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Resuscitation. 1998 Oct-Nov;39(1-2):91-8.

Failure of glutathione peroxidase to reduce transient ischemic injury in the rat hippocampal CA1 subfield.

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Department of Anesthesiology and Surgical Center, Kumamoto University School of Medicine, Honjo, Japan.


It has been postulated that oxygen radical species are produced by ischemia-reperfusion in the brain and play a critical role in neuronal damage. Glutathione peroxidase (GSHPx), one of the antioxidative enzymes, detoxifies hydrogen peroxide, which is the source of a hydroxyl radical that reacts with polyunsaturated fatty acids of the cell membrane, resulting in cell death. The present study was undertaken to investigate the postischemic effect of exogenous GSHPx upon rats subjected to global forebrain ischemia and reperfusion. GSHPx or artificial cerebrospinal fluid (aCSF) as a vehicle for GSHPx was administered into the left cerebral ventricle 15 min after a 5-min 4-vessel occlusion. Neuronal damage and apoptosis were assessed 4 days after ischemic insult using cresyl violet stain and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) method, respectively. Most pyramidal neurons in the hippocampal CA1 subfield were degenerated and their nuclei were stained by the TUNEL in both GSHPx- (80 and 200 units/kg) and aCSF-treated animals. Neurons in other subfields of the hippocampus and dentate gyrus survived. Our further attempt to improve the outcome with a higher dose of GSHPx was unsuccessful because all rats receiving 400 units/kg died soon after the intracerebroventricular injection due to respiratory insufficiency. We conclude that the postischemic treatment with GSHPx does not ameliorate the apoptotic neuronal death of hippocampal CA1 in this transient ischemia model under the conditions used here.

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