Starkov Anatoly A
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, Room A-501, New York Presbyterian Hospital, New York, NY 10021, United States.
Chem Biol Interact. 2006 Oct 27;163(1-2):133-44. doi: 10.1016/j.cbi.2006.08.015.
Mitochondrial production of reactive oxygen species (ROS) is a well-established fact of fundamental importance to aging and etiology of many pathologies with serious public health implications. The ROS production is an innate property of mitochondrial biochemistry inseparable from the oxidative metabolism. Recent discoveries indicate that in addition to several ROS-detoxifying enzyme systems, which remove ROS, mitochondria may also be able to limit their ROS production by the mechanism comprising several protein-mediated energy-dissipating ("uncoupling") pathways. Although the physiological significance and in vivo modus operandi of these pathways remain to be elucidated, several proteins potentially capable of energy dissipation are known. This mini-review addresses the identity of mitochondrial protein-mediated energy-dissipating pathways and the experimental evidence to their role in controlling ROS production.
线粒体产生活性氧(ROS)是一个已被充分证实的事实,对于衰老以及许多具有严重公共卫生影响的病理状况的病因学具有至关重要的意义。ROS的产生是线粒体生物化学的固有特性,与氧化代谢密不可分。最近的发现表明,除了几种可清除ROS的ROS解毒酶系统外,线粒体还可能通过包含几种蛋白质介导的能量耗散(“解偶联”)途径的机制来限制其ROS的产生。尽管这些途径的生理意义和体内作用方式仍有待阐明,但已知几种可能具有能量耗散能力的蛋白质。本综述探讨了线粒体蛋白质介导的能量耗散途径的身份及其在控制ROS产生中作用的实验证据。