TY - JOUR
T1 - Mitochondrial nitric-oxide synthase
T2 - Enzyme expression, characterization, and regulation
AU - Haynes, Virginia
AU - Elfering, Sarah
AU - Traaseth, Nathaniel
AU - Giulivi, Cecilia
N1 - Funding Information:
The authors thank the excellent technical assistance of Ms. Laura Yager. These studies had been supported by grants from National Institutes of Health (GM66768 and ES011407), Cottrell Research Corporation (CC5675), and American Chemical Society Petroleum Research Fund (37470-B4).
Copyright:
Copyright 2012 Elsevier B.V., All rights reserved.
PY - 2004/8
Y1 - 2004/8
N2 - Nitric oxide is generated in vivo by nitric-oxide synthase (NOS) during the conversion of L-Arg to citrulline. Using a variety of biological systems and approaches emerging evidence has been accumulated for the occurrence of a mitochondrial NOS (mtNOS), identified as the alpha isoform of neuronal or NOS-1. Under physiological conditions, the production of nitric oxide by mitochondria has an important implication for the maintenance of the cellular metabolism, i.e. modulates the oxygen consumption of the organelles through the competitive (with oxygen) and reversible inhibition of cytochrome c oxidase. The transient inhibition suits the continuously changing energy and oxygen requirements of the tissue; it is a short-term regulation with profound pathophysiological consequences. This review describes the identification of mtNOS and the role of posttranslational modifications on mtNOS' activity and regulation.
AB - Nitric oxide is generated in vivo by nitric-oxide synthase (NOS) during the conversion of L-Arg to citrulline. Using a variety of biological systems and approaches emerging evidence has been accumulated for the occurrence of a mitochondrial NOS (mtNOS), identified as the alpha isoform of neuronal or NOS-1. Under physiological conditions, the production of nitric oxide by mitochondria has an important implication for the maintenance of the cellular metabolism, i.e. modulates the oxygen consumption of the organelles through the competitive (with oxygen) and reversible inhibition of cytochrome c oxidase. The transient inhibition suits the continuously changing energy and oxygen requirements of the tissue; it is a short-term regulation with profound pathophysiological consequences. This review describes the identification of mtNOS and the role of posttranslational modifications on mtNOS' activity and regulation.
KW - Nitric oxide
KW - mitochondria
KW - nitric-oxide synthase
KW - oxygen
KW - oxygen consumption
KW - posttranslational modifications
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U2 - 10.1023/B:JOBB.0000041765.27145.08
DO - 10.1023/B:JOBB.0000041765.27145.08
M3 - Article
C2 - 15377869
AN - SCOPUS:10244222287
SN - 0145-479X
VL - 36
SP - 341
EP - 346
JO - Journal of Bioenergetics and Biomembranes
JF - Journal of Bioenergetics and Biomembranes
IS - 4 SPEC.ISS.
ER -