The effects of ageing and sulfur dioxide inhalation exposure on visual-evoked potentials, antioxidant enzyme systems, and lipid-peroxidation levels of the brain and eye.

The effects of ageing and 10 ppm sulfur dioxide (SO(2)) inhalation exposure on visual-evoked potentials (VEPs), thiobarbituric acid reactive substances (TBARS), a product of lipid peroxidation, and the activities of Cu, Zn superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) of brain and eye were investigated in young (3-month), adult (12-month), and mature (24-month) Swiss male albino rats. The experimental groups were placed in an exposure chamber containing a constant level of 10 ppm SO(2), while control groups were placed in an exposure chamber, which was continually pumped with filtered air, for 1 h/day x 7 days/week for 6 weeks. SO(2) inhalation exposure caused increased levels of brain, retina, and lens Cu, Zn SOD activity, and decreased levels of brain and lens GSH-Px activity in all experimental groups with respect to their corresponding control groups, whereas no change was observed in the level of retina GSH-Px activity. No alterations were observed in brain CAT activity. On the other hand, retina CAT activity was slightly decreased in SO(2)-exposed rats, but no change was observed in their lens CAT activity. The brain and lens TBARS levels of all SO(2)-exposed groups were significantly increased in comparison with their respective control groups. The amount of TBARS was only increased in the retina of the SO(2)-exposed 3-month group compared with its control. Of the SO(2)-exposed rats, the mean latencies of the P(1), N(1), P(2), and P(3) components of the 3-month group, P(1), N(1), and N(2) components of the 12-month group, and only P(3) of the 24-month group were significantly prolonged in comparison with those of their control groups. The amplitudes of N(1)P(2) and P(2)N(2) in the 12- and 24-month control groups were significantly decreased compared with those of the 3-month group. On the other hand, no differences were observed among those of SO(2)-exposed groups. These findings suggest that ageing and SO(2) inhalation exposure have the potential to induce antioxidant enzymes in the brain and eye, and VEP alterations, which are the primary target for air pollutants. It could be concluded that lipid peroxidation could play a critical role in the mechanism responsible for VEP alterations with ageing.