Erythrocytes (RBC) from untrained male Wistar rats and rat glomerular endothelial cells (EC) were used to investigate the effects of acute exercise (speed: 20 m/min, slope: 0, duration: 1 hour) on RBC membrane protein oxidation and adhesion to cultured EC. Experimental animals were divided into juvenile (age 10 weeks) and adult (age 30 weeks) groups for these studies. Immediately following exercise, juvenile rat RBC membrane protein oxidation was significantly enhanced. Adult rat RBC showed significantly higher basal protein oxidation than juvenile RBC; but the level of adult rat RBC membrane protein oxidation was unaffected by exercise. Prior to exercise, adult rat RBC showed significantly higher adhesion to EC than RBC of juvenile rat. There was no difference in plasma fibronectin or fibrinogen levels following exercise. Only juvenile rat RBC showed a significant decrease in sialic acid residue content following exercise. These experiments show that there are changes in RBC-EC interactions following exercise that are influenced by animal age.
In a previous study we demonstrated that acute footshock stress increased glutathione peroxidase activity in the prefrontal cortex and striatum of adult male rats. Adolescents may respond differently to stress as life stressors may be greater than at other ages. The present study examined the effects of the acute footshock stress on superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzyme activities and thiobarbituric acid reactive substances (TBARS) levels in adolescent male and female rat brains. We demonstrated that acute footshock stress increased SOD activity in the prefrontal cortex, and increased GPx activity in the hippocampus in female rats. In males, acute footshock stress increased GPx activity in the prefrontal cortex and hippocampus. Footshock stress did not change TBARS levels. These results indicate a strong role of gender in the response of adolescent subjects to various aspects of stress.
Melatonin has recently been suggested as an antioxidant that may protect neurons from oxidative stress. Acute ethanol administration produces both lipid peroxidation as an indicator of oxidative stress in the brain and impairs water-maze performance in spatial learning and memory tasks. The present study investigated the effect of melatonin against ethanol-induced oxidative stress and spatial memory impairment. The Morris water maze was used to evaluate the cognitive functions of rats. Thiobarbituric acid reactive substances (TBARS), which are the indicators of lipid peroxidation, and the activities of antioxidative enzymes (glutathione peroxidase and superoxide dismutase) were
measured in the rat hippocampus and prefrontal cortex which form
interconnected neural circuits for spatial memory. Acute administration of ethanol significantly increased TBARS levels in the hippocampus. Combined melatonin-ethanol treatment caused a significant increase in glutathione peroxidase activities and a significant decrease of TBARS
in the rat hippocampus. In the prefrontal cortex, there was only a significant decrease of TBARS levels in the combined melatonin-ethanol receiving group as compared to the ethanol-treated group. Melatonin did not affect the impairment of spatial memory due to acute ethanol exposure, but melatonin alone had a positive effect on water maze performances. Our study demonstrated that melatonin decreased ethanol-induced lipid peroxidation and increased glutathione peroxidase activity in the rat hippocampus.