Plasma Membrane Redox System in the Control of Stress-Induced Apoptosis

被引:92
作者
Villalba, Jose M. [2 ]
Navas, Placido [1 ]
机构
[1] Univ Pablo de Olavide, Lab Andaluz Biol, Seville 41013, Spain
[2] Univ Cordoba, Fac Ciencias, Dept Biol Celular Fisiol & Inmunol, Cordoba 14071, Spain
关键词
D O I
10.1089/ars.2000.2.2-213
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
The plasma membrane of animal cells contains an electron transport system based on coenzyme Q (CoQ) reductases. Cytochrome b(5) reductase is NADH-specific and reduces CoQ through a one-electron reaction mechanism. DT-diaphorase also reduces CoQ, although through a two-electron reaction mechanism using both NADH and NADP H, which may be particularly important under oxidative stress conditions. Because reduced CoQ protects membranes against peroxidations, and also maintains the reduced forms of exogenous antioxidants such as alpha-tocopherol and ascorbate, this molecule can be considered a central component of the plasma membrane antioxidant system. Stress-induced apoptosis is mediated by the activation of plasma membrane-bound neutral sphingomyelinase, which releases ceramide to the cytosol. Ceramide-dependent caspase activation is part of the apoptosis pathway. The reduced components of the plasma membrane antioxidant system, mainly CoQ, prevent both lipid peroxidation and sphingomyelinase activation. This results in the prevention of ceramide accumulation and caspase 3 activation and, as consequence, apoptosis is inhibited. W e propose the hypothesis that antioxidant protective function of the plasma membrane redox system can be enough to protect cells against the externally induced mild oxidative stress. If this system is overwhelmed, intracellular mechanisms of protection are required to avoid activation of the apoptosis pathway. Antiox. Redox Signal. 2, 213-230.
引用
收藏
页码:213 / 230
页数:18
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