| Zinc deficiency and neurodevelopment: the case of neurons. | |
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MedLine Citation:
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PMID: 20333753 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Zinc is essential for normal brain development. Gestational severe zinc deficiency can lead to overt fetal brain malformations. Although not teratogenic, suboptimal zinc nutrition during gestation can have long-term effects on the offspring's nervous system. This article will review current knowledge on the role of zinc in modulating neurogenesis and neuronal apoptosis as well as the proposed underlying mechanisms. A decrease in neuronal zinc causes cell cycle arrest, which in part involves a deregulation of select signals (ERK1/2, p53, and NF-kappaB). Zinc deficiency also induces apoptotic neuronal death through the intrinsic (mitochondrial) pathway, which can be triggered by the activation of the zinc-regulated enzyme caspase-3, and as a consequence of abnormal regulation of prosurvival signals (ERK1/2 and NF-kappaB). Alterations in the finely tuned processes of neurogenesis, neuronal migration, differentiation, and apoptosis, which involve the developmental shaping of the nervous system, could have a long-term impact on brain health. Zinc deficiency during gestation, even at the marginal levels observed in human populations, could increase the risk for behavioral/neurological disorders in infancy, adolescence, and adulthood. |
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Authors:
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Ana M Adamo; Patricia I Oteiza |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: BioFactors (Oxford, England) Volume: 36 ISSN: 1872-8081 ISO Abbreviation: Biofactors Publication Date: 2010 Mar-Apr |
Date Detail:
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Created Date: 2010-04-14 Completed Date: 2010-06-28 Revised Date: 2010-12-20 |
Medline Journal Info:
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Nlm Unique ID: 8807441 Medline TA: Biofactors Country: Netherlands |
Other Details:
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Languages: eng Pagination: 117-24 Citation Subset: IM |
Affiliation:
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Department of Biological Chemistry, IQUIFIB (UBA-CONICET), School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / physiology Cell Proliferation Humans Models, Biological NF-kappa B / metabolism Neurons / cytology*, metabolism* Tumor Suppressor Protein p53 / metabolism Zinc / deficiency*, metabolism, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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HD 01743/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/NF-kappa B; 0/Tumor Suppressor Protein p53; 7440-66-6/Zinc |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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