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Temperature controls oxidative phosphorylation and reactive oxygen species production through uncoupling in rat skeletal muscle mitochondria

机译:温度通过解偶联大鼠骨骼肌线粒体来控制氧化磷酸化和活性氧的产生

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摘要

Mitochondrial respiratory and phosphorylation activities, mitochondrial uncoupling, and hydrogen peroxide formation were studied in isolated rat skeletal muscle mitochondria during experimentally induced hypothermia (25 degrees C) and hyperthermia (42 degrees C) compared to the physiological temperature of resting muscle (35 degrees C). For nonphosphorylating mitochondria, increasing the temperature from 25 to 42 degrees C led to a decrease in membrane potential, hydrogen peroxide production, and quinone reduction levels. For phosphorylating mitochondria, no temperature-dependent changes in these mitochondrial functions were observed. However, the efficiency of oxidative phosphorylation decreased, whereas the oxidation and phosphorylation rates and oxidative capacities of the mitochondria increased, with increasing assay temperature. An increase in proton leak, including uncoupling protein-mediated proton leak, was observed with increasing assay temperature, which could explain the reduced oxidative phosphorylation efficiency and reactive oxygen species production. (C) 2015 Elsevier Inc. All rights reserved.
机译:与静息肌肉的生理温度(35摄氏度)相比,在实验诱导的低温(25摄氏度)和热疗(42摄氏度)期间,在孤立的大鼠骨骼肌线粒体中研究了线粒体呼吸和磷酸化活性,线粒体解偶联和过氧化氢的形成。 。对于非磷酸化的线粒体,将温度从25摄氏度提高到42摄氏度会导致膜电位,过氧化氢生成和醌还原水平降低。对于磷酸化线粒体,未观察到这些线粒体功能的温度依赖性变化。然而,随着测定温度的升高,氧化磷酸化的效率降低,而线粒体的氧化和磷酸化速率以及氧化能力增加。随着测定温度升高,观察到质子泄漏增加,包括解偶联蛋白介导的质子泄漏,这可以解释氧化磷酸化效率降低和活性氧产生降低。 (C)2015 Elsevier Inc.保留所有权利。

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