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Inhibition of palmityl carnitine oxidation in rat liver mitochondria by tert-butyl hydroperoxide

机译:叔丁基过氧化氢抑制大鼠肝线粒体中棕榈基肉碱的氧化

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摘要

Mitochondria as an energy generating cell device are very sensitive to oxidative damage. Our previous findings obtained in hepatocytes demonstrated that Complex I of the respiratory chain is more sensitive to oxidative damage than other respiratory chain complexes. We present additional data on isolated mitochondria showing that palmityl carnitine oxidation is strongly depressed at a low (200 mu M) tert butyl hydroperoxicle (tBHP) concentration, while oxidation of the flavoprotein-dependent substrate - succinate is not affected and neither is ATP synthesis inhibited by tBHP. In the presence of tBHP, the respiratory control index for palmityl carnitine oxidation is strongly depressed, but when succinate is oxidized the respiratory control index remains unaffected. Our findings thus indicate that flavoprotein-dependent substrates could be an important nutritional factor for the regeneration process in the necrotic liver damaged by oxidative stress.
机译:线粒体作为能量产生细胞的装置对氧化损伤非常敏感。我们先前在肝细胞中获得的发现表明,呼吸链复合物I比其他呼吸链复合物对氧化损伤更敏感。我们提供了有关分离的线粒体的其他数据,表明在低(200μM)叔丁基氢过氧化物(tBHP)浓度下,棕榈酰肉碱的氧化作用被强烈抑制,而黄酮蛋白依赖性底物-琥珀酸盐的氧化作用不受影响,ATP合成也不受抑制通过tBHP。在存在tBHP的情况下,棕榈酰肉碱氧化的呼吸控制指数会大大降低,但是琥珀酸被氧化时,呼吸控制指数仍然不受影响。因此,我们的发现表明,依赖黄素蛋白的底物可能是氧化应激所致坏死肝脏再生过程中的重要营养因子。

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