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Electron transport chain of Saccharomyces cerevisiae mitochondria is inhibited by H_2O_2 at succinate-cytochrome c oxidoreductase level without lipid peroxidation involvement

机译:H_2O_2在琥珀酸-细胞色素c氧化还原酶水平上抑制啤酒酵母线粒体的电子传输链,而没有脂质过氧化作用

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The deleterious effects of H_2O_2 on the electron transport chain of yeast mitochondria and on mitochondrial lipid peroxidation were evaluated. Exposure to H_2O_2 resulted in inhibition of the oxygen consumption in the uncoupled and phosphorylating states to 69% and 65%, respectively. The effect of H_2O_2 on the respiratory rate was associated with an inhibition of succinate-ubiquinone and succinate-DCIP oxidoreductase activities. Inhibitory effect of H_2O_2 on respiratory complexes was almost completely recovered by beta-mercaptoethanol treatment. H_2O_2 treatment resulted in full resistance to Qo site inhibitor myxothiazol and thus it is suggested that the quinol oxidase site (Qo) of complex III is the target for H_2O_2. H_2O_2 did not modify basal levels of lipid peroxidation in yeast mitochondria. However, H_2O_2 addition to rat brain and liver mitochondria induced an increase in lipid peroxidation. These results are discussed in terms of the known physiological differences between mammalian and yeast mitochondria.
机译:评估了H_2O_2对酵母线粒体电子传递链和线粒体脂质过氧化的有害作用。暴露于H_2O_2导致在未偶联和磷酸化状态下的耗氧量分别被抑制到69%和65%。 H_2O_2对呼吸频率的影响与琥珀酸-泛醌和琥珀酸-DCIP氧化还原酶活性的抑制有关。通过β-巯基乙醇处理,几乎可以完全恢复H_2O_2对呼吸道复合物的抑制作用。 H_2O_2处理导致对Qo站点抑制剂mythothiazol的完全抵抗,因此建议将配合物III的喹诺醇氧化酶站点(Qo)作为H_2O_2的目标。 H_2O_2不会改变酵母线粒体中脂质过氧化的基础水平。但是,大鼠脑和肝线粒体中的H_2O_2诱导脂质过氧化增加。根据哺乳动物和酵母线粒体之间的已知生理差异讨论了这些结果。

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