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• W2063760891 startingPage "659" @default.
• W2063760891 abstract "Arsenic and its methylated derivatives are contaminants of air, water, and food and are known as toxicants and carcinogens. Arsenic compounds are also being used as cancer chemotherapeutic agents. In humans, inorganic arsenic is metabolically methylated to mono-, di-, and trimethylated forms. Recent findings suggest that the methylation reactions represent a toxification rather than a detoxification pathway. In recent years, the correlation between arsenic exposure, cytotoxicity and genotoxicity, mutagenicity, and tumor promotion has been established, as well as the association of arsenic exposure with perturbation of physiologic processes, generation of reactive oxygen species, DNA damage, and apoptosis induction. Trivalent forms of arsenic have been found to induce apoptosis in several cellular systems with involvement of membrane-bound cell death receptors, activation of caspases, release of calcium stores, and changes of the intracellular glutathione level. It is well known that calcium ion deregulation plays a critical role in apoptotic cell death. A calcium increase in the nuclei might lead to toxic effects in the cell. In this review, we highlight the relationship between induced disturbances of calcium homeostasis, genomic damage, and apoptotic cell death caused by arsenic and its organic derivatives." @default.
• W2063760891 created "2016-06-24" @default.
• W2063760891 creator A5023144933 @default.
• W2063760891 creator A5073800403 @default.
• W2063760891 creator A5090040067 @default.
• W2063760891 date "2005-06-01" @default.
• W2063760891 modified "2023-10-11" @default.
• W2063760891 title "Intracellular Calcium Disturbances Induced by Arsenic and Its Methylated Derivatives in Relation to Genomic Damage and Apoptosis Induction" @default.
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• W2063760891 doi "https://doi.org/10.1289/ehp.7634" @default.
• W2063760891 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1257587" @default.
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• W2063760891 hasPublicationYear "2005" @default.
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