Lipid peroxidation in brain tissue following administration of low and high doses of arsenite and L-ascorbate in wistar strain rats

This study aimed at investigating the mechanism by which sodium arsenite induces brain injury and the role of L-ascorbate. Thirty adult (n=5) Wistar rats weighing between 140 and 160 g were used. Group 1 neither received sodium arsenite nor L-ascorbate (control), group 2 was administered low dose of arsenite only, group 3 received high dose of arsenite only, group 4 was administered L-ascorbate only, group 5 was administered low dose of arsenite and L-ascorbate, and group 6 received high dose of arsenite and L-ascorbate. M0 alon dialdehyde, MDA, levels were significantly increased in rats treated with high dose of arsenite when compared with those treated with low dose of arsenite. However, all treated groups except those treated with L-ascorbate only showed significant increase in MDA levels when compared with the control group. Rats treated with high dose of arsenite and L-ascorbate showed a significantly higher MDA level than those treated with low dose of arsenite and L-ascorbate. However, catalase activity, body weight gain, brain weight and mean food consumption were comparable across all groups. Brain tissue total protein was similar in all groups except in both groups treated with high dose of arsenite, where they were significantly reduced when compared with the control group. I0 n conclusion, sodium arsenite treatment induces brain injury via a mechanism associated with lipid peroxidation, but not catalase-dependent. However, L-ascorbate ameliorates arsenite-induced oxidative injury in the brain. L-ascorbate antioxidative potential in alleviating arsenite-induced brain injury is dependent on the concentration of arsenite.