During ischemia-reperfusion injury, the burst of ROS on reoxygenation is primarily generated by:

• A Complex I of the mitochondrial electron transport chain
• B Xanthine oxidase acting on hypoxanthine accumulated during ischemia ✓
• C NADPH oxidase in neutrophils infiltrating at 4-6 hours
• D Cyclooxygenase-2 induced by NF-κB

Explanation

During ischemia, ATP is catabolized to hypoxanthine, and xanthine dehydrogenase is converted (by Ca²⁺-activated proteases) to xanthine oxidase. On reperfusion with O2, xanthine oxidase converts accumulated hypoxanthine to xanthine and then to uric acid, generating O2•− and H2O2 — the immediate ROS burst responsible for early reperfusion injury. This mechanism is especially prominent in the heart and liver. Mitochondrial Complex I is a source of ROS but not the primary early burst mechanism. Neutrophil NADPH oxidase contributes later (hours) to inflammation-phase injury. COX-2 is an inflammatory amplifier, not the primary ROS generator.

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

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