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Related Experiment Videos

Mutagenesis and comutagenesis by lead compounds.

N K Roy1, T G Rossman

  • 1Institute of Environmental Medicine, NYU Medical Center, NY 10016.

Mutation Research
|December 1, 1992
PubMed
Summary

Lead(II) compounds show weak mutagenicity in Chinese hamster V79 cells. At non-toxic doses, lead(II) inhibits DNA repair, acting as a comutagen rather than an initiating carcinogen.

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Area of Science:

  • Environmental toxicology
  • Genetics and genomics
  • Molecular biology

Background:

  • Previous studies indicated lead(II) is weakly mutagenic to Chinese hamster V79 cells.
  • A transgenic G12 cell line with an E. coli gpt gene was developed, showing increased mutability compared to wild-type V79 cells.

Purpose of the Study:

  • To investigate the mutagenicity of lead acetate and lead nitrate at the gpt locus in G12 cells.
  • To explore the mechanisms of lead-induced DNA damage and its potential role in carcinogenesis.

Main Methods:

  • Mutagenicity assays on G12 cells treated with lead compounds.
  • Nick translation assays to detect DNA strand breaks.
  • In vitro assays using plasmid DNA and lead ions with hydrogen peroxide.

Main Results:

  • Lead acetate was mutagenic only at toxic doses; lead nitrate was not significantly mutagenic.
  • Both lead compounds induced DNA strand breaks (nicks) in chromosomal DNA.
  • Lead ions, in conjunction with hydrogen peroxide, induced DNA nicks in vitro, suggesting Fenton reaction involvement.
  • Non-mutagenic concentrations of lead acetate enhanced the mutagenicity of MNNG and UV light, indicating DNA repair inhibition.

Conclusions:

  • Lead(II) acts as a comutagen at biologically relevant, non-toxic doses by inhibiting DNA repair.
  • Lead(II) is unlikely to be an initiating genotoxic carcinogen but may act as a cocarcinogen.

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