The regulation of mitochondrial oxygen uptake by redox reactions involving nitric oxide and ubiquinol
The regulation of mitochondrial oxygen uptake by redox reactions involving nitric oxide and ubiquinol
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DOI：
10.1074/jbc.274.53.37709
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发表时间：
1999-12-31
影响因子：
4.8
通讯作者：
Boveris, A
中科院分区：
文献类型：
--
作者：
Poderoso, JJ;Lisdero, C;Boveris, A
一氧化氮的可逆抑制作用。NO)对线粒体细胞色素氧化酶的影响和O-2的摄取依赖于线粒体内。没有利用。本研究旨在建立线粒体途径。NO利用通过泛醇氧化和过氧亚硝酸盐（ONOO-）形成的还原和氧化反应调节O-2（自由基阴离子）的产生。为此，使用了由完整线粒体、泛素耗尽/重构的亚线粒体颗粒和ONOO补充的线粒体膜组成的实验模型。从这些实验方法中获得的结果强烈表明，存在独立的途径。一氧化氮在线粒体中的利用，它有效地与结合。NO向细胞色素氧化酶转移，从而释放这种抑制并恢复O-2的摄取。路径。在稳态水平上讨论了NO的利用率。NO和O-2（自由基阴离子），并估计为O-2张力的函数。这些计算表明线粒体。NO的衰变主要通过ONOO-形成和泛醇氧化途径，其次通过与细胞色素氧化酶的可逆结合。
The reversible inhibitory effects of nitric oxide (. NO) on mitochondrial cytochrome oxidase and O-2 uptake are dependent on intramitochondrial . NO utilization. This study was aimed at establishing the mitochondrial pathways for . NO utilization that regulate O-2(radical anion) generation via reductive and oxidative reactions involving ubiquinol oxidation and peroxynitrite (ONOO-) formation. For this purpose, experimental models consisting of intact mitochondria, ubiquinone-depleted/reconstituted submitochondrial particles, and ONOO--supplemented mitochondrial membranes were used.The results obtained from these experimental approaches strongly suggest the occurrence of independent pathways for . NO utilization in mitochondria, which effectively compete with the binding of . NO to cytochrome oxidase, thereby releasing this inhibition and restoring O-2 uptake. The pathways for . NO utilization are discussed in terms of the steady-state levels of . NO and O-2(radical anion) and estimated as a function of O-2 tension. These calculations indicate that mitochondrial . NO decays primarily by pathways involving ONOO- formation and ubiquinol oxidation and, secondarily, by reversible binding to cytochrome oxidase.