Mailloux Ryan J
Department of Biology, Faculty of Sciences, University of Ottawa, 30 Marie Curie, Ottawa, ON, Canada K1N 6N5.
Redox Biol. 2015;4:381-98. doi: 10.1016/j.redox.2015.02.001. Epub 2015 Feb 7.
Mitochondria fulfill a number of biological functions which inherently depend on ATP and O2(-•)/H2O2 production. Both ATP and O2(-•)/H2O2 are generated by electron transfer reactions. ATP is the product of oxidative phosphorylation whereas O2(-•) is generated by singlet electron reduction of di-oxygen (O2). O2(-•) is then rapidly dismutated by superoxide dismutase (SOD) producing H2O2. O2(-•)/H2O2 were once viewed as unfortunately by-products of aerobic respiration. This characterization is fitting considering over production of O2(-•)/H2O2 by mitochondria is associated with range of pathological conditions and aging. However, O2(-•)/H2O2 are only dangerous in large quantities. If produced in a controlled fashion and maintained at a low concentration, cells can benefit greatly from the redox properties of O2(-•)/H2O2. Indeed, low rates of O2(-•)/H2O2 production are required for intrinsic mitochondrial signaling (e.g. modulation of mitochondrial processes) and communication with the rest of the cell. O2(-•)/H2O2 levels are kept in check by anti-oxidant defense systems that sequester O2(-•)/H2O2 with extreme efficiency. Given the importance of O2(-•)/H2O2 in cellular function, it is imperative to consider how mitochondria produce O2(-•)/H2O2 and how O2(-•)/H2O2 genesis is regulated in conjunction with fluctuations in nutritional and redox states. Here, I discuss the fundamentals of electron transfer reactions in mitochondria and emerging knowledge on the 11 potential sources of mitochondrial O2(-•)/H2O2 in tandem with their significance in contributing to overall O2(-•)/H2O2 emission in health and disease. The potential for classifying these different sites in isopotential groups, which is essentially defined by the redox properties of electron donator involved in O2(-•)/H2O2 production, as originally suggested by Brand and colleagues is also surveyed in detail. In addition, redox signaling mechanisms that control O2(-•)/H2O2 genesis from these sites are discussed. Finally, the current methodologies utilized for measuring O2(-•)/H2O2 in isolated mitochondria, cell culture and in vivo are reviewed.
线粒体履行多种生物学功能,这些功能本质上依赖于ATP以及超氧阴离子(O2(-•))/过氧化氢(H2O2)的产生。ATP和O2(-•)/H2O2均由电子传递反应生成。ATP是氧化磷酸化的产物,而O2(-•)是通过氧分子(O2)的单电子还原产生的。随后,O2(-•)迅速被超氧化物歧化酶(SOD)歧化生成H2O2。O2(-•)/H2O2曾一度被视为有氧呼吸不幸的副产物。考虑到线粒体过量产生O2(-•)/H2O2与一系列病理状况及衰老相关,这种描述是恰当的。然而,O2(-•)/H2O2只有在大量存在时才具有危险性。如果以可控方式产生并维持在低浓度水平,细胞能够从O2(-•)/H2O2的氧化还原特性中受益匪浅。实际上,线粒体固有信号传导(例如线粒体过程的调节)以及与细胞其他部分的通讯需要低速率的O2(-•)/H2O2产生。抗氧化防御系统能极其高效地螯合O2(-•)/H2O2,从而使O2(-•)/H2O2水平得到控制。鉴于O2(-•)/H2O2在细胞功能中的重要性,必须考虑线粒体如何产生O2(-•)/H2O2以及O2(-•)/H2O2的生成如何随着营养和氧化还原状态的波动而受到调节。在此,我将讨论线粒体中电子传递反应的基本原理,以及关于线粒体O2(-•)/H2O2的11种潜在来源的新认识,同时探讨它们在健康和疾病状态下对整体O2(-•)/H2O2释放的贡献。还将详细考察按照等电位组对这些不同位点进行分类的可能性,这一分类最初由布兰德及其同事提出,本质上是由参与O2(-•)/H2O2产生的电子供体的氧化还原特性所定义。此外,还将讨论控制这些位点产生O2(-•)/H2O2的氧化还原信号传导机制。最后,对目前用于测量分离线粒体、细胞培养物和体内O2(-•)/H2O2的方法进行综述。