Following successful thrombolysis for acute myocardial infarction, myocardial injury paradoxically worsens. The principal source of the burst of superoxide generated during reperfusion of ischemic tissue is:

• A Lysosomal ceruloplasmin activated by low pH
• B Uncoupled ATP synthase in mitochondria
• C Myeloperoxidase released from infiltrating basophils
• D Xanthine oxidase acting on hypoxanthine accumulated during ischemia ✓

Explanation

During ischemia, ATP degradation raises tissue hypoxanthine while calcium influx converts xanthine dehydrogenase to xanthine oxidase. On reperfusion, oxygen returns and xanthine oxidase converts hypoxanthine to urate with massive superoxide generation, driving reperfusion injury. Myeloperoxidase comes from neutrophils, not basophils, and produces HOCl rather than superoxide, which eliminates that distractor.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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