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The time course of oxidative damage in different brain regions wasinvestigated in the gerbil model of transient cerebral ischemia. Animals weresubjected to both common carotid arteries occlusion for 5 min. After the end ofischemia and at different reperfusion times (2, 6, 12, 24, 48, 72, 96 h and 7days), markers of lipid peroxidation, reduced and oxidized glutathione levels,glutathione peroxidase, glutathione reductase, manganese-dependent superoxidedismutase (MnSOD) and copper/zinc containing SOD (Cu/ZnSOD) activities weremeasured in hippocampus, cortex and striatum. Oxidative damage in hippocampuswas maximal at late stages after ischemia (48-96 h) coincident with asignificant impairment in glutathione homeostasis. MnSOD increased inhippocampus at 24, 48 and 72 h after ischemia, coincident with the markedreduction in the activity of glutathione-related enzymes. The late disturbancein oxidant-antioxidant balance corresponds with the time course of delayedneuronal loss in the hippocampal CA1 sector. Cerebral cortex showed earlychanges in oxidative damage with no significant impairment in antioxidantcapacity. Striatal lipid peroxidation significantly increased as early as 2 hafter ischemia and persisted until 48 h with respect to the sham-operatedgroup. These results contribute significant information on the timing andfactors that influence free radical formation following ischemic brain injury,an essential step in determining effective antioxidant intervention.

Time course of oxidative damage in different brain regions following transient cerebral ischemia in gerbils