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Mechanisms participating in oxidative damage of isolated rat hepatocytes

机译：参与离体大鼠肝细胞氧化损伤的机制

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The aim of the study was to evaluate time course and dose dependence of peroxidative damage induced by tert-butyl hydroperoxide (tBHP) in rat hepatocytes cultured in suspension and in monolayer. At the lowest (0.1 mM) concentration, decrease of cytosolic glutathione and discharge of mitochondrial membrane potential (MMP) could be detected. Significant increases in leakage of lactate dehydrogenase and in malondialdehyde concentrations together with decrease of pyruvate-dependent respiration were detected at higher tBHP concentrations (above 0.5 mM) and after longer periods of incubation. Changes in plasma membrane integrity were observed at 1 mM concentration of tBHP. Succinate-dependent oxidation was most resistant to peroxidative damages. Opening of the mitochondrial permeability transition pore was responsible for the discharge of mitochondria membrane potential. In the presence of cyclosporine A and succinate, the membrane potential could be restored. Our data showed that the most sensitive indicators of the peroxidative damage are changes of cytosolic glutathione concentration and MMP.
机译：这项研究的目的是评估在悬浮和单层培养的大鼠肝细胞中由叔丁基氢过氧化物（tBHP）诱导的过氧化损伤的时程和剂量依赖性。在最低浓度（0.1 mM）下，可以检测到胞质谷胱甘肽的减少和线粒体膜电位（MMP）的释放。在较高的tBHP浓度（高于0.5 mM）和较长的孵育时间后，发现乳酸脱氢酶和丙二醛浓度的泄漏显着增加，丙酮酸依赖性呼吸作用降低。在浓度为1 mM的tBHP中观察到质膜完整性的变化。琥珀酸依赖性的氧化最能抵抗过氧化损伤。线粒体通透性过渡孔的开放负责线粒体膜电位的释放。在环孢菌素A和琥珀酸的存在下，膜电位可以恢复。我们的数据表明，对过氧化损伤最敏感的指标是细胞内谷胱甘肽浓度和MMP的变化。

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