Aspirin Inhibits Prostaglandin Synthesis

Aspirin, a widely used non-steroidal anti-inflammatory drug (NSAID), primarily works by blocking key enzymes in the eicosanoid pathway. The correct answer to the multiple-choice question is 2. Prostaglandins.

Correct Answer

Aspirin irreversibly inhibits cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) enzymes, preventing the conversion of arachidonic acid to prostaglandin H2 (PGH2), the precursor for prostaglandins. This action reduces prostaglandin levels, explaining aspirin’s anti-inflammatory, analgesic, antipyretic, and antiplatelet effects.

Option Explanations

1. Leukotrienes (Incorrect)

Leukotrienes derive from arachidonic acid via the 5-lipoxygenase pathway, not the cyclooxygenase pathway targeted by aspirin. Aspirin may indirectly influence lipoxins from modified COX-2 activity, but it does not directly inhibit leukotriene synthesis.

2. Prostaglandins (Correct)

Prostaglandins (e.g., PGE2, PGI2) form from PGH2 through COX enzyme action on arachidonic acid. Aspirin’s acetylation of a serine residue in COX-1 and COX-2 irreversibly blocks this, halting prostaglandin production.

3. Arachidonic Acid (Incorrect)

Arachidonic acid serves as the substrate released from membrane phospholipids by phospholipase A2. Aspirin acts downstream by inhibiting COX enzymes that metabolize arachidonic acid, without affecting its synthesis or levels directly.

4. 17-Eicosapentanoic Acid (EPA) (Incorrect)

EPA, an omega-3 fatty acid, competes with arachidonic acid for COX and lipoxygenase enzymes, producing less inflammatory mediators. Aspirin does not inhibit EPA synthesis; EPA is dietary and processed similarly but independently.​