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首页> 外文期刊>Archives of Biochemistry and Biophysics >Aging defect at the Q(o) site of complex III augments oxyradical production in rat heart interfibrillar mitochondria
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Aging defect at the Q(o) site of complex III augments oxyradical production in rat heart interfibrillar mitochondria

机译:复合物III Q(o)位点的衰老缺陷会增加大鼠心脏原纤维间线粒体的羟自由基生成

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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). [References: 35]
机译:线粒体电子传输链中的复合物III是增加活性氧的产生的拟议场所,活性氧有助于心脏的衰老。我们描述了复杂的III仅在心脏线粒体的原纤维间人口老化过程中细胞色素b中泛醇结合位点(Q(0))中的缺陷。该缺陷表现为通过噻噻唑阻滞使电子泄漏,从而还原了细胞色素b,并且观察到复合物III中的细胞色素b是从正向还是反向还原的。老化缺陷增加了原纤维间线粒体中复合物III的Q(0)位的活性氧种类的产生。泛醇氧化过程中,复合物III的电子泄漏量更大,这可能是线粒体产生氧化剂增加的机制,这可能导致大鼠心脏衰老。 (C)2003年由Elsevier Science(美国)出版。 [参考:35]

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