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What is the mechanism of action of Aspirin and how does it affect the decarboxylation of arachidonic acid?

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Aspirin, also known as acetylsalicylic acid, is a nonsteroidal anti-inflammatory drug  NSAID  that is commonly used for its analgesic, antipyretic, and anti-inflammatory properties. Its mechanism of action involves the irreversible inhibition of cyclooxygenase enzymes  COX-1 and COX-2 .Cyclooxygenase enzymes are responsible for the conversion of arachidonic acid into prostaglandins, which are lipid compounds that play a crucial role in mediating inflammation, pain, and fever. The decarboxylation of arachidonic acid is not directly affected by aspirin; however, the inhibition of COX enzymes by aspirin indirectly affects the production of prostaglandins from arachidonic acid.The mechanism of action of aspirin involves the acetylation of a serine residue in the active site of the COX enzymes. This acetylation leads to a conformational change in the enzyme, rendering it inactive and unable to catalyze the conversion of arachidonic acid to prostaglandins. As a result, the production of prostaglandins is reduced, leading to a decrease in inflammation, pain, and fever.In summary, aspirin does not directly affect the decarboxylation of arachidonic acid. Instead, it inhibits the cyclooxygenase enzymes responsible for converting arachidonic acid into prostaglandins, thereby reducing the production of these inflammatory mediators and alleviating pain, inflammation, and fever.
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