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.

The present study aims to evaluate the protective effect of methanolic leaf extract and flavonoid-rich leaf extract of Synsepalum dulcificum on lead-acetate-induced toxicity in Wistar albino rats. Forty-five animals were distributed into nine groups with five animals apiece. Group 1 served as the control and was given only distilled water throughout the course of the study. Group 2 served as the lead-induced group and was administered 50 mg/kg lead-acetate. Groups 3-8 were co-administered 50 mg/kg lead-acetate and various doses of the extracts. Group 9 was administered 40 mg/kg vitamin C in addition to 50 mg/kg lead-acetate. The study lasted for 14 days. Standard procedures were used to evaluate the hematological indices, serum total protein, urea, creatinine, as well as marker enzymes in liver and kidney of the animals. Malondialdehyde levels, superoxide dismutase, and glutathione-s-transferase activities were also estimated in the tissues. The results showed that the extracts, especially the high doses, significantly (p < 0.05) ameliorated the harmful effects of lead administration in the liver and kidney as well as in the hematological indices. The extract could, therefore, be considered as having protective effect on lead-induced toxicity in Wistar albino rats.