Abstract
Arsenic is a metalloid compound that is widely distributed in the environment. Human exposure of this compound has been associated with increased cancer incidence. Although the exact mechanisms remain to be investigated, numerous carcinogenic pathways have been proposed. Potential carcinogenic actions for arsenic include oxidative stress, genotoxic damage, DNA repair inhibition, epigenetic events, and activation of certain signal transduction pathways leading to abberrant gene expression. In this article, we summarize current knowledge on the molecular mechanisms of arsenic carcinogenesis with an emphasis on ROS and signal transduction pathways.
Original language | English |
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Pages (from-to) | 57-66 |
Number of pages | 10 |
Journal | Molecular and Cellular Biochemistry |
Volume | 255 |
Issue number | 1-2 |
DOIs | |
State | Published - Jan 2004 |
Bibliographical note
Funding Information:This work was supported by grants CA094964 and CA103180 from NIH/NCI.
Keywords
- Arsenic
- Carcinogenesis
- Gene expression
- Genetic toxicity
- Kinase
- Methylation
- Reactive oxygen species
- Signal transduction
ASJC Scopus subject areas
- Molecular Biology
- Clinical Biochemistry
- Cell Biology