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Abstract: This study was to investigate the effects of ascorbic acid on the hippocampus of suckling rats in the presence of lead (Pb)-induced oxidative stress. Pregnant Sprague–Dawley rats received treatment with drinking water, divided into three groups, as follows: (1) distilled water; (2) 0.2% Pb; (3) 0.2% Pb+ascorbic acid (100mg/kg/day). Rat pups were euthanized at the age of 21days and their brain tissue was examined using light microscopy. Protein levels of Cu/Zn superoxide dismutase (Cu/Zn SOD), manganese superoxide dismutase (Mn SOD), and catalase (CAT) in the hippocampus were determined by Western blotting. We found a significant decrease in levels of Cu/Zn SOD and Mn SOD among Pb-exposed pups. Ascorbic acid supplementation appeared to negate the decrease in protein levels for Cu/Zn SOD and Mn SOD. In the case of CAT, there was no effect from Pb administration alone and Pb plus ascorbic acid appeared to increase the levels. In histopathology, ascorbic acid decreased the number of damaged cells in cornu ammonis areas CA1, CA3, and the dentate gyrus (DG) in hippocampus. Our results showed that administration of ascorbic acid during pregnancy and lactation could ameliorate some of the oxidative damage induced by Pb exposure in the developing rat hippocampus. [Copyright &y& Elsevier]

Abstract: Lead is a neurotoxin that affects the developing central nervous system and may potentially induce apoptotic cell death. We investigated the effect of ascorbic acid against lead-induced neurotoxicity in the developing rat hippocampus. Female Sprague–Dawley rats were divided into three groups: control group, lead-treated group and lead plus ascorbic acid-treated group. Lead (0.2% lead acetate) was administered to female rats during pregnancy and lactation, in their drinking water. During this period, rats in the lead plus ascorbic acid-treated group received 100 mg/kg/day ascorbic acid, orally. At the end of the treatment, neuronal damage, apoptosis and blood lead levels were determined and the levels of Bax and Bcl-2 were immunodetected in the hippocampus of 21-day-old male pups. Histopathological evaluation demonstrated that ascorbic acid significantly attenuates apoptosis in the developing hippocampus and also spares hippocampal CA1, CA3 and dentate gyrus (DG) neurons. Simultaneous administration of ascorbic acid and lead lowered the level of Bax protein and increased Bcl-2 in pup hippocampus and reduced lead level in blood of dams compared with lead-treated only. Based on these results, it seems that ascorbic acid may potentially be beneficial in treating lead-induced brain injury in the developing rat brain. [Copyright &y& Elsevier]