Selenium Effect on Hyperoxia-Induced Glutathione Peroxidase Activity and Free Radicals Production in the Brain
DOI : 10.3844/ajessp.2013.439.445
American Journal of Environmental Sciences
Volume 9, Issue 5
The purpose of this study was to examine the behavior of Glutathione Peroxidase (GPx) activity and Free Radicals (FR) production in the brain during graded hyperoxia exposure with and without selenium preventive intake. Forty two adult male rats were assigned to seven groups, six animals each. The first group served as control and the second, third and fourth groups were exposed to hyperoxia for 24, 48 and 72 h, respectively. The fifth, six and seventh groups were exposed to hyperoxia for 24, 48 and 72 h with selenium treatment. Following the exposure period for each group animals were sacrificed and brain tissues were homogenized for GPx and FR analysis. The results of 2-way ANOVA showed that the main effects of both selenium and hyperoxia were significant (p<0.05) for GPx. However, FR production was significantly (p<0.05) affected by hyperoxia only. Pair-wise means comparisons showed that the corresponding means (±) SD of GPx activity decreased significantly (p<0.05), from baseline non-selenium values of 13841.72±1245.67 and 14594.89±6711.50 to 5741.72±949.31 and 4829.98±775.52 following 24 and 48 h of hyperoxia exposure respectively, then increased to 7846.19±2467.69, following 72 h of hyperoxia exposure, as compared with non-selenium mean value of 4346.38±349.14. These differences were attributed to the ability of brain tissue to use selenium to reduce the requirements for GPx during 24 and 48 h as such to spare the integrity of its antioxidant mechanism during 72 h. Based on the results of the present study selenium’s supplement and diet rich selenium are recommended for TBI patients.
© 2013 Ismaeel Bin-Jaliah. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.