Molecular mechanisms of arsenic carcinogenesis
| Autor: | Chuanshu Huang, Xianglin Shi, Max Costa, Qingdong Ke |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
DNA Repair
DNA Repair Inhibition Clinical Biochemistry chemistry.chemical_element Biology medicine.disease_cause Arsenic Mice Cricetinae medicine Animals Humans Epigenetics Molecular Biology Carcinogen Genetics Regulation of gene expression Arsenic toxicity Oncogenes Cell Biology General Medicine Rats Gene Expression Regulation Neoplastic Oxidative Stress Cell Transformation Neoplastic chemistry Cancer research Cytokines Environmental Pollutants Rabbits Signal transduction Reactive Oxygen Species Carcinogenesis Protein Kinases DNA Damage Mutagens Signal Transduction Transcription Factors |
| Zdroj: | Molecular and Cellular Biochemistry. 255:57-66 |
| ISSN: | 0300-8177 |
| DOI: | 10.1023/b:mcbi.0000007261.04684.78 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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