Aspirin's irreversible inhibition of COX in platelets achieves antiplatelet effect for the platelet lifetime (7–10 days) while endothelial cells recover within hours. The explanation for this differential recovery is that:

• A Platelet COX-1 has lower aspirin IC50 than endothelial COX-2 making it more sensitive
• B Aspirin is concentrated in platelets by a specific organic anion transporter absent in endothelial cells
• C Platelets are anucleate and cannot synthesize new COX protein; endothelial cells have nuclei and rapidly resynthesize COX ✓
• D Platelet thromboxane synthase is aspirin-sensitive but endothelial prostacyclin synthase is aspirin-resistant

Explanation

Mature platelets are anucleate cells (derived from megakaryocytes) and cannot synthesize new proteins, including COX-1. Once aspirin acetylates the active-site serine-529 of COX-1 in platelets, thromboxane A2 synthesis is permanently blocked for the platelet's remaining lifespan. Endothelial cells have nuclei and ribosomes; they re-synthesize COX-2 (the primary isoform for prostacyclin production in these cells) within hours of aspirin exposure. Low-dose aspirin exploits this difference to preferentially suppress platelet TXA2 while sparing endothelial PGI2 production, explaining its antiplatelet specificity at low doses.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.