Mitochondrial ROS and involvement of Bcl-2 as a mitochondrial ROS regulator

被引:107
作者
Chong, Stephen Jun Fei [1 ]
Low, Ivan Cherh Chiet [1 ]
Pervaiz, Shazib [1 ,2 ,3 ,4 ,5 ]
机构
[1] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Physiol, Clin Res Ctr, Singapore 117597, Singapore
[2] Ctr Life Sci CeLS, NUS Grad Sch Integrat Sci & Engn, Singapore 117576, Singapore
[3] Duke NUS Grad Med Sch, Canc & Stem Cell Biol Program, Singapore, Singapore
[4] Singapore MIT Alliance, Singapore, Singapore
[5] Natl Univ Singapore, Inst Canc, Singapore 117548, Singapore
关键词
Mitochondria; mitoROS; ROS; Superoxide; Bcl-2; Phosphorylation; PROTEIN-KINASE-C; SUCCINATE-UBIQUINONE OXIDOREDUCTASE; PROSTATE-CANCER CELLS; ALPHA ANTISENSE OLIGONUCLEOTIDE; STARVATION-INDUCED AUTOPHAGY; HYDROGEN-PEROXIDE FORMATION; OXIDANT-INDUCED ACTIVATION; BOVINE HEART-MITOCHONDRIA; OXYGEN SPECIES GENERATION; ELECTRON-TRANSPORT CHAIN;
D O I
10.1016/j.mito.2014.06.002
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitochondria are the major intracellular source of reactive oxygen species (ROS). While excessive mitochondrial ROS (mitoROS) production induces cell injury and death, there is accumulating evidence that non-toxic low levels of mitoROS could serve as important signaling molecules. Therefore, maintenance of mitoROS at physiological levels is crucial for cell homeostasis as well as for survival and proliferation. This review describes the various mechanisms that keep mitoROS in check, with particular focus on the role of the onco-protein Bcl-2 in redox regulation. In addition to its canonical anti-apoptotic activity, Bcl-2 has been implicated in mitoROS regulation by its effect on mitochondrial complex IV activity, facilitating the mitochondrial incorporation of GSH and interaction with the small GTPase-Rac1 at the mitochondria. We also discuss some of the plausible mechanism(s) which allows Bcl-2 to sense and respond to the fluctuations in mitoROS. (C) 2014 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
引用
收藏
页码:39 / 48
页数:10
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