Acute Co-Exposure of Lead and Cadmium Induce Pronounced Neurotoxicity in Wistar Rat

Abstract

Heavy metals are known to disrupt central nervous system (CNS) function; their precise mechanisms of toxicity remain unclear. This study examines the acute neurotoxic effects of lead (Pb) and cadmium (Cd) on the cerebral cortex, hippocampus, and hypothalamus of Wistar rats (Rattus norvegicus). To investigate their impact, rats were divided into four groups: Group-I (Control), Group-II (administered lead acetate at 180 mg/kg b. w.), Group-III (given cadmium chloride at 26.4 mg/kg b. w.), and Group-IV (administered a combination of lead acetate at 180 mg/kg and cadmium chloride at 26.4 mg/kg b. w.). The designated treatments were given over a four-day acute period. The results revealed significant reductions in tissue protein levels, along with catalase (CAT) and superoxide dismutase (SOD) activities, across all respective brain areas. Additionally, lipid peroxide levels were significantly elevated, indicating oxidative stress. Glutathione peroxidase activity also showed a slight decrease. Among the groups, the combined exposure to Pb and Cd caused the more pronounced effects, with the hippocampus and hypothalamus being the most affected regions. Histopathological analysis further confirmed damage in all brain sub-regions examined. This study highlights that Pb and Cd can traverse the blood-brain-barrier (BBB), triggering oxidative stress and histopathological damage, thereby adversely affecting brain tissue. The findings emphasize the heightened neurotoxic effects when these metals are present in combination.