Molecular NeuroscienceAPE/Ref-1 responses to ischemia in rat brainEdwards, Michael1; Kent, Thomas A.2; Rea, Harriet Charmaine1; Wei, Jinqua3; Quast, Mike3; Izumi, Tadahide1; Mitra, Sankar1; Perez-Polo, J Regino1,4Author Information 1Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-0652, USA 2Department of Neurology, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-0652, USA 3Department of Marine Biomedical Institute, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-0652, USA 4Corresponding Author: J. Regino Perez-Polo ACKNOWLEDGEMENTS: Thanks to K. Werrbach-Perez for technical assistance and D. Masters for manuscript preparation. Supported in part by NINDS NS33228. Received 14 July 1998; accepted 30 September 1998 NeuroReport: December 21st, 1998 - Volume 9 - Issue 18 - p 4015-4018 Buy Abstract 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, extra-cellular 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 6h of reperfusion following an induced ischemic insult. This specific inhibition of APE/Ref-1 expression may affect the extent of apoptosis after ischemia © 1998 Lippincott Williams & Wilkins, Inc.