen auf überlebende glattmuske-
223. Frederic, J. (1958) Recherches cytologiques sur le chondriome normal lige Organe. Arch. Exp. Pathol. Pharmakol. 85, 152–177.
ou soumis a l’experimentation dans des cellules vivantes cultivees in 250. Earle, W. R. (1928) Studies upon the effect of light on blood and
vitro. Arch. Biol. 69, 169–349. tissue cells. I. The action of light on white blood cells in vitro. J. Exp.
224. Kemp, T. and J. Juul (1932) Influence of ultraviolet rays upon mitosis Med. 48, 457–473.
in tissue cultures. Acta Pathol. Microbiol. Scand. 9, 222–235. 251. Earle, W. R. (1928) Studies upon the effect of light on blood and
225. Mayer, E. and H. Schreiber (1934) Die Wellenlängenabhängigkeit der tissue cells. III. The action of light on fibroblasts in vitro. J. Exp. Med.
Ultraviolettwirkung auf Gewebekulturen (‘‘Reinkulturen’’). Proto- 48, 683–693.
plasma 21, 34–61. 252. Büngeler, W. (1937) Über den Einfluss photosensibilisierender
226. Carlson, J. G. and A. Hollaender (1944) Immediate effects of low Substanzen auf die Entstehung von Hautgeschwülsten. Z. Krebs-
doses of ultraviolet radiation of wavelength 2537A on mitosis in the forsch. 46, 130–167.
grasshopper neuroblast. J. Cell. Comp. Physiol. 23, 157–166. 253. von Tappeiner, H. (1900) Ueber die Wirkung fluorescirender Stoffe
227. Wang, R. J., J. D. Stoien and F. Landa (1974) Lethal effect of near- auf Infusorien nach Versuchen von O. Raab. Munch. Med.
ultraviolet irradiation on mammalian cells in culture. Nature 247, 43– Wochenschr. 47, 5–7.
45. 254. von Tappeiner, H. and A. Jesionek (1903) Therapeutische Versuche
228. Parshad, R., K. K. Sanford, G. M. Jones and R. E. Tarone (1978) mit fluorescierenden Stoffen. Munch. Med. Wochenschr. 50, 2042–
2044.
Fluorescent light-induced chromosome damage and its prevention in
255. Dougherty, T. J. (2002) An update on photodynamic therapy
mouse cells in culture. Proc. Natl. Acad. Sci. USA 75, 1830–1833.
applications. J. Clin. Laser Med. Surg. 20, 3–7.
229. Sanford, K. K., R. Parshad and R. Gantt (1986) Responses of human
256. Schmarda, L. K. (1845) Der Einfluss des Lichtes auf die
cells in culture to hydrogen peroxide and related free radicals
Infusionsthierchen. Med. Jahrbücher des k. k. Österreichischen
generated by visible light: relationship to cancer susceptibility. In
Staates. 54, 257–270.
Free Radicals, Aging, and Degenerative Diseases, pp. 373–394. Liss,
257. Lessona, F. (1875) Dell’ azione della luce gugli animali. Turino.
New York. 258. Engelmann, T. W. (1879) Ueber Reizung contractilen Protoplasmas
230. Peak, J. G. and M. J. Peak (1991) Comparison of initial yields of durch plötzliche Beleuchtung. Pfluegers Arch. 19, 1–6 and 7–14.
DNA-to-protein crosslinks and single-strand breaks induced in 259. Engelmann, T. W. (1879) Ueber die Bewegungen der Oscillarien und
cultured human cells by far- and near-ultraviolet light, blue light Diatomeen. Pfluegers Arch. 19, 7–14.
and X-rays. Mutat. Res. 246, 187–191. 260. Hockberger, P. E. (2000) The discovery of the damaging effect of
231. Audait, J. (1931) Action des rayons ultra-violets sur l’excitabilite du sunlight on bacteria. J. Photochem. Photobiol. B. 58, 185–191.
nerf. C. R. Seances Soc. Biol. Fil. 107, 931–934. 261. Koch, R. (1890) Ueber bakteriologische Forschung. Hirschwald,
232. Hutton-Rudolph, M. (1943) Photochemische versuche an einzelnen Berlin.
Nervenfasern. Helv. Physiol. Pharmacol. Acta 1, C15–C19. 262. Tizzoni, G. and G. Cattani (1891) Ueber die Widerstandsfähigkeit der
233. Lüthy, H. and A. Von Muralt (1947) Ueber den ultraviolett Tetanusbacillen gegen physikalische unde chemische Einwirkungen.
