Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel, arsenic, and chromium.

Title	Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel, arsenic, and chromium.
Authors	Anatoly Zhitkovich, Konstantin Salnikow
Magazine	Chemical Research in Toxicology
Date	12/31/2007
DOI	10.1021/tx700198a
Introduction	Chronic exposure to nickel(II), chromium(VI), or inorganic arsenic (iAs) is associated with increased cancer risk. Recent studies indicate higher carcinogenic risks from chromate and iAs than previously thought, prompting revisions in regulatory standards for environmental and drinking water levels. The genotoxic effects of Cr(VI) and iAs are significantly influenced by their intracellular metabolism, generating reactive intermediates. Toxic metals selectively activate stress-signalling pathways, contributing to cancer development. Ascorbate can enhance or suppress toxic responses, depending on the metal. Metals cause genetic damage through oxidative and non-oxidative mechanisms and induce epigenetic changes, affecting gene expression. In vitro and animal studies support metals acting as cocarcinogens alongside non-metal carcinogens, likely due to interference with DNA repair. Metal carcinogenesis involves specific metal complex formation, chromosomal damage, and signal transduction pathway activation promoting altered cell survival and expansion.
Quote	Zhitkovich, A.; Salnikow, K. Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel, arsenic, and chromium. Chemical Research in Toxicology, 2007. DOI: 10.1021/tx700198a
Element	Nickel (Ni) , Arsenic (As) , Chromium (Cr)
Materials	Metals and Alloys
Topics	Biomedical Materials
Industry	Chemical & Pharmacy