During reperfusion after myocardial ischemia, the most damaging reactive oxygen species generated primarily by xanthine oxidase and NADPH oxidase is:
- A Superoxide anion (O2•-) and hydroxyl radical (•OH) via Fenton/Haber-Weiss reaction ✓
- B Hydrogen peroxide (H2O2) acting directly on contractile proteins
- C Nitric oxide (NO) causing vasodilation and tissue protection
- D Singlet oxygen generated by mitochondrial complex I
Explanation
Ischemia-reperfusion injury involves rapid generation of superoxide (O2•-) by xanthine oxidase (hypoxanthine + O2) and NADPH oxidase on neutrophils. Superoxide is converted to H2O2 by SOD; in the presence of Fe2+ (released from damaged mitochondria), the Fenton reaction generates the highly reactive hydroxyl radical (•OH), which initiates lipid peroxidation, protein oxidation, and DNA strand breaks. NO can be protective or harmful depending on context (forms peroxynitrite with O2•-). Mitochondrial complex I/III generate superoxide, not primarily singlet oxygen.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.