Aspirin and related salicylates produce their pharmacological effects predominantly by inhibiting the synthesis of prostaglandins and to a lesser extent synthesis of the thromboxanes (implicated in platelet aggregation). The prostanoids are mediators of inflammatory responses in many cell types. Aspirin is unique among NSAIDs in that it irreversibly acetylates COX-1 and COX-2, which are required for the synthesis of prostanoids from arachidonic acid. COX-2 is induced during inflammation and is therefore considered to mediate most inflammatory responses. Aspirin acetylation of COX-1 permanently inactivates the enzyme, while acetylated COX-2 is capable of producing 15-HETE. New enzyme must be synthesized to overcome the effects of aspirin, which in the case of platelets can take as long as 11 days. The metabolite of aspirin, salicylic acid, is a reversible inhibitor of COX. Other NSAIDs have reversible effects at different sites on COX-1 and on COX-2. In addition, aspirin interferes with kinin-induced modulation of the inflammatory response.
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