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HERO ID
511276
Reference Type
Journal Article
Subtype
Review
Title
The formation of peroxynitrite in the applied physiology of mitochondrial nitric oxide
Author(s)
Poderoso, JJ
Year
2009
Is Peer Reviewed?
Yes
Journal
Archives of Biochemistry and Biophysics
ISSN:
0003-9861
EISSN:
1096-0384
Publisher
ELSEVIER SCIENCE INC
Location
NEW YORK
Volume
484
Issue
2
Page Numbers
214-220
Language
English
PMID
19159609
DOI
10.1016/j.abb.2008.12.020
Web of Science Id
WOS:000265705800015
Abstract
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.
Keywords
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
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