Bagchi M, Prasad M R, Engelman R M, Das D K
Department of Surgery, University of Connecticut School of Medicine, Farmington 06032.
Free Radic Res Commun. 1989;7(3-6):375-80. doi: 10.3109/10715768909087964.
Free radicals, including superoxide anions (O2.-), hydroxyl radical (HO.), and hypohalite radical (OCl.), as well as oxidants such as hydrogen peroxide (H2O2) and hypochlorous acid (HOCl), have been indicated in the pathogenesis of myocardial ischemic and reperfusion injury. In this report, we compared the integrity of the myocardial membrane when exposed to these free radicals/oxidants. Isolated rat heart membrane preparations were exposed to chemically generated free radicals with or without their respective scavengers. Membrane fluidity was monitored by fluorescence polarization using the diphenylhexatriene probe, as well as by electron spin resonance (ESR) spectroscopy using 2,2,6,6-tetramethyl piperidine-n-oxyl as the spin labeling agent. HO., H2O2, and OCl. + HOCl increased the fluorescence polarization (FP) and microviscosity significantly by 1.7-fold, 1.8-fold, and 1.7-fold, respectively, as compared to an only 1.2-fold increase in FP by O2.-. O2.- did not alter the fatty acid profiles of the membrane phospholipids. However, HO. and H2O2 reduced the arachidonic acid contents in phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylinositol (PI). These radicals also stimulated the lipid peroxidation by several-fold, while that by O2.- was only insignificant. These results suggest that HO. and H2O2 decreased the membrane fluidity and induced lipid peroxidation by releasing the arachidonic acid from PC, PE, and PI.
自由基，包括超氧阴离子（O2.-）、羟自由基（HO.）和次卤酸根自由基（OCl.），以及氧化剂如过氧化氢（H2O2）和次氯酸（HOCl），已被证明与心肌缺血再灌注损伤的发病机制有关。在本报告中，我们比较了心肌膜在暴露于这些自由基/氧化剂时的完整性。将分离的大鼠心脏膜制剂暴露于化学产生的自由基中，同时或不添加各自的清除剂。使用二苯基己三烯探针通过荧光偏振监测膜流动性，以及使用2,2,6,6-四甲基哌啶氮氧化物作为自旋标记剂通过电子自旋共振（ESR）光谱进行监测。与O2.-仅使荧光偏振（FP）增加1.2倍相比，HO.、H2O2和OCl. + HOCl分别使荧光偏振（FP）和微粘度显著增加1.7倍、1.8倍和1.7倍。O2.-没有改变膜磷脂的脂肪酸谱。然而，HO.和H2O2降低了磷脂酰胆碱（PC）、磷脂酰乙醇胺（PE）和磷脂酰肌醇（PI）中的花生四烯酸含量。这些自由基还使脂质过氧化增加了几倍，而O2.-引起的脂质过氧化则微不足道。这些结果表明，HO.和H2O2通过从PC、PE和PI中释放花生四烯酸降低了膜流动性并诱导了脂质过氧化。
