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.

Abstract

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.

• Authors: Purnima Narasimhan, Taku Sugawara, Jing Liu, Takeshi Hayashi, Nobuo Noshita, Pak H Chan
• Journal: Journal of neurochemistry (J Neurochem) Vol. 93 Issue 2 Pg. 351-8 (Apr 2005) ISSN: 0022-3042 [Print] England
• PMID: 15816858 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Superoxide Dismutase
• DNA-(Apurinic or Apyrimidinic Site) Lyase

Topics

• Animals
• Brain Ischemia (enzymology, genetics)
• Cells, Cultured
• DNA-(Apurinic or Apyrimidinic Site) Lyase (biosynthesis, genetics)
• Gene Expression Regulation, Enzymologic (physiology)
• Humans
• Ischemic Attack, Transient (enzymology, genetics)
• Mice
• Mice, Transgenic
• Neurons (cytology, enzymology)
• Rats
• Rats, Sprague-Dawley
• Superoxide Dismutase (biosynthesis, genetics)