Oxidative damage to brain proteins, loss of glutamine synthetase activity, and production of free radicals during ischemia/reperfusion-induced injury to gerbil brain.

摘要: Free radical-mediated oxidative damage has been implicated in tissue injury resulting from ischemia/reperfusion events. Global cortical to Mongolian gerbil brains was produced by transient occlusion of both common carotid arteries. Protein oxidation, as measured protein carbonyl content, increased significantly during the reperfusion phase that followed 10 min ischemia. The activity glutamine synthetase, an enzyme known be inactivated metal-catalyzed oxidation reactions, decreased 65% control levels after 2 hr We also report free radical spin trap N-tert-butyl-alpha-phenylnitrone [300 mg/kg (body weight)] administered 60 before is initiated, partially prevents and protects loss synthetase activity. In addition, we a N-tert-butyl-alpha-phenylnitrone-dependent nitroxide obtained lipid fraction ischemia/reperfusion-lesioned brains, but there very little present comparable sham-operated brains. These data strengthen previous observation utilizing vivo-trapping methods, flux ischemia-lesioned brain. would expected increase brain L-glutamate. Thus, inactivation may critical factor neurotoxicity cerebral injury.