Dichroismus der peripheren Nervefaser. Schweiz. Med. Wochenschr. Arch. Exp. Pathol. Pharmakol. 28, 41–60.
77, 5–6. 263. Dandrieu, P. (1888) Influence de la lumiere dans la destruction des
234. Booth, J., A. Von Muralt and R. Stampfli (1950) The photochemical bacteries p. servir a l’etude du ‘‘tout a l’egout.’’ Ann. Hyg. Publ. Med.
action of ultraviolet light on isolated single nerve fibers. Helv. Physiol. Legale Ser. 3, 20, 448–451.
Pharmacol. Acta 8, 110–127. 264. Klebs, E. (1887) Die Allgemeine Pathologie, pp. 85, 97, 131. Fischer,
235. Boyarsky, L. L. (1952) Effect of ultraviolet on electrical properties of Jena.
nerve. Proc. Soc. Exp. Biol. Med. 79, 213–214. 265. Wesbrook, F. F. (1896) Some of the effects of sunlight on tetanus
236. Von Muralt, A. and R. Stämpfli (1953) Die photochemische Wirkung cultures. J. Pathol. Bacteriol. 3, 70–77.
von Ultraviolettlicht auf den erregten Ranvierschen Knoten der 266. Wesbrook, F. F. (1896) The growth of cholera (and other) bacilli in
einzelnen Nervenfaser. Helv. Physiol. Pharmacol. Acta 11, 182–193. direct sunlight. J. Pathol. Bacteriol. 3, 352–358.
237. Gasteiger, A. L. (1953) Effects of ultraviolet on electrical properties of 267. Richardson, A. (1893) The action of light in preventing putrefactive
invertebrate nerve. Fed. Proc. 12, 48–49. decomposition and in inducing the formation of hydrogen peroxide in
238. Lüttgau, H. C. (1956) Elektrophysiologische Analyse der Wirkung organic liquids. Trans. Chem. Soc. Lond. 63, 1109–1130.
von UV-Lichte auf die isolierte markhaltige Nervenfaser. Pfluegers 268. D’Arcy, R. F. and W. B. Hardy (1894) Note on the oxidizing powers
Arch. 262, 244–255. of different regions of the spectrum in relation to the bactericidal
239. Chalazonitis, N. (1957) Effects de la Lumiere sur l’Evolution des action of light and air. J. Physiol. 17, 390–393.
Potentiels Cellulaires et sur Quelques Vitesses d’Oxydoreduction 269. Bedford, T. H. (1927) The nature of the action of ultra-violet light on
dans les Neurones. Bosc Freres, Lyons. micro-organisms. Br. J. Exp. Pathol. 8, 437–444.
240. Ham, W. T., H. A. Mueller and D. H. Sliney (1976) Retinal sensitivity 270. Bie, V. (1900) Untersuchungen über die bakterientötende Wirkung
to damage from short wavelength light. Nature 260, 153–154. der verschiedenen Abteilungen des Spektrums. Mitt. Finsens Med.
241. Reme, C., J. Reinboth, M. Clausen and F. Hafezi (1996) Light Lysinst. 1, 40–77.
damage revisited: converging evidence, diverging views? Arch. Clin. 271. Bie, V. (1904) Über die bakterische Wirkung ultravioletter Strahlen.
Exp. Ophthamol. 234, 2–11. Mitt. Finsens Med. Lysinst. 7, 65–77.
