Aging defect at the Qo site of complex III augments oxyradical production in rat heart interfibrillar mitochondria
Aging defect at the Qo site of complex III augments oxyradical production in rat heart interfibrillar mitochondria
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DOI：
10.1016/s0003-9861(03)00166-8
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发表时间：
2003-06-01
影响因子：
3.9
通讯作者：
Lesnefsky, EJ
中科院分区：
文献类型：
--
作者：
Moghaddas, S;Hoppel, CL;Lesnefsky, EJ
线粒体电子传递链中的复合体III被认为是促进心脏衰老的活性氧物种产生的场所。我们描述了在衰老过程中，仅在心肌线粒体的纤维间群中，复合体III中细胞色素b内的泛喹酚结合位点(Q(0))的缺陷。缺陷表现为通过Myxthiiazol阻滞剂的电子泄漏来还原细胞色素b，并观察到络合物III中的细胞色素b是从正向还是从反向还原的。衰老缺陷增加了纤维间线粒体中复合体III的Q(0)位产生的活性氧物种。在泛喹酚的氧化过程中，络合物III的电子泄漏更多，这可能是线粒体产生氧化剂增加导致大鼠心脏衰老的一个可能机制。(C)2003年，爱思唯尔科学公司(美国)出版。
Complex III in the mitochondrial electron transport chain is a proposed site for the enhanced production of reactive oxygen species that contribute to aging in the heart. We describe a defect in the ubiquinol binding site (Q(0)) within cytochrome b in complex III only in the interfibrillar population of cardiac mitochondria during aging. The defect is manifested as a leak of electrons through myxothiazol blockade to reduce cytochrome b and is observed whether cytochrome b in complex III is reduced from the forward or the reverse direction. The aging defect increases the production of reactive oxygen species from the Q(0) site of complex III in interfibrillar mitochondria. A greater leak of electrons from complex III during the oxidation of ubiquinol is a likely mechanism for the enhanced oxidant production from mitochondria that contributes to aging in the rat heart. (C) 2003 Published by Elsevier Science (USA).