Perinatal Exposure to Lead: Reduction in Alterations of Brain Mitochondrial Antioxidant System with Calcium Supplement

Lead (Pb) is a potent neurotoxicant that causes several neurochemical and behavioral alterations. Previous studies showed that the gestational and lactational exposure to Pb reduces the cholinergic and aminergic systems, and behavior of rats. The present study was designed to examine the protective...

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Bibliographic Details
Published in:Biological trace element research 2014-12, Vol.162 (1-3), p.270-277
Main Authors: Gottipolu, Rajarami Reddy, Davuljigari, Chand Basha
Format: Article
Language:English
Subjects:
Animals
Antioxidants
Antioxidants - metabolism
Biochemistry
Biomedical and Life Sciences
Biotechnology
Brain
Brain - drug effects
Brain - metabolism
Calcium
Calcium - pharmacology
Dietary Supplements
Female
Hippocampus - drug effects
Lead
Lead - toxicity
Life Sciences
Male
Malondialdehyde - metabolism
Mitochondria - drug effects
Mitochondria - metabolism
Nutrition
Oncology
Oxidative stress
Oxidative Stress - drug effects
Pregnancy
Prenatal development
Rats
Toxicity
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Summary:Lead (Pb) is a potent neurotoxicant that causes several neurochemical and behavioral alterations. Previous studies showed that the gestational and lactational exposure to Pb reduces the cholinergic and aminergic systems, and behavior of rats. The present study was designed to examine the protective effects of calcium supplementation against Pb-induced oxidative stress in cerebellum and hippocampus of brain at postnatal day (PND) 21, PND 28, PND 35, and PND 60. Pregnant rats were exposed to 0.2 % Pb (Pb acetate in drinking water) from gestational day 6 (GD 6) and pups were exposed through maternal milk till weaning (PND 21). We found that the activity of serum ceruloplasmin oxidase (Cp), mitochondrial manganese superoxide dismutase (Mn-SOD), copper zinc superoxide dismutase (Cu/Zn-SOD), glutathione peroxidase (GPx), catalase (CAT), and xanthine oxidase (XO) enzyme activities were decreased, whereas the malondialdehyde (MDA) levels increased in the cerebellum and hippocampus of Pb-exposed rats. These changes were more prominent at PND 35 and greater in hippocampus compared to cerebellum. Among the enzyme activities, Mn-SOD and Cu/Zn-SOD showed maximum decrease compared to GPx, CAT, XO, and Cp. Furthermore, 0.02 % calcium supplementation together with 0.2 % Pb significantly reversed the Pb-induced alterations in the enzyme activities, and MDA levels. In conclusion, these data suggest that early life exposure to Pb induce alterations in the mitochondrial antioxidant system of brain regions which remain for long even after Pb exposure has stopped. Calcium supplementation may potentially be beneficial in treating Pb toxicity in the developing rat brain.
ISSN:0163-4984
1559-0720
DOI:10.1007/s12011-014-0112-7