engleski

Changes of oxidative stress parameters in different rat brain regions following traumatic brain injury

Introduction. Oxidative stress is considered to be important cause of secondary tissue damage following traumatic brain injury (TBI). Oxidative damage of cellular macromolecules, such as phospholipids, nucleic acids and proteins by reactive oxygen species, results in subsequent neuronal degeneration. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) are main intracellular enzymes responsible for endogenous antioxidant defense of the brain regions affected by TBI. Therefore, the aim of our study was to evaluate the levels of lipid oxidative damage and the antioxidant enzymes’ activities in different brain regions, at 24 h after the induction of TBI in rats. Materials & Methods. Experiments were performed on adult male Wistar rats. TBI of moderate severity was performed over the left parietal cortex using the lateral fluid percussion (LFP) brain injury model. Rats were sacrificed 24 h after the TBI induction. The brains were removed and the ipsilateral regions of interest (parietal cortex, hippocampus, thalamus, entorhinal cortex and cerebellum) were processed for spectrophotometric analyses of the thiobarbituric acid substances (TBARS) levels, as well as of the SOD and GSH-Px activities. Sham-operated animals were used as the control group. Results. TBI caused statistically significant increases of the TBARS levels in the ipsilateral cortex and hippocampus but it did not affect significantly the levels of the mentioned oxidative stress parameter in the thalamus, entorhinal cortex and cerebellum. GSH-Px activities were significantly increased in the injured parietal cortex and hippocampus, while this enzyme’s activities were not changed significantly in the other brain regions examined. SOD activities obtained from the injured animals were not significantly different in comparison to the levels measured in the sham-operated animals in any brain region tested. Conclusion. Our results suggest significant increases of the levels of oxidative lipid damage and the GSH-Px activities in the ipsilateral parietal cortex and hippocampus, at 24 h following TBI in rats. Thalamus, entorhinal cortex and cerebellum were not oxidatively altered in injured animals, at this time point in our experimental conditions.

traumatic brain injury; oxidative stress; brain regions; rats

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