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线粒体 Q 循环衍生的超氧自由基与化学渗透生物能学。

Mitochondrial Q cycle-derived superoxide and chemiosmotic bioenergetics.

机构信息

State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.

出版信息

Ann N Y Acad Sci. 2010 Jul;1201:84-95. doi: 10.1111/j.1749-6632.2010.05632.x.

DOI:10.1111/j.1749-6632.2010.05632.x
PMID:20649544
Abstract

We examined the intrinsic relation between two interdependent and interacted processes, namely, chemiosmotic energy coupling partition and redox signaling involved in mitochondrial respiration. The following aspects of research were conducted and discussed: generation sites and release sidedness of superoxide from the Q cycle of complex III of the mitochondrial respiratory chain; the different physiological roles of PMF components, DeltaPsi and DeltapH (DeltapH(S)), of the Q cycle in mitochondrial superoxide generating and partitioning; and direct feedback effects of Q cycle-derived O(2)(-) on PMF energy partition through its interaction with protons in DeltapH(S) to form HO(2)(), leading to decreasing DeltapH(S) and ATP synthesis due to its increasing effects of basic proton leak of mitochondria. The present experimental data give new evidence for our hypothesis of reactive oxygen species cycle cooperation with Q cycle and H(+) cycle in respiratory chain in keeping PMF energy partition and its equilibrium with redox signaling regulation of mitochondrial respiration.

摘要

我们研究了两个相互依存和相互作用的过程之间的内在关系,即参与线粒体呼吸的化学渗透能量偶联分配和氧化还原信号。进行并讨论了以下研究方面:来自线粒体呼吸链复合物 III 的 Q 循环中超氧化物的产生部位和释放偏向性;Q 循环中 PMF 成分(DeltaPsi 和 DeltapH(DeltapH(S)))在生成和分配线粒体超氧化物中的不同生理作用;以及 Q 循环衍生的 O(2)(-)通过与 DeltapH(S)中的质子相互作用形成 HO(2)(),对 PMF 能量分配的直接反馈效应,导致 DeltapH(S)和 ATP 合成减少,因为它增加了线粒体的基本质子漏的影响。本实验数据为我们的假设提供了新的证据,即活性氧物质循环与呼吸链中的 Q 循环和 H(+)循环合作,以保持 PMF 能量分配及其与线粒体呼吸的氧化还原信号调节的平衡。

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