Carcinogenic metal compounds: recent insight into molecular and cellular mechanisms

@article{Beyersmann2008CarcinogenicMC,
  title={Carcinogenic metal compounds: recent insight into molecular and cellular mechanisms},
  author={Detmar Beyersmann and Andrea Hartwig},
  journal={Archives of Toxicology},
  year={2008},
  volume={82},
  pages={493-512}
}
Mechanisms of carcinogenicity are discussed for metals and their compounds, classified as carcinogenic to humans or considered to be carcinogenic to humans: arsenic, antimony, beryllium, cadmium, chromium, cobalt, lead, nickel and vanadium. Physicochemical properties govern uptake, intracellular distribution and binding of metal compounds. Interactions with proteins (e.g., with zinc finger structures) appear to be more relevant for metal carcinogenicity than binding to DNA. In general, metal… Expand
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References

SHOWING 1-10 OF 147 REFERENCES
Interactions by carcinogenic metal compounds with DNA repair processes: toxicological implications.
TLDR
Cobalt, arsenic, nickel and cadmium interfere with base and nucleotide excision repair, even though they affect different steps of the respective repair systems and act by different, not yet completely understood mechanisms. Expand
Molecular and cellular mechanisms of cadmium carcinogenesis.
TLDR
It becomes clear that there exist multiple mechanisms which contribute to the carcinogenicity of cadmium, although the relative weights of these contributions are difficult to estimate. Expand
Role of cellular antioxidants in metal-induced damage
  • M. Sugiyama
  • Chemistry, Medicine
  • Cell Biology and Toxicology
  • 2004
TLDR
The cellular antioxidant defense system, which removes free radicals, may play an important role in the genotoxicity and toxic effects of metal compounds. Expand
Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel, arsenic, and chromium.
TLDR
Overall, metal carcinogenesis appears to require the formation of specific metal complexes, chromosomal damage, and activation of signal transduction pathways promoting survival and expansion of genetically/epigenetically altered cells. Expand
Is the capacity of lead acetate and cadmium chloride to induce genotoxic damage due to direct DNA-metal interaction?
TLDR
An induction of lipid peroxidation and an increase in free radical levels in the different organs of CD-1 male mice after inhalation of lead acetate or cadmium chloride for 1 h is found, suggesting the induction of genotoxicity and carcinogenicity by indirect interactions, such as oxidative stress. Expand
Differential effects of toxic metal compounds on the activities of Fpg and XPA, two zinc finger proteins involved in DNA repair.
TLDR
Even though other mechanisms of protein inactivation cannot be completely excluded, zinc finger structures may be sensitive targets for toxic metal compounds, but each zinc finger protein has unique sensitivities. Expand
Metal-induced oxidative stress and signal transduction.
TLDR
This review covers recent advances in metal-induced generation of reactive oxygen species; the receptors, kinases, and nuclear transcription factors affected by metals andMetal-induced oxidative stress; and global cellular phenomena associated with metal- induced ROS production and gene expression. Expand
Oxidative mechanisms in the toxicity of chromium and cadmium ions.
  • S. Stohs, D. Bagchi, E. Hassoun, M. Bagchi
  • Chemistry, Medicine
  • Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer
  • 2001
TLDR
The results clearly indicate that although different mechanisms lead to the production of reactive oxygen species by chromium and cadmium, similar subsequent mechanisms and types of oxidative tissue damage are involved in the overall toxicities. Expand
Induction and repair inhibition of oxidative DNA damage by nickel(II) and cadmium(II) in mammalian cells.
TLDR
Since oxidative DNA damage is continuously induced during aerobic metabolism, an impaired repair of these lesions might well explain the carcinogenic action of nickel(II) and cadmium(II). Expand
The genetic toxicology of cobalt.
TLDR
Evidence for the interference of Co(II) with DNA repair processes is discussed, regarded as relevant for the risk assessment of human exposure to cobalt in combination with other agents. Expand
...
1
2
3
4
5
...