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511276 
Journal Article 
Review 
The formation of peroxynitrite in the applied physiology of mitochondrial nitric oxide 
Poderoso, JJ 
2009 
Yes 
Archives of Biochemistry and Biophysics
ISSN: 0003-9861
EISSN: 1096-0384 
ELSEVIER SCIENCE INC 
NEW YORK 
484 
2 
214-220 
English 
19159609 
WOS:000265705800015 
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. 
Nitric oxide; Peroxynitrite; Mitochondria; Mitochondrial nitric oxide; synthase; Insulin; Thyroid hormones; Aging; Nitration; Oxygen uptake; ob(-)/ob(-) mice; cytochrome-c-oxidase; complex-i; superoxide-dismutase; reversible; inhibition; heart mitochondria; respiratory-chain; energy-metabolism; synthase activity; cell-death; life-span