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Tridimensional model of the chemical structure of aspirin.
Aspirin causes several different effects in the body, mainly the reduction of inflammation, analgesia (relief of pain), the prevention of clotting, and the reduction of fever. Much of this is believed to be due to decreased production of prostaglandins and TXA2. Aspirin's ability to suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the cyclooxygenase (COX) enzyme. Cyclooxygenase is 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 COX enzyme.[1] This makes aspirin different from other NSAIDs (such as diclofenac and ibuprofen), which are reversible inhibitors; aspirin creates an allosteric change in the structure of the COX enzyme.[2] However, other effects of aspirin, such as uncoupling oxidative phosphorylation in mitochondria,[3] and the modulation of signaling through NF-κB, are also being investigated. Some of its effects are like those of salicylic acid, which is not an acetylating agent.
^Tóth L, Muszbek L, Komáromi I (March 2013). "Mechanism of the irreversible inhibition of human cyclooxygenase-1 by aspirin as predicted by QM/MM calculations". Journal of Molecular Graphics & Modelling. 40: 99–109. doi:10.1016/j.jmgm.2012.12.013. PMID 23384979.
^Giménez-Bastida JA, Boeglin WE, Boutaud O, Malkowski MG, Schneider C (January 2019). "Residual cyclooxygenase activity of aspirin-acetylated COX-2 forms 15 R-prostaglandins that inhibit platelet aggregation". FASEB Journal. 33 (1): 1033–1041. doi:10.1096/fj.201801018R. PMC 6355089. PMID 30096040.
^Jörgensen TG, Weis-Fogh US, Nielsen HH, Olesen HP (November 1976). "Salicylate- and aspirin-induced uncoupling of oxidative phosphorylation in mitochondria isolated from the mucosal membrane of the stomach". Scandinavian Journal of Clinical and Laboratory Investigation. 36 (7): 649–654. doi:10.1080/00365517609054490. PMID 1019575.
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