The protective role of ascorbic acid on hippocampal CA1 pyramidal neurons in a rat model of maternal lead exposure |
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| Affiliation: | 1. Golestan Neuroscience Research Center, Golestan University of Medical Sciences, Gorgan, Iran;2. Department of Biology, Faculty of Science, Golestan University, Gorgan, Iran;1. Center for Neuroscience, Cell Biology, University of Coimbra, 3004 517 Coimbra, Portugal;2. Faculty of Pharmacy, University of Coimbra, 3000 548 Coimbra, Portugal;1. Fisheries Division, Department of Natural Resources, Isfahan University of Technology, Isfahan 8415683111, Iran;2. Young Researchers and Elites Club, Science and Research Branch, Islamic Azad University, Tehran, Iran;1. Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil;2. Department of Basic Sciences, School of Dentistry, UNESP − Universidade Estadual Paulista, Rodovia, Araçatuba, SP, Brazil;1. School of Anatomical Sciences, Faculty of Health Sciences, University of the Witwatersrand, 7 York Road, Parktown, 2193 Johannesburg, South Africa;2. South African Research Chair of Mammal Behavioural Ecology and Physiology, University of Pretoria, Pretoria 0002, South Africa;3. KSU Mammals Research Chair, Department of Zoology, King Saud University, Riyadh 11451, Saudi Arabia;4. Faculté des Sciences, University of Kisangani, B.P 1232 Kisangani, Congo;5. Department of African Zoology, Royal Museum for Central Africa, Leuvensesteenweg 13, B-3080 Tervuren, Belgium;6. Laboratory of Histology and Neuropathology, Université Libre de Bruxelles, 1070 Brussels, Belgium;7. Department of Anthropology, University of Arkansas, Fayetteville, AR 72701, USA;8. Saudi Wildlife Authority, Riyadh 11575, Saudi Arabia;9. Queensland Brain Institute, University of Queensland, St. Lucia 4072, Australia;1. Laboratoire Neurosciences, Pharmacology and Environment, Faculté des Sciences Semlalia, Université Cadi Ayyad, Marrakech BP 2390, Morocco;2. Laboratoire de Chimie Organique Appliquée, Faculté des Sciences Semlalia, Université Cadi Ayyad, Marrakech, Morocco;1. Neurobiology Laboratory, Department of Healthcare Biotechnology, Atta-ur-Rahman School of Applied Biosciences, National University of Sciences and Technology, Sector H-12, Islamabad, 44000, Pakistan;2. Department of Pharmacy, COMSATS Institute of Information Technology, Abbottabad, 22060, K.P.K, Pakistan |
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| Abstract: | Oxidative stress is a major pathogenic mechanism of lead neurotoxicity. The antioxidant ascorbic acid protects hippocampal pyramidal neurons against cell death during congenital lead exposure; however, critical functions like synaptic transmission, integration, and plasticity depend on preservation of dendritic and somal morphology. This study was designed to examine if ascorbic acid also protects neuronal morphology during developmental lead exposure. Timed pregnant rats were divided into four treatment groups: (1) control, (2) 100 mg/kg ascorbic acid once a day via gavage, (3) 0.05% lead acetate in drinking water, and (4) 0.05% lead + 100 mg/kg oral ascorbic acid. Brains of eight male pups (P25) per treatment group were processed for Golgi staining. Changes in hippocampal CA1 pyramidal neurons’ somal size were estimated by cross-sectional area and changes in dendritic arborization by Sholl’s analysis. One-way ANOVA was used to compare results among treatment groups. Lead-exposed pups exhibited a significant decrease in somal size compared to controls (P < 0.01) that was reversed by cotreatment with ascorbic acid. Sholl’s analysis revealed a significant increase in apical dendritic branch points near cell body (P < 0.05) and a decreased total dendritic length in both apical and basal dendritic trees of CA1 neurons (P < 0.05). Ascorbic acid significantly but only partially reversed the somal and dendritic damage caused by developmental lead exposure. Oxidative stress thus contributes to lead neurotoxicity but other pathogenic mechanisms are also involved. |
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| Keywords: | Lead exposure Hippocampus Dendrite arborisation Ascorbic acid |
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