OXIDATIVE BALANCE IN BRAIN AFTER CHRONIC EXPOSURE TO ARSENIC

The effect of chronic As exposure in brain, the specific oxidants production and oxidative stress still needs more attention. In the present study, male wistar rats were chronically exposed to As bythe drinking water during 60 days. The rats receiving a dose of 10 mg As/l showed a 9- and 18-fold increase in the content of As in blood and brain, respectively, as compared to the control group. Histopathological changes were detected in brain samples isolated from animals treated with Asas compared to control animals. The oxidation rate of 2ʹ,7ʹ-Dichlorofluorescein diacetate (DCFH-DA) showed no significant changes after the treatment. A significant increase (13%) in the steady state concentration of ascorbyl radical (A•) was determined in the brain isolated from animals exposed to 50 mg As/l. The lipid radical (LR•) generation rate and the content of malondialdehyde (MDA) were increased by 34% and 32%, respectively in brain isolated from rats receiving 50 mg As/l. The content of ascorbate (AH-) in brain was not affected by the exposure to As.However, the content of glutathione (GSH) and the lipophilic antioxidant α-tocopherol (α-T), were significantly decreased after As supplementation, as compared to control brains. The A•/AH- content ratio in rat brain showed no changes associated to the As supplementation. Nevertheless, a significant increase of 44% and 55% was determined in the LR•/α-T and MDA/α-T content ratios, respectively, suggesting that the oxidative imbalance in the lipophilic cellular medium could be the primarily effect of As associated to membrane damage.