272. Bie, V. (1905) Ist die Bactericide Wirkung des Lichtes ein 299. Hartman, P. S. (1986) In situ hydrogen peroxide production may
Oxydationprozess? Mitt. Finsens Med. Lysinst. 9, 5–74. account for a portion of NUV (300–400 nm) inactivation of stationary
273. Strebel, H. (1901) Untersuchungen über die bakterizide Wirkung phase Escherichia coli. Photochem. Photobiol. 43, 87–89.
des Hochspannung-funkenenlichtes. Dtsch. Med. Wochenschr. 27, 300. Galland, P. and H. Senger (1988) New trends in photobiology: The
69–72. role of flavins as photoreceptors. J. Photochem. Photobiol. B 1, 277–
274. Bang, S. (1901) Die Wirkungen des Lichtes auf Mikrooganismen. 294.
Mitt. Finsens Med. Lysinst. 2, 1–107. 301. Beukers, R. and W. Berends (1960) Isolation and identification of the
275. Bang, S. (1903) Über die Wirkungen des Lichtes auf Mikroben. II. irradiation product of thymine. Biochim. Biophys. Acta 41, 550–551.
Eine verbesserte Untersuchungs methode. Mitt. Finsens Med. Lysinst. 302. Setlow, R. B. (1966) Cyclobutane-type pyrimidine dimmers in
3, 97–112. polynucleotides. Science 153, 379–386.
276. Barnard, J. E. and H. Morgan (1903) Upon the bactericidal action of 303. Hanawalt, P. C. and R. B. Setlow (1960) Effect of monochromatic
some ultraviolet radiations as produced by the continuous current arc. UV on macromolecular synthesis in E. coli. Biochim. Biophys. Acta
Proc. R. Soc. Lond. B. 72, 126–128. 41, 283–294.
277. Thiele, H. and K. Wolf (1906) Über die Abtötung von Bakterien 304. Setlow, R. B. and W. L. Carrier (1964) The disappearance of thymine
durch Licht. I. Arch. Hyg. Bakteriol. 57, 29–55. dimmers from DNA: an error correcting mechanism. Proc. Natl.
278. Thiele, H. and K. Wolf (1907) Über die Abtötung von Bakterien Acad. Sci. USA 51, 226–231.
durch Licht. II. Arch. Hyg. Bakteriol. 60, 29–39. 305. Pettijohn, D. and P. C. Hanawalt (1964) Evidence for repair-
279. Cernovodeanu, P. and V. Henri (1910) Action des rayons ultraviolets replication of ultraviolet damaged DNA in bacteria. J. Mol. Biol. 9,
sur les microorganisms et sur differents cellules. Etude micro- 395–410.
chimique. C. R. Hebd. Seances Acad. Sci. 150, 52–54. 306. Sancar, A. (1996) DNA excision repair. Annu. Rev. Biochem. 65,
280. Cenovodeanu, P. and V. Henri (1910) Etude de l’action des rayons 43–81.
ultraviolets sur les microbes. C. R. Hebd. Seances Acad. Sci. 150, 307. Kelner, R. (1949) Effect of visible light on the recovery of
729–731. Streptomyces griseus conidia from ultraviolet irradiation injury. Proc.
281. Henri, V. and V. Moycho (1914) Action des rayons ultraviolets Natl. Acad. Sci. USA 35, 73–79.
monochromatique sur les tissues. Mesure de l’energie de rayonnement 308. Sancar, A. (1996) No ‘end of history’ for photolyase. Science 272,
correspondant au coup de soleil. C. R. Hebd. Seances Acad. Sci. 158, 48–49.
1509–1511. 309. Cleaver, J. E. (1968) Defective repair replication of DNA in
282. Henri, Mme. V. and V. Henri (1914) Variation du pouvoir abiotique xeroderma pigmentosum. Nature 218, 652–656.
des rayons ultraviolets avec leur longueur d’onde. C. R. Seances Soc. 310. Cleaver, J. E. and K. H. Kraemer (1995) Xeroderma pigmentosum
Biol. Fil. 73, 321–322. and Cockayne syndrome. In The Metabolic and Molecular Bases
283. Browning, C. H. and S. Russ (1917) The germicidal action of ultra- of Inherited Disease, 7th ed. (Edited by C. R. Scriver, A. L. Beaudet,
violet radiation, and its correlation with selective absorption. Proc. R. W. S. Sly and D. Valle), pp. 4393–4419. McGraw-Hill, New York.
