ABSTRACT
Lead (Pb) is a highly toxic heavy metals found in every facet of environmental and biological systems. Evidence suggests that most of lead's effects on a child's central nervous system are irreversible. In this study we examined the effect of post-natal lead exposure on the hippocampus of developing Wistar rat. Nine Pregnant rats were randomly distributed into three experimental groups of three rats each, consisting of a control group (1) and experimental groups (2 and 3). After parturition, dams in Group 2 were administered 60mg/kg body weight (bwt) of lead acetate and Group 3 were administered 90mg/kg bwt of lead acetate. The pups of the dams in the experimental groups (2 and 3) were exposed to lead acetate via lactation from dams' that were administered lead (Pb) acetate via oral gavage from post-natal day (PND) 1 - PND 21.The control group (1) was given distilled water (2ml/kg bwt) throughout the experimental period. On PND 22, the pups were weighed and sacrificed after anaesthesia with 75mg/kg of ketamine. The brain tissue was excised and separated into halves along its longitudinal fissure. One half of the brain was homogenized for analysis of lead concentration via Atomic Absorption Spectrophotometry and oxidative stress markers such as Malondialdehyde (MDA), Superoxide Dismutase (SOD) and Reduced Glutathione (GSH). The hippocampus was isolated from the other half of the brain and were fixed in Bouin's fluid and paraformaldehyde fixatives for histological studies. The hippocampus was then processed routinely and stained using H and E for general cytoarchitecture, Cresyl violet stain for Nissl substance and Tomato lectin stain for microglia cells. The volume of the hippocampus and the number of activated microglia cells was then determined using stereology. The result from the present study showed a signicant decrease (p<0.05) in body weight,significant (p<0.05) increase in brain somatic index and an insignificant (p>0.05)decrease in brain weight of Wistar rat's pups exposed to lead acetate via lactation from PND 1-21 when compared with the control. It also revealedsignificant x (p<0.05)increase in accumulation of lead deposit in the brain of the Wistar rat pups exposed to increasing doses of lead acetate. Lead exposure also induced oxidative stress in Wistar rat pups by causing an increase in free radicals production and a significant (p<0.05) decrease in the antioxidant enzymes. Neurotoxicity of lead was also evident as it caused weak staining for Nissl substanceand distortion in cytoarchitecture of the CA3 region of the hippocampus with presence of necrotic pyramidal cell, cell loss and pyknotic nucleus. In comparison with the controls, there was an insignificant (p>0.05) increase in the number of activated microglia cells in Wistar rat pups exposed to lead acetate via lactation from dams from PND 1-21. In conclusion, it can be inferred that exposure of Wistar rat pups to increasing doses of lead acetate from post-natal day 1-21 did not significantly trigger microglia activation but caused distortion in the cytoarchitecture of the CA3 region of the hippocampus of developing Wistar rats.