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The effect of exposure to carcinogenic metals on histone tail modifications and gene expression in human subjects

Adriana Arita1, Magdy Y Shamy, Yana Chervona

  • 1Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY 10987, USA.

Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS)
|May 29, 2012
PubMed

Insights

Nickel and arsenic exposure alters epigenetic mechanisms, specifically histone modifications in peripheral blood mononuclear cells (PBMCs). These changes may contribute to metal-induced carcinogenesis.

Area of Science:

  • Environmental Toxicology
  • Epigenetics
  • Carcinogenesis

Background:

  • The carcinogenic mechanisms of nickel and arsenic compounds are not fully understood.
  • Epigenetic alterations, including DNA methylation and histone modifications, are increasingly implicated in metal-induced carcinogenesis.
  • Previous studies suggest in vitro exposure to nickel or arsenic can alter epigenetic patterns.

Purpose of the Study:

  • To review recent findings on alterations in global posttranslational histone modifications in peripheral blood mononuclear cells (PBMCs) from individuals occupationally exposed to nickel or exposed to arsenic in drinking water.
  • To investigate the association between nickel and arsenic exposure and specific changes in histone modifications.
  • To explore potential sex-specific differences in histone modification patterns following arsenic exposure.

Main Methods:

  • Analysis of global levels of posttranslational histone modifications in PBMCs.
  • Comparison of histone modification patterns between occupationally nickel-exposed subjects and controls.
  • Comparison of histone modification patterns between arsenic-exposed subjects and controls, with stratification by sex.

Main Results:

  • Occupational nickel exposure was linked to increased H3K4me3 and decreased H3K9me2 levels in PBMCs.
  • Arsenic exposure was associated with increased global H3K9me2 and decreased H3K9ac levels.
  • Arsenic exposure induced sex-specific opposing changes in several histone modifications.

Conclusions:

  • Exposure to nickel and arsenic compounds can induce global changes in posttranslational histone modifications in PBMCs.
  • These epigenetic alterations may play a role in the carcinogenic effects of these metals.
  • Further research into metal-induced epigenetic changes could elucidate carcinogenesis mechanisms and inform risk assessment.

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