The document discusses micronutrients, specifically vitamins. It provides details on fat soluble and water soluble vitamins. The majority of the document focuses on vitamin A, including its chemistry, sources, absorption, transport, functions, and deficiency symptoms.
The document discusses micronutrients, specifically vitamins. It provides details on fat soluble and water soluble vitamins. The majority of the document focuses on vitamin A, including its chemistry, sources, absorption, transport, functions, and deficiency symptoms.
The document discusses micronutrients, specifically vitamins. It provides details on fat soluble and water soluble vitamins. The majority of the document focuses on vitamin A, including its chemistry, sources, absorption, transport, functions, and deficiency symptoms.
The document discusses micronutrients, specifically vitamins. It provides details on fat soluble and water soluble vitamins. The majority of the document focuses on vitamin A, including its chemistry, sources, absorption, transport, functions, and deficiency symptoms.
Bsc; Msc Micronutrients •Vitamins •Minerals Vitamins are defined as small organic molecules present in diet which are required in small amounts. Most of the vitamins are not synthesized in the body and hence they must be supplied in the diet. However, few vitamins are synthesized in the body. Though most of them are present in diet as such, some are present as precursors. The precursor forms of vitamins are called provitamins. In the body these provitamins are converted to vitamins. Vitamins are divided into two groups: Fat soluble and water soluble vitamins. Fat Soluble Vitamins Vitamins A, D, E and K. They have some common properties. 1. Fat soluble. 2. Require bile salts for absorption. 3. Stored in liver. 4. Stable to normal cooking conditions. Water Soluble Vitamins Members of vitamin B complex and Vitamin C. Common properties: 1. Water solubility. 2. Except Vitamin B12, others are not stored. 3. Unstable to normal cooking conditions. 4. Excreted in urine. FAT SOLUBLE VITAMINS VITAMIN A Chemistry Vitamin A refers to a group of compounds which exhibit Vitamin A activity. They are retinol (Vitamin A alcohol), retinal (Vitamin A aldehyde) and retinoic acid (Vitamin A acid). They are also referred as retinoids. Retinal and Retinoic acid are formed from retinol. Further retinal and retinol are inter convertible. But retinoic acid cannot be converted to either retinal or retinol. The three forms of Vitamin A are derivatives of a 20 carbon compound which is composed of β−ionine ring (methyl substituted cyclohexenyl ring) and side chain containing two isoprene units with four conjugated double bonds. Due to the presence of double bonds in isoprenoid side chain, vitamin A exhibits cis-trans (geometric) isomerism (Fig). Due to the presence of 4 double bonds vitamin A can be oxidized by air or light slowly. In nature, vitamin A occurs in two forms. In the foods of animal origin it is present as retinol esters. In plant foods it is present in provitamin form which is known as carotenes. There are three types of carotenes present in plants. They are α- carotenes, β-carotenes and γ-carotenes. These carotenes are called carotenoids. β-carotenes are most potent source of retinol because one molecule of β-carotene yields two molecules of Vitamin A in vivo (Fig). However α, γ-carotenes can yield only one molecule of vitamin A. Fig: Structures of vit. A. Geometric isomers of vit A are also shown Fig: Conversion of β-carotene to retinal Absorption of Vitamin A In the intestine, pancreatic esterase hydrolyzes retinol esters present in the diet to retinol and free fatty acid in presence of bile salts. Retinol is absorbed by mucosal cells. β-carotenes are also absorbed by mucosal cells. A dioxygenase present in the intestinal mucosal cells cleaves most of the β-carotene of dietary origin to two molecules of retinal in presence of oxygen. The conversion of β-carotene is limited. Six μg of β-carotene is converted to 1μg of retinal. Retinal formed is reduced to retinol by NAD(P)H dependent reductase present in mucosal cells of intestine. The reaction is a reversible one. Retinal can be oxidized to retinoic acid by using NAD+ or FAD as hydrogen acceptor. Retinoic acid formed is absorbed through portal venous system and transported to target cells after binding with albumin. A part of β-carotene absorbed does not undergo conversion to retinal and it is associated with lipoproteins and transported to target tissues where it is converted to retinal Fig: Absorption and fate of dietary vit A. FFA : Free fatty acid. PA : Palmitic acid In the mucosal cells of intestine the retinol generated from animal and plant sources is esterified with fatty acids and incorporated into chylomicrons which enter blood stream via lymph. In the circulation chylomicron remnants formed from chylomicrons contain virtually all retinyl esters. These chylomicron remnants are taken up by the liver. In the liver, retinyl esters are liberated from chylomicron remnants and are hydrolysed to retinol and free fatty acid. Retinyl ester is resynthesized in liver with palmitic acid and stored as lipoglycoprotein in lipocytes of liver Transport of Vitamin A Under normal conditions retinyl esters are constantly broken down and resynthesized in the liver. Free retinol formed in the liver is transported to target cells by way of protein complex. It is a multistage process. In hepatocyte retinol combines with apo retinol binding protein (APRB) to form holo retinol binding protein (HRBP) which is a binary complex. This binary complex is processed by golgi complex and it is secreted (Fig). In the plasma the binary complex combines with pre-albumin to form ternary complex which reaches target cells. The ternary complex then binds to specific receptor on cell membrane of target tissues and retinol is released into cell. In target cells some of the retinol is converted to retinal and retinoic acid. Within cells retinol and retinoic acid combine with cellular retinol binding protein (CRBP) and cellular retinoic acid binding protein (CRABP) respectively. Then these complexes enter the nucleus to exert their action Functions of Vitamin A Three major retinoids: retinal, retinol and retinoic acid have unique functions. 