Effect of vitamin E supplementation on hypoxia-induced oxidative damage inmale albino rats

Background: There is growing evidence that free radicals mediated oxidative injury due to inadequate oxygen availability is an important factor in var ious pathologies at high altitude. Since vitamin E is known to protect the cells from oxidative damage due to its potent antioxidant properties, the p resent study was carried out to explore the effect of vitamin E supplementa tion on various hematological and biochemical parameters in hypoxia-induced oxidative stress in albino rats. Methods: The experiments were conducted o n male albino rats by intermittently exposing them to a simulated altitude of 7576 m (25,000 ft), daily for 6 h for 15 d at 32 +/- 2 degreesC. The con trol group was fed vehicle only (1% Tween 80) and the experimental group wa s given vitamin E (40 mg per rat (.) d(-1)) orally, 5 d prior to and during the period of hypoxic exposure. The variables studied include: hemoglobin, hematocrit, RBC deformability index, a-tocopherol level, malondialdehyde ( MDA), reduced glutathione (GSH), oxidized glutathione (GSSG), lactate dehyd rogenase (LDH) and protein level in blood/plasma and various tissues. Resul ts: Significant increase in hematocrit and hemoglobin and decrease in RBC d eformability index was observed on exposure to hypoxia while vitamin E supp lementation maintained them at the normal level. Hypoxia led to the decreas e in plasma vitamin E and blood glutathione (GSH) level and two-fold increa se in the plasma malondialdehyde (MDA) level. Vitamin E supplementation, on the other hand, resulted in less of an increase in MDA and increased the G SH concentration significantly. LDH activity, which was elevated on exposur e to hypoxia, was arrested on vitamin E supplementation. Conclusion: The re sults indicate that vitamin E supplementation results in preventing oxidati ve damage due to high altitude stress.