Role of peroxynitrite and neuronal nitric oxide synthase in the activation of poly(ADP-ribose) synthetase in a murine model of cerebral ischemia-reperfusion.
Neurosci Lett
; 248(1): 41-4, 1998 May 22.
Article
em En
| MEDLINE
| ID: mdl-9665659
ABSTRACT
Poly(ADP-ribose) synthetase (PARS) activation, a downstream event of nitric oxide (NO) neurotoxicity has been implicated in cerebral reperfusion injury. The aim of our study was to identify the trigger of PARS activation during stroke. Formation of poly(ADP-ribose) profoundly increased in the early phase of reperfusion. Poly(ADP-ribose) formation was attenuated in mice deficient for neuronal NO synthase (nNOS). We next tested in glioma cells whether NO, or peroxynitrite (a cytotoxic oxidant formed from NO and superoxide) is the actual trigger of PARS activation. Peroxynitrite, but not various NO donors, activated PARS and suppressed cellular viability in a PARS-dependent fashion. Thus, nNOS is responsible for PARS activation in stroke. PARS activation, however, is not a direct result of NO production, but it occurs via peroxynitrite formation.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Isquemia Encefálica
/
Poli(ADP-Ribose) Polimerases
/
Óxido Nítrico Sintase
/
Proteínas do Tecido Nervoso
/
Neurônios
/
Nitratos
Limite:
Animals
Idioma:
En
Revista:
Neurosci Lett
Ano de publicação:
1998
Tipo de documento:
Article
País de afiliação:
Estados Unidos