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Molecular biology of nickel carcinogenesis

M Costa1, J E Sutherland, W Peng

  • 1Department of Environmental Medicine, New York University School of Medicine, NY 10016, USA.

Molecular and Cellular Biochemistry
|October 27, 2001
PubMed

Insights

This review details nickel carcinogenesis mechanisms, focusing on cellular uptake, dissolution, and effects on DNA. Nickel induces gene silencing via DNA hypermethylation and inhibited histone acetylation.

Area of Science:

  • Environmental Health Sciences
  • Molecular Biology
  • Toxicology

Background:

  • Nickel compounds are known human carcinogens.
  • Understanding nickel carcinogenesis is crucial for public health and occupational safety.
  • Decades of research have elucidated various molecular pathways involved.

Purpose of the Study:

  • To review the molecular mechanisms underlying nickel-induced carcinogenesis.
  • To consolidate findings on nickel's interaction with cellular components and genetic material.
  • To provide a comprehensive overview based on extensive laboratory research.

Main Methods:

  • Review of existing research on nickel uptake (soluble and insoluble forms).
  • Analysis of nickel's dissolution within cells.
  • Examination of nickel's effects on cellular heterochromatin.
  • Discussion of nickel's role in gene silencing through epigenetic modifications.

Main Results:

  • Nickel uptake and dissolution are key initial steps in carcinogenesis.
  • Nickel interacts with and alters cellular heterochromatin structure.
  • Nickel induces gene silencing in mammalian cells via DNA hypermethylation.
  • Nickel inhibits histone acetylation in yeast cells, contributing to genetic instability.

Conclusions:

  • Nickel carcinogenesis involves complex molecular events, including epigenetic alterations.
  • Nickel's ability to induce DNA hypermethylation and affect histone acetylation are critical mechanisms.
  • Further research into nickel's genotoxic and epigenetic effects is warranted.

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