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 endon
uclease (APE/Ref-1) decreased significantly in the hippocampus but not othe
r 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. (C) 1998 Lippincott Williams & Wilkins.