Silver E H, Szabo S
Exp Mol Pathol. 1983 Feb;38(1):69-76. doi: 10.1016/0014-4800(83)90099-0.
Ischemia and anoxia are associated with decreased concentrations of cellular antioxidants. The hypothesis that recirculation of oxygenated blood to previously ischemic tissue may result in enhanced free-radical reactions leading to lipid peroxidation and tissue damage was investigated. Elevated hepatic conjugated diene concentrations were detected 60 min after treatment of rats with carbon tetrachloride, a positive control, but were not found after 90 min ischemia or at 5 or 60 min after reperfusion of ischemic tissue. These findings suggest that lipid peroxidation may not be an early event in ischemia-induced necrosis but do not rule out a role of other free-radical reactions in the pathogenesis of ischemic necrosis.
缺血和缺氧与细胞抗氧化剂浓度降低有关。研究了向先前缺血组织输送含氧血液再灌注可能导致自由基反应增强，进而引起脂质过氧化和组织损伤这一假说。用四氯化碳（阳性对照）处理大鼠60分钟后，检测到肝脏共轭二烯浓度升高，但在缺血90分钟后或缺血组织再灌注5分钟及60分钟后未发现这种情况。这些发现表明脂质过氧化可能不是缺血诱导坏死的早期事件，但不排除其他自由基反应在缺血性坏死发病机制中的作用。
