Abstract

Nickel has been linked to various neurodevelopmental deficits. Therefore, this study aims to unravel the mechanism through which prenatal exposure Ni may trigger neurodevelopmental disruptions in postnatal life. Ten pregnant Wistar rats were divided into two groups; control and Ni-treated groups. The control group was administered normal saline while the Ni group was treated with 20 mg/kg body weight of NiCl2 from gestational day 7 – 21. After parturition, pups were sacrificed on postnatal days 21 and 42. Their brains were excised for biochemical estimation of malondialdehyde, nitric oxide and glutathione as well as histological analysis of the hippocampal CA3. Our findings revealed elevated malondialdehyde and NO activity with depleted GSH level in the brains prenatally exposed to Ni. Histological distortions from oxidative damage were prominent in this group. We concluded that prenatal exposure to Ni could induce neurodevelopmental abnormality via oxidative stress in the rat brain to provoke neuronal injury.