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The purpose of the present study was to investigate the effect of lipoic acid on lipid peroxidation, nitric oxide production, and visual evoked potentials (VEPs) in rats exposed to chronic restraint stress and to examine whether lipoic acid could prevent VEP alterations that occurred in stress together with lipid peroxidation. Forty male wistar rats, aged three months, were used in the present study. They were equally divided into four groups: control (C), the group treated with lipoic acid (L), the group exposed to restraint stress (S), and the group exposed to stress and treated with lipoic acid (LS). Chronic restraint stress was applied for 21 days (1 h/day) and lipoic acid (100 mg/kg/day) was injected intraperitonally to the L and LS groups for the same period. Brain and retina TBARS levels were significantly increased in the S group compared with the C group. Lipoic acid reduced retina and brain TBARS levels in the L and LS groups compared with their corresponding control groups. Restraint stress significantly increased nitrite and nitrate levels in both brain and retina in the stress group with respect to the control group. Lipoic acid produced a significant decrease in brain and retina nitrite and nitrate levels of the L and LS groups comparing with their corresponding control groups. All latencies of VEP components were prolonged in the S group with respect to the C group. The study found significant correlations between VEPs latencies and TBARS and nitrite and nitrate levels of retina and brain. Lipoic acid decreased the latencies of all VEP components in the LS group whereas it did not affect them in the L group with respect to their control groups. In summary, lipoic acid treatment was found effective in preventing VEP and TBARS alterations caused by stress.

The aim of this study was to investigate the effect of chronic restraint stress (RS) on spatial learning and memory. Fifty healthy male Wistar rats, aged three months were used. They were equally divided into five groups--C: Control, W: Water Maze, CS-1: Restrained for 21 days (1 h/day) + water maze protocol following stress period, CS-2: Restrained for 28 days (1 h/day) + water maze protocol during last 7 days of stress period, CS-3: Restrained for 21 days and allowed to recovery for 7 days (1 h/day). Corticosterone levels were higher in all stress groups than in C and W groups. Nitrite levels of frontal cortex and hippocampus were found to be elevated in chronic stress groups with respect to C and W groups. Thiobarbituric acid reactive substances (TBARS) of both tissues were increased significantly in CS1 and CS2 groups compared with C, W, and CS3 groups. Escape latencies of CS1 and CS2 groups were longer than those of the W group on each day of acquisition. In transfer test, CS1 and CS2 groups stayed significantly shorter in target quadrant according to the W group. Significant correlations between corticosterone and either nitrite or TBARS of hippocampus and frontal cortex were found. Both acquisition and memory performances were negatively correlated with plasma corticosterone level, nitrite, and TBARS levels of hippocampus and frontal cortex. The results of this study suggest that stress-induced lipid peroxidation may affect the acquisition and memory performances.

The effect of sulfur dioxide (SO(2)) on hippocampus antioxidant status, lipid peroxidation and learning and memory was investigated in diabetic rats. A total of 40 rats were divided into four equal groups: Control (C), SO(2) + C (SO(2)), diabetic (DM) and SO(2) + D (DMSO(2)). Experimental diabetes mellitus (DM) was induced by i.v injection of alloxan with a dose of 50 mg/kg body weight. Ten ppm SO(2) was administered to the rats in the sulfur dioxide groups in an exposure chamber. Exposure occurred 1 h/d, 7 d/wk, for 6 wk; control rats were exposed to filtered air during the same time periods. SO(2) exposure, while markedly increasing Cu-Zn Superoxide dismutase activity, significantly decreased glutathione peroxidase activity in diabetic and non-diabetic groups compared with the C group; hippocampus catalase activity was unaltered. Hippocampus thiobarbituric acid reactive substances (TBARS) were found to be elevated in all experimental groups with respect to control group. The active avoidance training results indicated that diabetic condition has been associated with learning and memory impairment. SO(2) exposure caused deficits of learning and memory. Diabetes mellitus-induced impairment of learning and memory were potentiated by SO(2) exposure. These findings suggest that exposure to SO(2) by increasing lipid peroxidation, can change antioxidant enzyme activities and can elevated intensity of deficits of learning and memory in diabetic rats.