Mitochondrial electron transport complex I is a potential source of oxygen free radicals in the failing myocardium
Mitochondrial electron transport complex I is a potential source of oxygen free radicals in the failing myocardium
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DOI：
10.1161/01.res.85.4.357
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发表时间：
1999-08-20
影响因子：
20.1
通讯作者：
Takeshita, A
中科院分区：
文献类型：
--
作者：
Ide, T;Tsutsui, H;Takeshita, A
心肌氧化应激可能在充血性心力衰竭(HF)的发病机制中起重要作用。然而，衰竭心肌中增强产生活性氧物种(ROS)的细胞来源和机制仍不清楚。犬快速心脏起搏4周后，心内硫代巴比妥酸反应物质增多，4-羟基-2-壬烯醛ROS诱导的过氧化脂质免疫组织化学染色在心衰大鼠心肌细胞中可见，而间质细胞中未见。用自旋捕捉剂5，5‘-二甲基-1-吡咯啉-N-氧化物，在NADH和琥珀酸作底物的NADH-泛醌氧化还原酶(复合体I)和琥珀酸-泛醌氧化还原酶(复合体II)的存在下，用电子自旋共振波谱直接研究线粒体亚组分中超氧阴离子的产生。超氧化物歧化产生量增加2.8倍(P
Oxidative stress in the myocardium may play an important role in the pathogenesis of congestive heart failure (HF). However, the cellular sources and mechanisms for the enhanced generation of reactive oxygen species (ROS) in the failing myocardium remain unknown. The amount of thiobarbituric acid reactive substances increased in the canine HF hearts subjected to rapid ventricular pacing for 4 weeks, and immunohistochemical staining of 4-hydroxy-2-nonenal ROS-induced lipid peroxides was detected in cardiac myocytes but not in interstitial cells of HF animals. The generation of superoxide anion was directly assessed in the submitochondrial fractions by use of electron spin resonance spectroscopy with spin trapping agent, 5,5'-dimethyl-1-pyrroline-N-oxide, in the presence of NADH and succinate as a substrate for NADH-ubiquinone oxidoreductase (complex I) and succinate-ubiquinone oxidoreductase (complex II), respectively. Superoxide production was increased 2.8-fold (P