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Changes in superoxide dismutase and glutathione peroxidase activities in the parietal cortex and hippocampus of rats exposed to focal cerebral ischemia

Reactive oxygen species are an important cause of tissue injury during cerebral ischemia and reperfusion (I/R). Superoxide dismutase (SOD) and glutathione peroxidase (GPX) are the main intracellular enzymes responsible for endogenous antioxidant defense of tissues affected by I/R. The aim of this study was to examine temporal and regional changes of SOD and GPX activities in animals exposed to temporary focal cerebral ischemia. Male Wistar Hannover rats were subjected to right middle cerebral artery (MCA) occlusion for 2 h. Animals were sacrificed immediately, 0.5, 1, 2, 3, 6, 24, 48, 72 or 168 h after ischemic procedure. SOD and GPX activities were determined spectrophotometrically in the parietal cortex and hippocampus, both ipsilaterally and contralaterally to the occlusion. Sham-operated animals were used as the control group. The level of SOD activity increased significantly in the period from 0.5 to 48 h of reperfusion, in the right parietal cortex. In the same region, a statistically significant rise of GPX activity was recorded 1 h after ischemia. After a transient decrease, second rise in enzymatic activity was determined 72 and 168 h after ischemia. In the hippocampus, a statistically significant increase in SOD activity was found in the period from 0.5 to 72 h after MCA occlusion, both ipsilaterally and contralaterally. The level of hippocampal GPX activity did not change significantly throughout the reperfusion times examined. These results indicate that temporary focal cerebral ischemia caused significant changes in the SOD and GPX activities in the parietal cortex and hippocampus during different periods of reperfusion.

focal cerebral ischemia; SOD; GPX; rat

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