Aspirin

Abstract

Aspirin exerts its effect primarily by interfering with the biosynthesis of cyclic prostanoids, ie, thromboxane A₂ (TXA₂), prostacyclin, and other prostaglandins. These prostanoids are generated by the enzymatically catalyzed oxidation of arachidonic acid, which is itself derived from membrane phospholipids⁴ (Figure ⇓ ). Arachidonic acid is metabolized by the enzyme prostaglandin (PG) H-synthase, which, through its cyclooxygenase (COX) and peroxidase activities, results in the production of PGG₂ and PGH₂, respectively. PGH₂ is then modified by specific synthases, thus producing prostaglandins D₂, E₂, F_2α, I₂ (prostacyclin), and TXA₂, all of which mediate specific cellular functions.