Hyperglycemia increases superoxide production in the CA1 pyramidal neurons after global cerebral ischemia
Department of Cell, John A. Burns School of Medicine, University of Hawaii at Manoa, 1960 East-West Road, Biomedical Tower T514, Honolulu, HI 96822, USA. Neuroscience Letters
(Impact Factor: 2.03).
02/2006; 393(2-3):119-21. DOI: 10.1016/j.neulet.2005.09.079
Transient global cerebral ischemia results in selective neuronal death in the vulnerable hippocampal CA1 pyramidal neurons in a delayed manner. Hyperglycemia accelerates and exacerbates neuronal damage in this region. The object of this study was to determine whether hyperglycemia-enhanced damage is associated with increased production of superoxide anion after ischemia. The results showed that hyperglycemic ischemia caused a significant increase of superoxide production in the hippocampal CA1 neurons compared to normoglycemic animals after 18 h of recirculation, suggesting that enhanced superoxide anion production may mediate the hyperglycemia-accelerated and -enhanced neuronal death in the hippocampal CA1 area after ischemia and reperfusion.
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