Mechanisms in cadmium-induced carcinogenicity: recent insights

Cadmium is an environmental pollutant, with relevant exposures at workplaces and in the general population. The carcinogenicity has been long established, most evident for tumors in the lung and kidney, but with increasing evidence also for other tumor locations. While direct interactions with DNA a...

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Bibliographic Details
Published in:Biometals 2010-10, Vol.23 (5), p.951-960
Main Author: Hartwig, Andrea
Format: Article
Language:English
Subjects:
Animals
apoptosis
Biochemistry
Biomedical and Life Sciences
Cadmium
Cadmium - toxicity
Carcinogenicity
Carcinogens
Carcinogens, Environmental - toxicity
Cell Biology
Cell cycle control
Cell Proliferation - drug effects
Deoxyribonucleic acid
Deregulation
DNA
DNA Damage
DNA repair
DNA Repair - drug effects
gene expression
Gene Expression - drug effects
Genomic instability
Humans
Life Sciences
Medicine/Public Health
Microbiology
Models, Biological
Mutagens
Mutagens - toxicity
Neoplasms - chemically induced
Oxidative Stress - drug effects
Pharmacology/Toxicology
Plant Physiology
Tumors
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Summary:Cadmium is an environmental pollutant, with relevant exposures at workplaces and in the general population. The carcinogenicity has been long established, most evident for tumors in the lung and kidney, but with increasing evidence also for other tumor locations. While direct interactions with DNA appear to be of minor importance, the interference with the cellular response to DNA damage, the deregulation of cell growth as well as resistance to apoptosis have been demonstrated in diverse experimental systems. With respect to DNA repair processes, cadmium has been shown to disturb nucleotide excision repair, base excision repair and mismatch repair; consequences are increased susceptibility towards other DNA damaging agents and endogenous mutagens. Furthermore, cadmium induces cell proliferation, inactivates negative growth stimuli, such as the tumor suppressor protein p53, and provokes resistance towards apoptosis. Particularly the combination of these multiple mechanisms may give rise to a high degree of genomic instability in cadmium-adapted cells, relevant not only for tumor initiation, but also for later steps in tumor development. Future research needs to clarify the relevance of these interactions for low exposure conditions in humans.
ISSN:0966-0844
1572-8773
DOI:10.1007/s10534-010-9330-4