The article by Konstantin Salnikow and Anatoly Zhitkovich discusses the genetic and epigenetic mechanisms involved in the carcinogenic effects of nickel, arsenic, and chromium. Chronic exposure to these metals has been linked to increased cancer incidence, with recent studies revealing higher carcinogenic risks than previously thought. The genotoxic effects of these metals are influenced by their intracellular metabolism, which creates reactive intermediates and byproducts. These metals can activate stress-signaling pathways, contributing to the development of human cancers. Ascorbate (vitamin C) can either enhance or suppress toxic responses in human cells, depending on the metal. Metals can also cause significant changes in DNA methylation and histone modifications, leading to epigenetic silencing or reactivation of gene expression. In vitro and animal studies support the idea that metals can act as cocarcinogens, interfering with DNA repair processes. Overall, metal carcinogenesis involves the formation of specific metal complexes, chromosomal damage, and activation of signal transduction pathways promoting the survival and expansion of genetically/epigenetically altered cells. The article provides detailed insights into the mechanisms of nickel, arsenic, and chromium carcinogenesis, highlighting the importance of epigenetic changes and DNA repair inhibition in their carcinogenic processes.The article by Konstantin Salnikow and Anatoly Zhitkovich discusses the genetic and epigenetic mechanisms involved in the carcinogenic effects of nickel, arsenic, and chromium. Chronic exposure to these metals has been linked to increased cancer incidence, with recent studies revealing higher carcinogenic risks than previously thought. The genotoxic effects of these metals are influenced by their intracellular metabolism, which creates reactive intermediates and byproducts. These metals can activate stress-signaling pathways, contributing to the development of human cancers. Ascorbate (vitamin C) can either enhance or suppress toxic responses in human cells, depending on the metal. Metals can also cause significant changes in DNA methylation and histone modifications, leading to epigenetic silencing or reactivation of gene expression. In vitro and animal studies support the idea that metals can act as cocarcinogens, interfering with DNA repair processes. Overall, metal carcinogenesis involves the formation of specific metal complexes, chromosomal damage, and activation of signal transduction pathways promoting the survival and expansion of genetically/epigenetically altered cells. The article provides detailed insights into the mechanisms of nickel, arsenic, and chromium carcinogenesis, highlighting the importance of epigenetic changes and DNA repair inhibition in their carcinogenic processes.