[解偶联蛋白在氧化应激保护机制中的作用]。

Iu V Hoshovs'ka
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引用次数: 3

摘要

解偶联蛋白(Uncoupling proteins, UCPs)位于线粒体内膜,催化质子穿过线粒体内膜渗漏。虽然来自棕色脂肪组织(BAT)的UCP1作为产热的热介导过程耗散质子梯度能量,但UCPs的心脏同工异构体的功能仍存在争议。由于心脏组织中UCPs的含量远低于BAT,因此UCPs对呼吸链的轻度解偶联可能调节心脏线粒体的膜电位,防止活性氧的过量产生。本文综述了在缺血再灌注和衰老条件下UCPs活化对氧化应激的保护作用。讨论了UCPs参与缺血预处理诱导的内源性心脏保护机制。
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[The role of uncoupling proteins in mechanisms of protection from oxidative stress].

Uncoupling proteins, UCPs, are located in the inner mitochondrial membrane and catalize proton leak across the inner mitochondrial membrane. While UCP1 from brown adipose tissue (BAT) dissipates energy of proton gradient as heat mediating process of thermogenesis, the function of cardiac isoforms of UCPs is still debated. Since the content of UCPs in heart tissue is much lesser then in BAT mild uncoupling of respiratory chain by UCPs might regulate membrane potential of cardiac mitochondria, preventing excessive production of reactive oxygen species. The review is focused on own and literature evidences suggesting the protective role of UCPs activation from oxidative stress under ischemia-reperfusion conditions and aging. Participation of UCPs in endogenous mechanisms of cardioprotection induced by ischemic preconditioning is discussed.

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