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首页> 外文期刊>American Journal of Physiology >Ischemic defects in the electron transport chain increase the production of reactive oxygen species from isolated rat heart mitochondria
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Ischemic defects in the electron transport chain increase the production of reactive oxygen species from isolated rat heart mitochondria

机译：电子传输链中的缺血性缺陷会增加离体大鼠心脏线粒体中活性氧的产生

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First published December 12, 2007; doi:10.1152/ajpcell.00211.2007.-Cardiac ischemia decreases complex III activity, cytochrome c content, and respiration through cytochrome oxidase in subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM). The reversible blockade of electron transport with amobarbital during ischemia protects mitochondrial respiration and decreases myocardial injury during reperfu-sion. These findings support that mitochondrial damage occurs during ischemia and contributes to myocardial injury during reperfusion. The current study addressed whether ischemic damage to the electron transport chain (ETC) increased the net production of reactive oxygen species (ROS) from mitochondria. SSM and IFM were isolated from 6-mo-old Fisher 344 rat hearts following 25 min global ischemia or following 40 min of perfusion alone as controls. H_2o_2 release from SSM and IFM was measured using the amplex red assay. With glutamate as a complex I substrate, the net production of H_2O_2 wasincreased by 178 +- 14% and 179 +- 17% in SSM and IFM (n = 9), respectively, following ischemia compared with controls (n - 8). With succinate as substrate in the presence of rotenone, H_2O_2 increased by 272 +- 22% and 171 +- 21% in SSM and IFM, respectively, after ischemia. Inhibitors of electron transport were used to assess maximal ROS production. Inhibition of complex I with rotenone increased H_2O_2 production by 179 +- 24% and 155 +- 14% in SSM and IFM, respectively, following ischemia. Ischemia also increased the antimycin A-stimulated production of H_2O_2 from complex HI. Thus ischemic damage to the ETC increased both the capacity and the net production of H_2O_2 from complex I and complex III and sets the stage for an increase in ROS production during reperfusion as a mechanism of cardiac injury.
机译：首次发布于2007年12月12日; doi：10.1152 / ajpcell.00211.2007.-心肌缺血可降低肌膜下线粒体（SSM）和原纤维间线粒体（IFM）中的复杂III活性，细胞色素c含量以及通过细胞色素氧化酶的呼吸作用。缺血期间可逆的电子转运被阿莫巴比妥阻滞，可保护线粒体呼吸并减少再灌注期间的心肌损伤。这些发现支持线粒体损伤发生在局部缺血过程中，并在再灌注过程中导致心肌损伤。当前的研究探讨了缺血对电子传输链（ETC）的损害是否增加了线粒体的活性氧（ROS）的净产量。在25分钟的整体缺血后或在单独灌注40分钟后，从6个月大的Fisher 344大鼠心脏分离SSM和IFM。使用am红色测定法测量了SSM和IFM中H_2o_2的释放。与对照（n-8）相比，缺血后SSM和IFM（n = 9）中以谷氨酸为复杂的I底物的H_2O_2的净产量分别增加了178±14％和179±17％。在鱼藤酮存在下以琥珀酸酯为底物，缺血后，SSM和IFM中H_2O_2分别增加272±22％和171±21％。使用电子传输抑制剂来评估最大的ROS产生。缺血后，用鱼藤酮抑制复合物I分别使SSM和IFM中H_2O_2的产生增加了179±24％和155±14％。局部缺血还增加了抗霉素A刺激的H_2O_2的产生。因此，对ETC的缺血性损伤既增加了复合物I和复合物III产生的H_2O_2的能力，又增加了其净产量，为心脏再灌注过程中ROS产生的增加奠定了基础。

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