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温度通过大鼠骨骼肌线粒体解偶联作用来控制氧化磷酸化和活性氧的产生。

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

作者信息

Jarmuszkiewicz Wieslawa, Woyda-Ploszczyca Andrzej, Koziel Agnieszka, Majerczak Joanna, Zoladz Jerzy A

机构信息

Department of Bioenergetics, Faculty of Biology, Adam Mickiewicz University, 61-614 Poznan, Poland.

Department of Bioenergetics, Faculty of Biology, Adam Mickiewicz University, 61-614 Poznan, Poland.

出版信息

Free Radic Biol Med. 2015 Jun;83:12-20. doi: 10.1016/j.freeradbiomed.2015.02.012. Epub 2015 Feb 17.

DOI:10.1016/j.freeradbiomed.2015.02.012
PMID:25701433
Abstract

Mitochondrial respiratory and phosphorylation activities, mitochondrial uncoupling, and hydrogen peroxide formation were studied in isolated rat skeletal muscle mitochondria during experimentally induced hypothermia (25 °C) and hyperthermia (42 °C) compared to the physiological temperature of resting muscle (35 °C). For nonphosphorylating mitochondria, increasing the temperature from 25 to 42 °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.

摘要

在实验诱导的低温(25°C)和高温(42°C)条件下,研究了分离的大鼠骨骼肌线粒体中的线粒体呼吸和磷酸化活性、线粒体解偶联以及过氧化氢生成,并与静息肌肉的生理温度(35°C)进行了比较。对于非磷酸化线粒体,将温度从25°C升高至42°C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随温度的变化。然而,随着测定温度升高,氧化磷酸化效率降低,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生成减少的原因。

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