Literature DB >> 17315243

Oxidative stress as a mechanism of teratogenesis.

Jason M Hansen1.   

Abstract

Emerging evidence shows that redox-sensitive signal transduction pathways are critical for developmental processes, including proliferation, differentiation, and apoptosis. As a consequence, teratogens that induce oxidative stress (OS) may induce teratogenesis via the misregulation of these same pathways. Many of these pathways are regulated by cellular thiol redox couples, namely glutathione/glutathione disulfide, thioredoxinred/thioredoinox, and cysteine/cystine. This review outlines oxidative stress as a mechanism of teratogenesis through the disruption of thiol-mediated redox signaling. Due to the ability of many known and suspected teratogens to induce oxidative stress and the many signaling pathways that have redox-sensitive components, further research is warranted to fully understand these mechanisms. Copyright (c) 2007 Wiley-Liss, Inc.

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Year:  2006        PMID: 17315243     DOI: 10.1002/bdrc.20085

Source DB:  PubMed          Journal:  Birth Defects Res C Embryo Today        ISSN: 1542-975X


  40 in total

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7.  Association between maternal occupational exposure to organic solvents and congenital heart defects, National Birth Defects Prevention Study, 1997-2002.

Authors:  Suzanne M Gilboa; Tania A Desrosiers; Christina Lawson; Philip J Lupo; Tiffany J Riehle-Colarusso; Patricia A Stewart; Edwin van Wijngaarden; Martha A Waters; Adolfo Correa
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9.  Arsenate-induced maternal glucose intolerance and neural tube defects in a mouse model.

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10.  Developmental origin of chronic diseases: toxicological implication.

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