Folic acid (Vitamin B9) and cobalamin (Vitamin B12) ameliorate Lead Acetate-induced oxidative stress in the cerebellum of Wistar Rats

Abstract

Heavy metals such as lead-Acetate (PbA) poses a major risk, particularly in developing countries, through contaminated water, industrial emissions, and poor waste management. The cerebellum, crucial for balance and coordination, undergoes oxidative stress and neuronal damage from Pb exposure. This study examined whether folic acid (vitamin B9) and vitamin B12 supplements could counteract lead-induced cerebellar damage in adult Wistar rats. Thirty rats were divided into five groups (n=6): Control, PbA (120 mg/kg), FA + VB12 (100 mg/kg), PbA (120 mg/kg) + FA + VB12 (100 mg/kg), and PbA (120 mg/kg) + FA + VB12 (400 mg/kg). Treatments were administered orally for 14 days. Some brain tissue homogenate was used for biochemical studies, while some was used for histological studies. The results showed a significant (p˂ 0.05) rise in lead (PbA) concentration and Malondialdehyde in the PbA-treated group when compared to the control. A significant (p˂ 0.05) decline was observed in FA + VB12 (100 mg/kg) and Pb (120 mg/kg) + FA + VB12 (400 mg/kg) treated groups. Superoxide dismutase, Catalase, and Glutathione Peroxidase activity decreased significantly (p˂ 0.05) in the Pb-treated group when compared to the control, while a significant (p˂ 0.05) increase was observed in Pb (120 mg/kg) + FA + VB12 (400 mg/kg).  Histologically, PbA caused cerebellar neuronal shrinkage, and gliosis. FA + VB12 treatment attenuated these changes, preserving neuronal structure. In conclusion, folic acid and vitamin B12 synergistically relieve Pb-induced cerebellar oxidative stress, restore antioxidant defenses, maintain histological integrity, and support motor function, highlighting their therapeutic potential.