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Titolo:
Mitochondrial nitric-oxide synthase stimulation causes cytochrome c release from isolated mitochondria - Evidence for intramitochondrial peroxynitrite formation
Autore:
Ghafourifar, P; Schenk, U; Klein, SD; Richter, C;
Indirizzi:
Swiss Fed Inst Technol, Inst Biochem, CH-8092 Zurich, Switzerland Swiss Fed Inst Technol Zurich Switzerland CH-8092 92 Zurich, Switzerland
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 44, volume: 274, anno: 1999,
pagine: 31185 - 31188
SICI:
0021-9258(19991029)274:44<31185:MNSSCC>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT-LIVER MITOCHONDRIA; LIPID-PEROXIDATION; MEDIATED APOPTOSIS; HL-60 CELLS; SUPEROXIDE; CALCIUM; DYSFUNCTION; NEUROTOXICITY; CALMODULIN; ACTIVATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Ghafourifar, P Swiss Fed Inst Technol, Inst Biochem, CH-8092 Zurich, Switzerland Swiss Fed Inst Technol Zurich Switzerland CH-8092 zerland
Citazione:
P. Ghafourifar et al., "Mitochondrial nitric-oxide synthase stimulation causes cytochrome c release from isolated mitochondria - Evidence for intramitochondrial peroxynitrite formation", J BIOL CHEM, 274(44), 1999, pp. 31185-31188

Abstract

Nitric oxide (NO) is synthesized by members of the NO synthase (NOS) family. Recently the existence of a mitochondrial NOS (mtNOS), its Ca2+ dependence, and its relevance for mitochondrial bioenergetics was reported (Ghafourifar, P., and Richter, C. (1997) FEBS Lett. 418, 291-296; Giulivi, C., Poderoso, J. J., and Boveris, A. (1998) J. Biol. Chem. 273, 11038-11043). Here we report on the possible involvement of mtNOS in apoptosis. We show that uptake of Ca2+ by mitochondria triggers mtNOS activity and causes the release of cytochrome c from isolated mitochondria in a Bcl-2-sensitive manner. mtNOS-induced cytochrome c release was paralleled by increased lipid peroxidation. The release of cytochrome c as well as increase in lipid peroxidation were prevented by NOS inhibitors, a superoxide dismutase mimic, and a peroxynitrite scavenger. We show that mtNOS-induced cytochrome c release is not mediated via the mitochondrial permeability transition pore because the release was aggravated by cyclosporin A and abolished by blockade of mitochondrial calcium uptake by ruthenium red. We conclude that, upon Ca2+-inducedmtNOS activation, peroxynitrite is formed within mitochondria, which causes the release of cytochrome c from isolated mitochondria, and we propose a mechanism by which elevated Ca2+ levels induce apoptosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 10:39:54