APE/Ref-1 responses to ischemia in rat brain

Michael Edwards, Thomas A. Kent, Harriet Charmaine Rea, Jinqua Wei, Mike Quast, Tadahide Izumi, Sankar Mitra, J. Regino Perez-Polo

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


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, extracellular 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 6 h of reperfusion following an induced ischemic insult. This specific inhibition of APE/Ref-1 expression may affect the extent of apoptosis after ischemia.

Original languageEnglish (US)
Pages (from-to)4015-4018
Number of pages4
Issue number18
StatePublished - Dec 21 1998
Externally publishedYes


  • APE/Ref-1
  • DNA repair
  • Hypoxia
  • Ischemia
  • Reperfusion
  • Stroke

ASJC Scopus subject areas

  • General Neuroscience


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