APE/Ref‐1 responses to ischemia in rat brain
作者:
Michael Edwards,
Thomas Kent,
Harriet Rea,
Jinqua Wei,
Mike Quast,
Tadahide Izumi,
Sankar Mitra,
J Perez-Polo,
期刊:
NeuroReport
(OVID Available online 1998)
卷期:
Volume 9,
issue 18
页码: 4015-4018
ISSN:0959-4965
年代: 1998
出版商: OVID
关键词: APE/Ref-1;DNA repair;Hypoxia;Ischemia;Reperfusion;Stroke
数据来源: OVID
摘要:
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, extra-cellular 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 6h 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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