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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
Author(s) -
Narasimhan Purnima,
Sugawara Taku,
Liu Jing,
Hayashi Takeshi,
Noshita Nobuo,
Chan Pak H.
Publication year - 2005
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2005.03039.x
Subject(s) - ap site , dna (apurinic or apyrimidinic site) lyase , superoxide dismutase , oxidative stress , base excision repair , dna damage , ap endonuclease , dna repair , ischemia , xrcc1 , biology , chemistry , microbiology and biotechnology , biochemistry , dna , medicine , gene , genotype , single nucleotide polymorphism
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.