Metal carcinogenesis: mechanistic implications.
Cancer epidemiology has identified several metal compounds as human carcinogens. Recent evidence suggests that carcinogenic metals induce genotoxicity in a multiplicity of ways, either alone or by enhancing the effects of other agents. This review summarizes current information on the genotoxicity of arsenic, chromium, nickel, beryllium and cadmium compounds and their possible roles in carcinogenesis. Each of these metals is distinct in its primary modes of action; yet there are several mechanisms induced by more than one metal, including: the induction of cellular immunity and oxidative stress, the inhibition of DNA metabolism and repair and the formation of DNA- and/or protein-crosslinks.
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Nelson Institute of Environmental Medicine, New York University Medical Center, Tuxedo 10987.
D000818:Animals; D001682:Biological Availability; D002273:Carcinogens / Q000378:metabolism / Q000493:pharmacokinetics / Q000633:toxicity*; D004249:DNA Damage; D004260:DNA Repair; D004781:Environmental Exposure; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006801:Humans; D008670:Metals / Q000378:metabolism / Q000493:pharmacokinetics / Q000633:toxicity*; D009369:Neoplasms / Q000139:chemically induced / Q000453:epidemiology; D009784:Occupational Diseases / Q000139:chemically induced / Q000453:epidemiology
D002273:Carcinogens; D008670:Metals