1. Retinal is required for normal and color vision. 2. Retinol is required for reproduction and growth. Retinol supports spermatogenesis, oogenesis and placental development. 3. Retinol is required for differentiation and function as steroid hormone. Fig: Transport of vit A from liver to target cells. RE : Receptor 4. Retinoic acid is required for the synthesis of glycoproteins or mucopolysaccharides. Retinoyl phosphate act as glycosyl carrier. 5. Retinoic acid also acts as a steroid hormone. It also promotes growth and differentiation but only to some extent. 6. Retinol and retinoic acid are involved in regulation of gene expression. 7. Vitamin A has several other important functions which are not yet clear. Some of them are given below. (a) Vitamin A is required for integrity of epithelial cells of gastro-intestinal tract, skin, respiratory tract and urinary tract and salivary glands. (b) Vitamin A is required for maintenance of nervous tissue particularly myelin sheath formation. (c) Vitamin A is required for tooth formation and bone growth. (d) Cancer. Retinoids are found to prevent chemical carcinogenesis. Synthetic retinoids are found to prevent breast cancer and bladder cancer. β-carotenes function as antioxidants (Free radical scavenger). They eliminate reactive oxygen species. (f) Acne and psoriasis. Vitamin A is useful in treatment of skin disorders like acne and psoriasis Retinal and vision Rods and cones present in the retina are responsible for normal and colour vision. Rods are responsible for vision in dim light where as cones are responsible for visual acuity and color vision. The rods contain visual pigment rhodopsin which is made up of 11-cis retinal and opsin a glycoprotein. Rhodopsin is an integral membrane glycoprotein. 11-cis retinal is attached to apoprotein opsin through ε-amino group of lysine. When photon (light) strikes, it undergoes conversion to all trans retinol. At the same time apoprotein dissociates as opsin. The conversion of rhodopsin to opsin and all trans retinal occurs through several intermediates whose life span ranges from picoseconds to a minute. So in the first stage of visual process a light signal is converted into atomic motion. In the next stage this atomic motion is converted into nerve impulse. Symptoms of Vitamin A deficiency 1. Night blindness. In early stages of Vitamin A deficiency the affected individual is not able to see clearly in dim light or night due to block in the resynthesis of rhodopsin. In the later stage of deficiency the affected individual cannot see or read in dim light. Thus loss of night vision (night blindness) is the major initial symptom of Vitamin A deficiency. Night blindness in adults or in preschool children is common in some areas where intake of vitamin A is low. If the night blindness is not treated, it progresses to xerophthalmia in which conjunctival and corneal epithelium of the eye is keratinised. Due to keratinisation of epithelium, conjunctiva is dry, thickens, wrinkled and pigmented. This condition is called xerosis conjunctiva. Further in affected children of below 6 years age Bitot’s spots a triangular shaped white plaques on conjunctiva are seen. Due to keratinisation of epithelium, cornea is dry and gives dull appearance (xerosis cornea). When xerosis of conjuctiva and cornea is not treated it leads to keratomalacia which is characterized by degenerated corneal epithelium. Finally permanent blindness results from corneal perforation or ulceration and scarring. 2. Growth of bone and formation of tooth are defective. Thick and long bones are formed. 3. Nerve growth also affected. Degeneration of myelin sheath occurs. 4. Keratinisation of mucous secreting epithelial cells (hyperkeratosis) lining respiratory tract and reproductive tract occurs. Mucous secretion by salivary and lacrymal glands is also affected. 5. Deposition of keratin in skin (xeroderma) gives rise to characteristic toad skin appearance. 6. Reproductive disorders like testicular degeneration, resorption of foetus or foetal malformation are observed. 7. Degenerative changes in kidneys. Vit. A deficiency anemia Anemia due to Vitamin A deficiency. Prevalence of Vitamin A deficiency anemia is high in populations of developing countries. Vitamin A appears to be involved in pathogenesis of anemia through diverse biological mechanisms like: (a) Growth and differentiation of erythrocytes. (b) Proliferation of immune cells. (c) Mobilization of iron stores. Vit. A supplementation reduces severity of anemia. Sources (a) Animal sources. As mentioned earlier it is present as retinol esters in animal foods. Marine fish oils like halibut liver oil, cod liver oil and shark liver oils are excellent sources. Liver of sheep or goat or pig is also excellent source. Butter, egg, and milk are good sources. Freshwater fish contain Vitamin A2 (dehydroretinol) which is only 40% active. (b) Plant sources. In plant foods, vitamin A is present as carotenes. Plant oil like red palm oil is excellent source. Other plant sources are Leafy vegetables. Amarnath leaves, coriander leaves, curry leaves, drumstick leaves, spinach and cabbage are good sources. Yellow vegetables like carrot, pumpkin and sweet potatoes and other vegetables like bottle gouard, drum sticks and ripe tomatoes also contain appreciable amounts of vitamin A. Fruits. Yellow pigmented fruits papaya, mango, jackfruit, banana and oranges also contain vitamin A in good amounts Daily requirement (RDA) Adults (men and women). 750 μg of retinol or 3 mg of carotene (2500 I.U) (International units, 1 I.U = 0.3 μg of retinol) Vit A toxicity (Hyper vitaminosis) It occurs when mega doses of Vitamin A (about 10-20 times of RDA) are taken or other vitamin A containing preparations are taken. Signs and symptoms of vitamin A toxicity are weakness, headache, muscle stiffness, increased intracranial pressure and hypertension. Fortunately symptoms disappear within a week after stopping excess intake. Antagonists of Vit A Some chemically unrelated compounds are found to antagonize vitamin A in experimental animals. Some are citral, sodium benzoate and monobromobenzene. Thank you