APE/Ref-1 responses to ischemia in rat brain.
Neuroreport
; 9(18): 4015-8, 1998 Dec 21.
Article
em En
| MEDLINE
| ID: mdl-9926839
Cerebral ischemia and the aftermath of reperfusion form a hypoxic/hyperoxic sequence of events that can trigger oxidative stress response cascades in neurons of the central nervous system. After transient ischemia there is an increase in intracellular Ca2+ release, extracellular glutamate, reactive oxygen species (ROS) and nitric oxide, genotoxic events that stimulate DNA repair. Increased oxidative stress and interrupted blood flow in ischemia, like DNA repair, also deplete cellular ATP and commit neurons to apoptosis. We report that levels of the DNA repair enzyme apurinic/apyrimidinic endonuclease (APE/Ref-1) decreased significantly in the hippocampus but not other brain areas after 6 h of reperfusion following an induced ischemic insult. This specific inhibition of APE/Ref-1 expression may affect the extent of apoptosis after ischemia.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Encéfalo
/
Isquemia Encefálica
/
Carbono-Oxigênio Liases
/
DNA Liase (Sítios Apurínicos ou Apirimidínicos)
Limite:
Animals
Idioma:
En
Revista:
Neuroreport
Assunto da revista:
NEUROLOGIA
Ano de publicação:
1998
Tipo de documento:
Article
País de afiliação:
Estados Unidos
País de publicação:
Reino Unido