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辅酶Q同系物对线粒体产生活性氧的影响。

Effect of CoQ homologues on reactive oxygen generation by mitochondria.

作者信息

Imada Isuke, Sato Eisuke F, Kira Yukimi, Inoue Masayasu

机构信息

Department of Biochemistry and Molecular Pathology, Osaka City University Medical School, Osaka, Japan.

出版信息

Biofactors. 2008;32(1-4):41-8. doi: 10.1002/biof.5520320106.

Abstract

Effect of CoQ compounds (Qs) on reactive oxygen (ROS) generation by mitochondrial complex I was studied using rat liver mitochondria and chemiluminescence probe L012. Kinetic analysis revealed that short chain Qs, such as Q2 and idebenone enhanced ROS generation by mitochondrial NADH oxidase system by a succinate-inhibitable mechanism. Lipid peroxidation in mitochondrial membranes induced by NADH and iron was inhibited by short chain Qs. The inhibitory activity was enhanced by co-oxidation of succinate as determined by chemiluminescence method and by electron spin resonance spectroscopy. These results suggested that the reduced form of short chain Qs inhibited mitochondrial ROS generation and lipid peroxidation.

摘要

使用大鼠肝脏线粒体和化学发光探针L012研究了辅酶Q化合物(Qs)对线粒体复合体I产生活性氧(ROS)的影响。动力学分析表明,短链Qs,如Q2和艾地苯醌,通过琥珀酸抑制机制增强了线粒体NADH氧化酶系统产生的ROS。短链Qs抑制了由NADH和铁诱导的线粒体膜脂质过氧化。通过化学发光法和电子自旋共振光谱法测定,琥珀酸的共氧化增强了抑制活性。这些结果表明,短链Qs的还原形式抑制了线粒体ROS的产生和脂质过氧化。

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