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[摘要]：Mitochondria require nitric oxide ((NO)-N-center dot) 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)-N-center dot steady state concentration as provided by mitochondrial (mtNOS) and cytosolic sources (eNOS) and reduced by forming superoxide anion and H2O2 and a low perozynitrite (ONOO-) yield. We review herein the biochemical pathways involved in the control of (NO)-N-center dot mitochondrial level and its biological and physiological significance in hormone effects and aging. At high (NO)-N-center dot, 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)-N-center dot modulation of mitochondrial respiration supports then, a platform for prevalent neurodegenerative and metabolic diseases. (C) 2009 Elsevier Inc. All rights reserved. |
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