Ghafourifar Pedram, Cadenas Enrique
Department of Pharmacology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25704, USA.
Trends Pharmacol Sci. 2005 Apr;26(4):190-5. doi: 10.1016/j.tips.2005.02.005.
Mitochondria produce nitric oxide (NO) through a Ca(2+)-sensitive mitochondrial NO synthase (mtNOS). The NO produced by mtNOS regulates mitochondrial oxygen consumption and transmembrane potential via a reversible reaction with cytochrome c oxidase. The reaction of this NO with superoxide anion yields peroxynitrite, which irreversibly modifies susceptible targets within mitochondria and induces oxidative and/or nitrative stress. In this article, we review the current understanding of the roles of mtNOS as a crucial biochemical regulator of mitochondrial functions and attempt to reconcile apparent discrepancies in the literature on mtNOS.
线粒体通过一种对钙离子(Ca(2+))敏感的线粒体一氧化氮合酶(mtNOS)产生一氧化氮(NO)。mtNOS产生的NO通过与细胞色素c氧化酶的可逆反应来调节线粒体的氧消耗和跨膜电位。这种NO与超氧阴离子反应生成过氧亚硝酸盐,它会不可逆地修饰线粒体内的易感靶点,并诱导氧化和/或硝化应激。在本文中,我们综述了目前对mtNOS作为线粒体功能关键生化调节因子作用的理解,并试图调和文献中关于mtNOS的明显差异。