| Literature DB >> 17315243 |
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.Entities:
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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