Poderoso Juan J
Director of the Laboratory of Oxygen Metabolism, University Hospital, CONICET and University of Buenos Aires, Córdoba 2351, 1120 Buenos Aires, Argentina.
Arch Biochem Biophys. 2009 Apr 15;484(2):214-20. doi: 10.1016/j.abb.2008.12.020. Epub 2009 Jan 6.
Mitochondria require nitric oxide ((.)NO) to exert a delicate control of metabolic rate as well as to regulate life functions, cell cycle activation and arrest, and apoptosis. All activities depend on the matrical (.)NO steady state concentration as provided by mitochondrial (mtNOS) and cytosolic sources (eNOS) and reduced by forming superoxide anion and H2O2 and a low peroxynirite (ONOO(-)) yield. We review herein the biochemical pathways involved in the control of (.)NO mitochondrial level and its biological and physiological significance in hormone effects and aging. At high ()NO, the cost of this physiological regulation is that ONOO(-) excess will lead to nitrosation/nitration and oxidization of mitochondrial and cell proteins and lipids. The disruption of (.)NO modulation of mitochondrial respiration supports then, a platform for prevalent neurodegenerative and metabolic diseases.
线粒体需要一氧化氮（·NO）来精确控制代谢率以及调节生命功能、细胞周期激活与停滞和细胞凋亡。所有这些活动都依赖于线粒体基质中由线粒体一氧化氮合酶（mtNOS）和胞质来源（eNOS）提供的·NO稳态浓度，该浓度会通过形成超氧阴离子和过氧化氢以及低产率的过氧亚硝酸根（ONOO⁻）而降低。我们在此综述了控制线粒体·NO水平所涉及的生化途径及其在激素效应和衰老中的生物学和生理学意义。在高·NO水平时，这种生理调节的代价是ONOO⁻过量会导致线粒体和细胞蛋白质及脂质的亚硝化/硝化和氧化。线粒体呼吸的·NO调节紊乱进而为常见的神经退行性疾病和代谢疾病提供了一个平台。
