GLUTATHIONE-DEPENDENT PROTECTION BY RAT-LIVER MICROSOMAL PROTEIN AGAINST LIPID-PEROXIDATION
GLUTATHIONE-DEPENDENT PROTECTION BY RAT-LIVER MICROSOMAL PROTEIN AGAINST LIPID-PEROXIDATION
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DOI：
10.1016/0304-4165(83)90148-4
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发表时间：
1983-01-01
期刊：
影响因子：
--
通讯作者：
BURK, RF
中科院分区：
文献类型：
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作者：
BURK, RF
GSH [谷胱甘肽]是一种重要的细胞防御氧化损伤。观察其对大鼠肝微粒体脂质过氧化系统的影响。用抗坏血酸和ADP螯合铁孵育新鲜大鼠肝微粒体，延迟2-5分钟后微粒体脂质过氧化（产生硫代巴比妥酸反应物质和破坏多不饱和脂肪酸）。添加0.1 mM GSH的系统延长了滞后期5-15分钟，而不影响脂质过氧化的速率或程度。GSH不能被半胱氨酸、巯基乙醇、二硫苏糖醇、丙基硫氧嘧啶或GSSG [还原型谷胱甘肽]所替代。GSH对滞后的影响被废除加热或胰蛋白酶消化的微粒体，表明微粒体蛋白质是其表达所必需的。随着GSH浓度从0.1-5 mM增加，观察到逐渐更长的滞后，但没有证据表明GSH氧化是防止脂质过氧化的结果。GSH保护微粒体蛋白的热失活，负责GSH效应。用O2电极的实验表明，GSH保护并没有改变消耗的O2与产生的硫代巴比妥酸反应物质的比率。这暗示自由基清除是保护机制。存在一个谷胱甘肽依赖性大鼠肝微粒体蛋白，清除自由基的指示。这种蛋白质可能是一个重要的防御自由基损伤的微粒体膜。
GSH [glutathione] is an important cellular defense against oxidant injury. Its effect in the rat liver microsomal lipid peroxidation system was examined. Incubation of fresh rat liver microsomes with ascorbic acid and ADP-chelated Fe leads to the peroxidation of microsomal lipids (production of thiobarbituric acid-reactive substances and destruction of polyunsaturated fatty acids) following a 2-5 min lag. Addition of 0.1 mM GSH to the system lengthened the lag period by 5-15 min without affecting the rate or the extent of lipid peroxidation. GSH could not be replaced in prolonging the lag by cysteine, mercaptoethanol, dithiothreitol, propylthiouracil or GSSG [reduced glutathione]. The GSH effect on the lag was abolished by heating or trypsin digestion of the microsomes, indicating that microsomal protein is required for its expression. Progressively longer lags were observed as the GSH concentration was increased from 0.1-5 mM, but there was no evidence of GSH oxidation as a consequence of the protection against lipid peroxidation. GSH protected against heat inactivation of the microsomal protein responsible for the GSH effect. Experiments with an O2 electrode revealed that the GSH protection did not alter the ratio of O2 consumed to thiobarbituric acid-reactive substances produced. This implicated free radical scavenging as the mechanism of protection. The existence of a GSH-dependent rat liver microsomal protein which scavenges free radicals is indicated. This protein may be an important defense against free radical injury to the microsomal membrane.