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.
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.
Narasimhan
Purnima
P
Department of Neurosurgery, Stanford University School of Medicine, Stanford, California 943005, USA.
Sugawara
Taku
T
Liu
Jing
J
Hayashi
Takeshi
T
Noshita
Nobuo
N
Chan
Pak H
PH
D000818:Animals; D002545:Brain Ischemia / Q000201:enzymology / Q000235:genetics; D002478:Cells, Cultured; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase / Q000096:biosynthesis* / Q000235:genetics; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology*; D006801:Humans; D002546:Ischemic Attack, Transient / Q000201:enzymology* / Q000235:genetics; D051379:Mice; D008822:Mice, Transgenic; D009474:Neurons / Q000166:cytology / Q000201:enzymology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000096:biosynthesis* / Q000235:genetics
D013482:Superoxide Dismutase; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase