A wave of reactive oxygen species (ROS)-induced ROS release in a sea of excitable mitochondria

被引:153
作者
Brady, Nathan R.
Hamacher-Brady, Anne
Westerhoff, Hans V.
Gottlieb, Roberta A.
机构
[1] Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA
[2] Vrije Univ Amsterdam, Fac Earth & Life Sci, Inst Mol Cell Biol, Dept Mol Cell Physiol, Amsterdam, Netherlands
[3] Univ Manchester, Manchester Ctr Integrat Syst Biol, Manchester M13 9PL, Lancs, England
关键词
D O I
10.1089/ars.2006.8.1651
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Once considered simply as the main source of ATP, mitochondria are now implicated in the control of many additional aspects of cell physiology, such as calcium signaling, and pathology, as in injury incurred on ischemia and subsequent reperfusion (I/R). Mitochondrial respiration is ordinarily accompanied by low-level ROS production, but they can respond to elevated ROS concentrations by increasing their own ROS production, a phenomenon termed ROS-induced ROS release (RIRR). Two modes of RIRR have been described. In the first mode of RIRR, enhanced ROS leads to mitochondrial depolarization via activation of the MPTP, yielding a short-lived burst of ROS originating from the mitochondrial electron transport chain (ETC). The second mode of RIRR is MPTP independent but is regulated by the mitochondrial benzodiazepine receptor (mBzR). Increased ROS in the mitochondrion triggers opening of the inner mitochondrial membrane anion channel (IMAC), resulting in a brief increase in ETC-derived ROS. Both modes of RIRR have been shown to transmit localized mitochondrial perturbations throughout the cardiac cell in the form of oscillations or waves but are kinetically distinct and may involve different ROS that serve as second messengers. In this review, we discuss the mechanisms of these different modes of RIRR.
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页码:1651 / 1665
页数:15
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共 126 条
[41]  
DROBINSKI G, 1989, THERAPIE, V44, P263
[42]   Mitochondria and calcium: from cell signalling to cell death [J].
Duchen, MR .
JOURNAL OF PHYSIOLOGY-LONDON, 2000, 529 (01) :57-68
[43]   RO 5-4864 AND PK 11195, BUT NOT DIAZEPAM, DEPRESS CARDIAC-FUNCTION IN AN ISOLATED WORKING RAT-HEART MODEL [J].
EDOUTE, Y ;
GIRIS, J ;
BENHAIM, SA ;
LOCHNER, A ;
WEIZMAN, A ;
HAYAM, G ;
KATZ, Y ;
GAVISH, M .
PHARMACOLOGY, 1993, 46 (04) :224-230
[44]   The mitochondrial permeability transition initiates autophagy in rat hepatocytes [J].
Elmore, SP ;
Qian, T ;
Grissom, SF ;
Lemasters, JJ .
FASEB JOURNAL, 2001, 15 (10) :2286-+
[45]   Bax-induced cytochrome C release from mitochondria is independent of the permeability transition pore but highly dependent on Mg2+ ions [J].
Eskes, R ;
Antonsson, B ;
Osen-Sand, A ;
Montessuit, S ;
Richter, C ;
Sadoul, R ;
Mazzei, G ;
Nichols, A ;
Martinou, JC .
JOURNAL OF CELL BIOLOGY, 1998, 143 (01) :217-224
[46]   Mitochondrial reactive oxygen species in cell death signaling [J].
Fleury, C ;
Mignotte, B ;
Vayssière, JL .
BIOCHIMIE, 2002, 84 (2-3) :131-141
[48]   BIOLOGY OF OXYGEN RADICALS [J].
FRIDOVICH, I .
SCIENCE, 1978, 201 (4359) :875-880
[49]   SUPEROXIDE RADICAL - AN ENDOGENOUS TOXICANT [J].
FRIDOVICH, I .
ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY, 1983, 23 :239-257
[50]   PK11195 potently sensitizes to apoptosis induction independently from the peripheral benzodiazepin receptor [J].
Gonzalez-Polo, RA ;
Carvalho, G ;
Braun, T ;
Decaudin, D ;
Fabre, C ;
Larochette, N ;
Perfettini, JL ;
Djavaheri-Mergny, M ;
Youlyouz-Marfak, I ;
Codogno, P ;
Raphael, M ;
Feuillard, J ;
Kroemer, G .
ONCOGENE, 2005, 24 (51) :7503-7513