Protective Effect of Rutin and Vitamin E on Cobalt Chloride Induced Neurotoxicity

Toxic exposures to cobalt chloride could occur from dietary, occupational, and medical sources. This study evaluated the ameliorative effect of oral administration of rutin and vitamin E on cobalt chloride (CoCl2)-induced oxidative stress in the brain of rats following exposure to cobalt chloride (CoCl2) toxicity. Wistar rats were randomly divided into five groups. Group 1 received only water, while group 2 received cobalt chloride (300 ppm) in drinking water. Groups 3, 4 and 5 also received cobalt chloride, but were treated with rutin (100 mg/kg body weight), rutin (200 mg/kg BW) and vitamin E (50 mg/kg BW) respectively for seven consecutive days. The rats were euthanized 24 hours after the last treatment. The brain was collected for biochemical and histopathological evaluations. The study demonstrated that cobalt chloride caused a significant (P<0.05) decrease in the activities of superoxide dismutase (SOD), glutathione S-transferase (GST), glutathione peroxidase (GPx) and glutathione level, whereas the levels of malondialdehyde (MDA) and hydrogen peroxide (H2O2) increased significantly (P<0.05). However, rutin and vitamin E treatment attenuated CoCl2-induced oxidative stress. Histopathological findings also revealed the ameliorative effect of rutin and Vitamin E on the neuronal damage caused by CoCl2 treatment.