Thromboxane A2 (TXA2) and prostacyclin (PGI2) have opposing effects on platelet aggregation. The enzyme that produces TXA2 in platelets and is inhibited by low-dose aspirin is:

• A COX-1 (cyclo-oxygenase-1) → thromboxane synthase ✓
• B Lipoxygenase
• C Phospholipase A2
• D Prostacyclin synthase in platelet microsomes

Explanation

Arachidonic acid released by phospholipase A2 is converted by platelet COX-1 to PGH2, which thromboxane synthase converts to TXA2 (potent platelet aggregator and vasoconstrictor). Aspirin irreversibly acetylates COX-1 Ser529; platelets (anucleate) cannot synthesise new COX-1, so low-dose aspirin permanently inhibits platelet TXA2 production for the platelet's 7–10-day lifespan. Vascular endothelium regenerates COX-1, maintaining PGI2 (antiplatelet). Lipoxygenase produces leukotrienes.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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