We examined whether non-enzymatic antioxidant defense systems are disrupted in the brain of rats with water-immersion restraint stress. When rats were exposed to water-immersion restraint stress for 1.5, 3 or 6 h, the brain had decreased ascorbic acid and reduced glutathione contents and increased lipid peroxide and nitric oxide metabolites contents at 3 h and showed further changes in these components with a reduction of vitamin E content at 6 h. Increased serum levels of stress markers were found at 1.5, 3 or 6 h of WIRS. Oral pre-administration of L-ascorbic acid (1.5 mmol/kg) or vitamin E (0.5 mmol/kg) to rats with 6 h of water-immersion restraint stress attenuated the increases in lipid peroxide and nitric oxide metabolites contents and the decrease in vitamin E content in the brain. Pre-administered L-ascorbic acid attenuated the decreases in brain ascorbic acid and reduced glutathione contents at 6 h of water-immersion restraint stress, while pre-administered vitamin E enhanced the decreases in those contents. Pre-administered L-ascorbic acid or vitamin E did not affect the increased serum levels of stress markers in rats with 6 h of water-immersion restraint stress. These results indicate that water-immersion restraint stress causes disruption of non-enzymatic antioxidant defense systems through enhanced lipid peroxidation and nitric oxide generation in the brain of rats with water-immersion restraint stress.
All Science Journal Classification (ASJC) codes
- Medicine (miscellaneous)
- Nutrition and Dietetics
- Clinical Biochemistry