Overexpression of human copper/zinc-superoxide dismutase in transgenic animals attenuates the reduction of apurinic/apyrimidinic endonuclease expression in neurons after in vitro ischemia and after transient global cerebral ischemia

被引：12
|
作者：
Narasimhan, P
Sugawara, T
Liu, J
Hayashi, T
Noshita, N
Chan, PH
机构：
[1] Stanford Univ, Neurosurg Labs, Sch Med, Dept Neurosurg, Stanford, CA 94305 USA
[2] Stanford Univ, Dept Neurol & Neurol Sci, Sch Med, Stanford, CA 94305 USA
[3] Stanford Univ, Program Neurosci, Sch Med, Stanford, CA 94305 USA
来源：
JOURNAL OF NEUROCHEMISTRY | 2005年 / 93卷 / 02期
关键词：
cell death; DNA repair; hypoxia; ischemia; neurons;
D O I：
10.1111/j.1471-4159.2005.03039.x
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Oxidative stress after ischemia/reperfusion has been shown to induce DNA damage and subsequent DNA repair activity. Apurinic/apyrimidinic endonuclease (APE) is a multifunctional protein in the DNA base excision repair pathway which repairs apurinic/apyrimidinic sites in DNA. We investigated the involvement of oxidative stress and expression of APE in neurons after oxygen-glucose deprivation and after global cerebral ischemia. Our results suggest that overexpression of human copper/zinc-superoxide dismutase reduced oxidative stress with a subsequent decrease in APE expression. Production of oxygen free radicals and inhibition of the base excision repair pathway may play pivotal roles in the cell death pathway after ischemia.
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页码：351 / 358
页数：8
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