Soc. Lond. B. 90, 33–38. 311. Pfiefer, G. P., R. Drouin, A. D. Riggs and G. P. Holmquist (1992)
284. Bovie, W. T. and D. M. Hughes (1918) The effect of quartz ultraviolet Binding of transcription factors creates hotspots for UV photo-
light on the rate of division of Paramecium caudatum. J. Med. Res. 39, products. Mol. Cell. Biol. 12, 1798–1804.
223–231. 312. Pfeifer, G. P. (1997) Formation and processing of UV photoproducts:
285. Henri, V. (1919) Etudes de Photochemie. Gauthier Villars et Cie, Paris. effects of DNA sequence and chromatin environment. Photochem.
286. Burge, W. E. (1917) The action of ultra-violet radiation in killing Photobiol. 65, 270–283.
living cells such as bacteria. Am. J. Physiol. 43, 429–432. 313. Engelmann, T. W. (1883) Ueber Licht- und Farbenperception
287. Bayne-Jones, S. and J. S. Van Der Lingen (1923) The bactericidal niederster Organismen. Pfluegers Arch. 29, 387–400.
action of ultra-violet light. Bull. Johns Hopkins Hosp. 34, 11–16. 314. Engelmann, T. W. (1888) I. Ueber Bacteriopurpurin und seine
288. Coblentz, W. W. and H. R. Fulton (1924) A radiometric investigation physiologische Bedeutung. Pfluegers Arch. 42, 183–186.
of the germicidal action of ultra-violet radiation. U.S. Bur. Stand. Sci. 315. Loeb, J. (1888) Der Einfluss des Lichtes auf die Oxydationsvorgänge
Pap., no. 495, 19, 641–680. in thierischen Organismen. Pfluegers Arch. 42, 393–407.
289. Wykoff, R. W. (1930) The killing of certain bacteria by X-rays. J. 316. Mast, S. O. (1911) Light and the Behavior of Organisms. Wiley, New
Exp. Med. 52, 435–446. York.
290. Wykoff, R. W. (1932) The killing of certain bacteria by ultraviolet 317. Buder, J. (1915) Zur Kenntnis des Thiospirillum jenense und seiner
light. J. Gen. Physiol. 15, 351–361. Reaktionen auf Lichtreize. Jahrbücher Wiss. Bot. 56, 529–584.
291. Gates, F. L. (1929) A study of the bactericidal action of ultraviolet 318. Brucker, W. (1954) Beiträge zur Kenntnis der Phototaxis grüner
light. I. The reaction to monochromatic light. J. Gen. Physiol. 13, Schwärmzellen. I. Die Lichtempfindlichkeit von Lepocinclis texta und
231–248. ihre Abhängigkeit von der Vorbelichtung und vom Kohlensäuregehalt
292. Gates, F. L. (1929) A study of the bactericidal action of ultraviolet des Mediums. Arch. Protistenkd. 99, 294–327.
light. II. The effect of various environmental factors and conditions. J. 319. Clayton, R. K. (1964) Phototaxis in microorganisms. In Photo-
Gen. Physiol. 13, 249–260. physiology, Vol. 2 (Edited by A. C. Giese), pp. 51–77. Academic
293. Gates, F. L. (1930) A study of the bactericidal action of ultraviolet Press, New York.
light. III. The absorption of ultra violet by bacteria. J. Gen. Physiol. 320. Beijerinck, M. W. (1902) Photobacteria as a reactive in the
14, 31–42. investigation of the chlorophyll-function. Proc. Acad. Sci. Amst. 4,
294. Tatum, E. L. and G. W. Beadle (1945) Biochemical genetics of 45–49.
Neurospora. Ann. MO Bot. Gard. 32, 125–129. 321. Metzner, P. (1919) Über die Wirkung photodynamischer Stoffe auf
295. Hollaender, A. (1943) Effect of long ultraviolet and short visible Spirillum volutans und die Beziehungen der photodynamischen
radiation (3500 to 4900A) on Escherichia coli. J. Bacteriol. 46, 531– Erscheinung zur Phototaxis. Biochem. Z. 101, 33–53.
