Oxidative stress as a mechanism of teratogenesis.
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.
Hansen
Jason M
JM
Department of Pediatrics, Emory School of Medicine, Emory University, Atlanta, Georgia 30322, USA. jhansen@emory.edu
D000014:Abnormalities, Drug-Induced / Q000209:etiology* / Q000378:metabolism*; D000818:Animals; D002451:Cell Compartmentation; D002453:Cell Cycle; D005260:Female; D006801:Humans; D008954:Models, Biological; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D011247:Pregnancy; D017382:Reactive Oxygen Species / Q000378:metabolism; D015290:Second Messenger Systems; D015398:Signal Transduction; D013723:Teratogens / Q000633:toxicity*; D013792:Thalidomide / Q000633:toxicity
D017382:Reactive Oxygen Species; D013723:Teratogens; D013792:Thalidomide