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→COX-1 and COX-2 inhibition: Altered the text to use a consistent naming convention. COX-2 and PTGS2 (as well as COX-1 and PTGS1) are two names for the same thing. While there might be technical reasons why one might be preferred over another, depending on context and the jargon of a given specialization or context, using them interchangeably in this context only causes confusion. COX was chosen over PTGS as that seems to be the preferred convention in the article overall. Tags: Mobile edit Mobile web edit Advanced mobile edit |
→Prostaglandins and thromboxanes: Additional conversion of PTGS to COX for consistency Tags: Mobile edit Mobile web edit Advanced mobile edit |
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===Prostaglandins and thromboxanes===
Aspirin's ability to suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the [[cyclooxygenase]] (COX; officially known as prostaglandin-endoperoxide synthase, PTGS) enzyme required for prostaglandin and thromboxane synthesis. Aspirin acts as an acetylating agent where an acetyl group is covalently attached to a [[serine]] residue in the active site of the
Low-dose aspirin use irreversibly blocks the formation of [[thromboxane A2|thromboxane A<sub>2</sub>]] in platelets, producing an inhibitory effect on platelet aggregation during the lifetime of the affected platelet (8–9 days). This antithrombotic property makes aspirin useful for reducing the incidence of heart attacks in people who have had a heart attack, unstable angina, ischemic stroke or transient ischemic attack.<ref>{{cite web |url=http://www.americanheart.org/presenter.jhtml?identifier=4456 |title=Aspirin in heart attack and stroke prevention |access-date=8 May 2008 |publisher=American Heart Association |archive-url=https://web.archive.org/web/20080331031146/http://www.americanheart.org/presenter.jhtml?identifier=4456 |archive-date=31 March 2008 }}</ref> 40{{nbsp}}mg of aspirin a day is able to inhibit a large proportion of maximum thromboxane A<sub>2</sub> release provoked acutely, with the prostaglandin I2 synthesis being little affected; however, higher doses of aspirin are required to attain further inhibition.<ref>{{cite journal | vauthors = Tohgi H, Konno S, Tamura K, Kimura B, Kawano K | title = Effects of low-to-high doses of aspirin on platelet aggregability and metabolites of thromboxane A2 and prostacyclin | journal = Stroke | volume = 23 | issue = 10 | pages = 1400–3 | date = October 1992 | pmid = 1412574 | doi = 10.1161/01.STR.23.10.1400 | doi-access = free | title-link = doi }}</ref>
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