541. 322. Manten, A. (1948) Phototaxis in the purple bacterium Rhodospirillum
296. Jagger, J., W. C. Wise and R. S. Stafford (1964) Delay in growth and rubrum, and the relation between phototaxis and photosynthesis.
division induced by near ultraviolet radiation in Escherichia coli B Antonie Leeuwenhoek 14, 65–86.
and its role in photoprotection and liquid holding recovery. Photo- 323. Schlegel, H. G. (1956) Vergleichende Untersuchungen über die
chem. Photobiol. 3, 11–24. Lichtempfindlichkeit einiger Purpurbakterien. Arch. Protistenkd. 101,
297. Webb, R. B. and J. S. Bhorjee (1967) The effect of 3000–4000A light 69–97.
on the synthesis of b-galactosidase and bacteriophages by Escherichia 324. Clayton, R. K. (1959) Phototaxis of purple bacteria. In Handbuch der
coli. Can. J. Microbiol. 13, 69–79. Pflanzenphysiologie Part 1, Vol. 17 (Edited by W. Rushland), pp.
298. D’Aoust, J. Y., W. G. Martin, J. Giroux and H. Schneider (1980) 371–387. Springer, Berlin.
Protection from visible light damage to enzymes and transport in 325. Zalokar, M. (1955) Biosynthesis of carotenoids in Neurospora: action
Escherichia coli. Photochem. Photobiol. 31, 471–474. spectrum of photoactivation. Arch. Biochem. Biophys. 56, 318–325.
326. Curry, G. M. and H. E. Gruen (1959) Action spectra for the positive 333. Bünning, E. (1937) Phototropismus und carotinoide. I. Phototropische
and negative phototropism of Phycomyces sporangiophores. Proc. Wirksamkeit von Strahlen versciedener Wellenlange und Strahlum-
Natl. Acad. Sci. USA 45, 797–804. gasabsorption im Pigment bei Pilobolus. Planta 26, 710–736.
327. Delbrück, M. and W. Shropshire (1960) Action and transmission 334. Galston, A. W. (1950) Riboflavin, light, and the growth of plants.
spectra of Phycomyces. Plant Physiol. 35, 194–203. Science 111, 619–624.
328. Sargent, M. L. and W. R. Briggs (1967) The effects of light on 335. Galland, P. (1992) Forty years of blue-light research and no
a circadian rhythm of conidiation in Neurospora. Plant Physiol. 42, anniversary. Photochem. Photobiol. 56, 847–853.
336. Gurwitsch, A. G., S. Grabje and S. Salkind (1923) Die Natur des
1504–1510.
spezifischen Erregers der Zellteilung. Arch. Entwicklungsmech. Org.
329. Diehn, B. (1969) Action spectra of the phototactic responses in
100, 11–40.
Euglena. Biochim. Biophys. Acta 177, 136–143. 337. Alpatov, W. W. and O. K. Nastjukova (1933) The influence of
330. Bialcyzyk, J. (1979) An action spectrum for light avoidance by different quantities of ultra-violet radiation on the division rate in
Physarum nudum plasmodia. Photochem. Photobiol. 30, 301–303. Paramecium. Protoplasma 18, 281–285.
331. Selbach, M. and H. W. Kuhlmann (1999) Structure, fluorescent 338. Hollaender, A. and W. Claus (1937) An experimental study of the
properties and proposed function in phototaxis of the stigma apparatus problem of mitogenic radiation. Bull. Natl. Res. Council 100, 3–96.
in the ciliate Chlamydodon mnemosyne. J. Exp. Biol. 202, 919–922. 339. Hollaender, A. (1939) Present status of mitogenic radiation.
332. Castle, E. S. (1935) Photic excitation and phototropism in single plant Radiology 32, 404–410.
cells. Cold Spring Harbor Symp. Quant. Biol. 3, 224–229. 340. Popp, F.-A. (1988) Biophoton emission. Experientia 44, 543–544.
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A History of Ultraviolet Photobiology for Humans, Animals and

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