Mitochondrial ROS-induced ROS release: An update and review
Mitochondrial ROS-induced ROS release: An update and review
复制标题
DOI：
10.1016/j.bbabio.2006.04.029
复制
发表时间：
2006-05-01
影响因子：
4.3
通讯作者：
Sollott, Steven J.
中科院分区：
文献类型：
--
作者：
Zorov, Dmitry B.;Juhaszova, Magdalena;Sollott, Steven J.
在包括缺血/再灌注损伤和毒素暴露在内的损伤后，可能发生不稳定的线粒体膜电位和氧化还原转换，对线粒体完整性和细胞存活产生负面影响。这些转换可能涉及机制，如最近描述的过程，“活性氧（ROS）诱导的ROS释放”（RIRR），并产生的电路，其中涉及线粒体渗透性转换（MPT）孔和内膜阴离子通道（IMAC）。暴露于过度的氧化应激导致ROS增加，达到触发必需的线粒体通道之一打开的阈值水平。反过来，这导致线粒体膜电位的同时崩溃和电子转移链瞬时增加的ROS产生。产生的ROS可以释放到胞质溶胶中并触发邻近线粒体中的RIRR。这种ROS信号传导构成了增强ROS产生的正反馈机制，导致潜在的显著线粒体和细胞损伤。本综述和更新考虑了各种RIRR机制（涉及MPT，INIAC和线粒体瞬时超极化发作）。RIRR可能是与程序性线粒体破坏和细胞死亡过程相关的一般细胞生物学现象，并可能导致缺血后病理学的其他机制，包括心律失常。由爱思唯尔公司出版
Unstable mitochondrial membrane potential and redox transitions can occur following insults including ischemia/reperfusion injury and toxin exposure, with negative consequences for mitochondrial integrity and cellular survival. These transitions can involve mechanisms such as the recently described process, "Reactive Oxygen Species (ROS)-induced ROS-release" (RIRR), and be generated by circuits where the mitochondrial permeability transition (MPT) pore and the inner membrane anion channel (IMAC) are involved. The exposure to excessive oxidative stress results in an increase in ROS reaching a threshold level that triggers the opening of one of the requisite mitochondrial channels. In turn, this leads to the simultaneous collapse of the mitochondrial membrane potential and a transient increased ROS generation by the electron transfer chain. Generated ROS can be released into cytosol and trigger RIRR in neighboring mitochondria. This mitochondrion-to-mitochondrion ROS-signaling constitutes a positive feedback mechanism for enhanced ROS production leading to potentially significant mitochondrial and cellular injury. This review and update considers a variety of RIRR mechanisms (involving MPT, INIAC and episodes of mitochondrial transient hyperpolarization). RIRR could be a general cell biology phenomenon relevant to the processes of programmed mitochondrial destruction and cell death, and may contribute to other mechanisms of post-ischemic pathologies, including arrhythmias. Published by Elsevier B.V.