PURPOSE: The aim of the study was to investigate the effects of vitamin E on stress-induced changes in visual evoked potentials (VEPs) and lipid peroxidation. METHODS: Eight experimental groups of 10 rats per group were formed. These consisted of the control group (C); the group treated with vitamin E (E); groups exposed to cold stress (CS), immobilization stress (IS) and both cold and immobilization stress (CIS), and groups exposed to equivalent stresses and treated with vitamin E (CSE, ISE, CISE). Vitamin E was injected intramuscularly in a dose of 30 mg/kg/day. RESULTS: Following chronic stress (15 days), plasma corticosterone concentrations in all experimental groups were significantly increased over those in C group. Vitamin E significantly decreased corticosterone levels in all stress groups compared with their respective control groups. Brain nitrite levels were significantly more elevated in all stress groups than in the C group. Vitamin E reduced retina and brain nitrite levels in all stress and E groups compared with their respective control groups. Vitamin E decreased glutathione peroxidase (GSH-Px) activity in retina and brain tissues in the CSE group, but increased it in the ISE group compared with their respective control groups. Lipid peroxidation was increased in brain and retina tissues in all stress groups as indicated by the significant increase in thiobarbituric acid-reactive substance (TBARS) levels with respect to the C group. Vitamin E produced a significant decrease in brain and retina TBARS levels in all stress groups with respect to their corresponding control groups. The mean latencies of P1, N1, P2, N2 and P3 components were significantly prolonged in all stress groups compared with the C group. CONCLUSION: Vitamin E returned the VEP latencies in the stress groups to control values. Our findings clearly indicated that vitamin E has the potential to prevent VEP changes caused by stress.
PURPOSE: The aim of the study was to investigate the effects of vitamin E on stress-induced changes in visual evoked potentials (VEPs) and lipid peroxidation. METHODS: Eight experimental groups of 10 rats per group were formed. These consisted of the control group (C); the group treated with vitamin E (E); groups exposed to cold stress (CS), immobilization stress (IS) and both cold and immobilization stress (CIS), and groups exposed to equivalent stresses and treated with vitamin E (CSE, ISE, CISE). Vitamin E was injected intramuscularly in a dose of 30 mg/kg/day. RESULTS: Following chronic stress (15 days), plasma corticosterone concentrations in all experimental groups were significantly increased over those in C group. Vitamin E significantly decreased corticosterone levels in all stress groups compared with their respective control groups. Brain nitrite levels were significantly more elevated in all stress groups than in the C group. Vitamin E reduced retina and brain nitrite levels in all stress and E groups compared with their respective control groups. Vitamin E decreased glutathione peroxidase (GSH-Px) activity in retina and brain tissues in the CSE group, but increased it in the ISE group compared with their respective control groups. Lipid peroxidation was increased in brain and retina tissues in all stress groups as indicated by the significant increase in thiobarbituric acid-reactive substance (TBARS) levels with respect to the C group. Vitamin E produced a significant decrease in brain and retina TBARS levels in all stress groups with respect to their corresponding control groups. The mean latencies of P1, N1, P2, N2 and P3 components were significantly prolonged in all stress groups compared with the C group. CONCLUSION:Vitamin E returned the VEP latencies in the stress groups to control values. Our findings clearly indicated that vitamin E has the potential to prevent VEP changes caused by stress.