Abstract
Nickel is a widely distributed metal that is industrially applied in many forms. Accumulated epidemiological evidence confirms that exposures to nickel compounds are associated with increased nasal and lung cancer incidence, both in mostly occupational exposures. Although the molecular mechanisms by which nickel compounds cause cancer are still under intense investigation, the carcinogenic actions of nickel compounds are thought to involve oxidative stress, genomic DNA damage, epigenetic effects, and the regulation of gene expression by activation of certain transcription factors related to corresponding signal transduction pathways. The present review summarizes our current knowledge on the molecular mechanisms of nickel carcinogenesis, with special emphasis on the role of nickel induced reactive oxygen species (ROS) and signal transduction pathways.
Original language | English |
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Pages (from-to) | 45-67 |
Number of pages | 23 |
Journal | Molecular and Cellular Biochemistry |
Volume | 279 |
Issue number | 1-2 |
DOIs | |
State | Published - Nov 2005 |
Bibliographical note
Funding Information:This work was supported in part by Grants from NIH/NCI CA112557, CA103180, and CA094964, and from NIH/NIEHS ES012451, ES000260.
Keywords
- Carcinogenesis
- Nickel
- Reactive oxygen species
- Signal transduction
- Transcription factor
ASJC Scopus subject areas
- Molecular Biology
- Clinical Biochemistry
- Cell Biology