Ravindranath V, Reed D J
Dept. of Neurochemistry, National Institute of Mental Health & Neuro Sciences, Bangalore, India.
Biochem Biophys Res Commun. 1990 Jun 29;169(3):1075-9. doi: 10.1016/0006-291x(90)92004-j.
t-Butyl hydroperoxide was utilized to alter the thiol homeostasis in rat brain mitochondria. Following exposure to t-butyl hydroperoxide (50-500 microM), intramitochondrial GSH content decreased rapidly and irreversibly with a major portion of the depleted GSH being accounted for as protein-SS-Glutathione mixed disulfide. Formation of GSSG was not observed nor was efflux of GSSG or GSH from the mitochondria detected in the incubation medium. The loss of intramitochondrial GSH was accompanied by loss of protein thiols. Unlike liver mitochondria, which can reverse t-butyl hydroperoxide induced formation of GSSG, addition of 50 microM t-butyl hydroperoxide resulted in irreversible loss; indicating greater susceptibility of brain mitochondria to oxidative stress than liver mitochondria.
叔丁基过氧化氢被用于改变大鼠脑线粒体中的硫醇稳态。在暴露于叔丁基过氧化氢（50 - 500微摩尔）后，线粒体内谷胱甘肽（GSH）含量迅速且不可逆地下降，耗尽的GSH的主要部分以蛋白质 - SS - 谷胱甘肽混合二硫化物的形式存在。未观察到谷胱甘肽二硫化物（GSSG）的形成，在孵育培养基中也未检测到GSSG或GSH从线粒体流出。线粒体内GSH的损失伴随着蛋白质硫醇的损失。与能够逆转叔丁基过氧化氢诱导的GSSG形成的肝线粒体不同，添加50微摩尔叔丁基过氧化氢会导致不可逆的损失；这表明脑线粒体比肝线粒体对氧化应激更敏感。
