Lu Chao, Zhang Dawei, Whiteman Matthew, Armstrong Jeffrey S
Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Republic of Singapore.
Antioxid Redox Signal. 2008 Mar;10(3):651-60. doi: 10.1089/ars.2007.1865.
MitoQ has been developed as a mitochondrial targeted antioxidant for diseases associated with oxidative stress. Here we show that MitoQ blocks the generation of reactive oxygen species (ROS) and mitochondrial protein thiol oxidation, and preserves mitochondrial function and ultrastructure after glutathione (GSH) depletion. Furthermore, the antioxidant effect of MitoQ is conserved in cells lacking mitochondrial DNA, indicating that its antioxidant properties do not depend on a functional electron transport chain (ETC). Our results elucidate the antioxidant mechanism of MitoQ and suggest that it may be a useful therapeutic for disorders associated with a dysfunctional ETC and increased ROS production.
MitoQ已被开发为一种针对与氧化应激相关疾病的线粒体靶向抗氧化剂。在此我们表明，MitoQ可阻断活性氧（ROS）的生成及线粒体蛋白硫醇氧化，并在谷胱甘肽（GSH）耗竭后维持线粒体功能和超微结构。此外，MitoQ的抗氧化作用在缺乏线粒体DNA的细胞中得以保留，这表明其抗氧化特性不依赖于功能性电子传递链（ETC）。我们的结果阐明了MitoQ的抗氧化机制，并表明它可能是治疗与ETC功能失调和ROS生成增加相关疾病的有效药物。
