Abstract
Background: The most critical effects of lead (Pb) toxicity occur among children exposed during fetal development, postnatal development or both. Malnutrition is a common problem worldwide and occurs in both developing and developed countries. Zinc is an essential mineral and a fundamental component of the endogenous enzymatic antioxidant system. Objective: To evaluate the possible protective effects of zinc against postnatal Pb-induced alterations in the physical and neurobehavioral development in both normally-fed (NF) and protein malnourished (PM) rats. Methods: Protein sufficient diet (20% casein) for NF groups and protein deficient one (8% casein) for PM groups were utilized. Both NF and PM groups were subdivided to 3 groups 6 dams/each and received daily from parturition until weaning (together with diet); saline for control, 1 ml lead acetate (12 mg/ml) and zinc sulphate (32 mg/kg) with Pb. Pups were evaluated for physical and neurobehavioral development as well as for performance in Neonatal T-maze and Open-field test (OFT). Results: Postnatal Pb exposure inhibited most physical and neurobehavioral development of both NF and PM pups. It also reduced number of correct choices as well as ambulation and rearing frequencies in both pups, the effect was more pronounced in PM pups. However, Zinc increased these parameters in NF and PM pups but increased body weight, ambulation and rearing frequencies while decreased time of appearance of eye opening and grooming time in NF pups only. Conclusion: Postnatal Pb exposure caused alteration in some aspect of physical and neurobehavioral development as well as in some behavioral functions as learning, emotionality as well as locomotor and exploratory activities. The alterations were much greater under the condition of protein malnutrition. Zinc was shown to protect against these lead-induced alterations in both NF and PM rat pups. However the protective effect of Zinc sometimes declined under concomitant protein malnutrition.
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