In utero-initiated cancer: the role of reactive oxygen species.
It is becoming more evident that not only can drugs and environmental chemicals interfere with normal fetal development by causing structural malformations, such as limb defects, but that xenobiotic exposure during development can also cause biochemical and functional abnormalities that may ultimately lead to cancer later on in life. Fetal toxicity may be partly mediated by the embryonic bioactivation of xenobiotics to free radical intermediates that can lead to oxidative stress and potentially lead, in some cases, to carcinogenesis. Using a number of examples, this review will focus on the role of reactive oxygen species (ROS) in the mechanisms pertaining to in utero initiated cancers.
Wan
Joanne
J
Department of Pharmacology and Toxicology, School of Environmental Studies, Queen's University, Kingston, Ontario, Canada.
Winn
Louise M
LM
D000818:Animals; D002648:Child; D004249:DNA Damage; D005260:Female; D006801:Humans; D009369:Neoplasms / Q000209:etiology* / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D012907:Smoking / Q000009:adverse effects; D015262:Xenobiotics / Q000633:toxicity
D017382:Reactive Oxygen Species; D015262:Xenobiotics