Aspirin, or acetylsalicylic acid, is a nonsteroidal anti-inflammatory drug NSAID that is commonly used for its analgesic, antipyretic, and anti-inflammatory properties. It inhibits the formation of prostaglandins and thromboxanes by irreversibly inhibiting the cyclooxygenase COX enzymes, which are involved in the synthesis of these molecules.Prostaglandins and thromboxanes are lipid mediators derived from arachidonic acid, a polyunsaturated fatty acid. They play important roles in various physiological processes, such as inflammation, pain, fever, and blood clotting. The synthesis of prostaglandins and thromboxanes is catalyzed by the COX enzymes, which exist in two isoforms: COX-1 and COX-2.COX-1 is constitutively expressed in most tissues and is involved in the maintenance of normal physiological functions, such as gastric mucosal protection and platelet aggregation. COX-2 is induced in response to inflammatory stimuli and is responsible for the production of prostaglandins involved in inflammation, pain, and fever.Aspirin exerts its inhibitory effect on the COX enzymes by acetylating a serine residue Ser-530 in COX-1 and Ser-516 in COX-2 in the active site of the enzymes. This acetylation leads to a conformational change in the enzyme structure, which prevents the access of arachidonic acid to the active site and thus inhibits the formation of prostaglandins and thromboxanes.The acetylation of the serine residue by aspirin is an irreversible process, which means that the enzyme activity can only be restored through the synthesis of new COX enzymes. This is in contrast to other NSAIDs, such as ibuprofen and naproxen, which reversibly inhibit the COX enzymes by competing with arachidonic acid for binding to the active site.The inhibition of COX-1 by aspirin leads to a decrease in the production of thromboxane A2 TXA2 , a potent vasoconstrictor and platelet aggregator. This effect contributes to the antithrombotic properties of aspirin, which is used in low doses for the prevention of cardiovascular events, such as myocardial infarction and stroke.In summary, aspirin inhibits the formation of prostaglandins and thromboxanes by irreversibly acetylating a serine residue in the active site of the cyclooxygenase enzymes, COX-1 and COX-2. This modification prevents the access of arachidonic acid to the active site and thus inhibits the synthesis of these lipid mediators, leading to the analgesic, antipyretic, anti-inflammatory, and antithrombotic effects of aspirin.