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Characterization of mouse cell lines resistant to nickel(II) ions

X W Wang1, R J Imbra, M Costa

  • 1Institute of Environmental Medicine, New York University Medical Center, New York 10016.

Cancer Research
|December 1, 1988
PubMed

Insights

Nickel exposure creates resistant cells with centromeric abnormalities. This nickel resistance is linked to heterochromatin changes, potentially an early step in nickel carcinogenesis.

Area of Science:

  • Cell Biology
  • Toxicology
  • Carcinogenesis

Background:

  • Nickel chloride (NiCl2) is a known toxicant.
  • Understanding cellular resistance mechanisms is crucial for toxicology and cancer research.

Purpose of the Study:

  • To investigate the mechanisms of nickel resistance in BALB/c-3T3 cells.
  • To explore the relationship between nickel resistance, cellular uptake, metallothionein expression, and chromosomal abnormalities.
  • To assess the potential role of nickel-induced heterochromatin changes in nickel carcinogenesis.

Main Methods:

  • Isolation and characterization of NiCl2-resistant BALB/c-3T3 cell lines.
  • Measurement of Ni(II) cellular uptake in wild-type and resistant cells.
  • Analysis of metallothionein expression.
  • Cytogenetic analysis including C-banding and in situ hybridization to detect heterochromatic abnormalities.
  • Long-term culture to assess stability of resistance and associated chromosomal changes.

Main Results:

  • NiCl2-resistant cell lines were established with 6- to 11-fold resistance.
  • Resistance was not attributed to altered Ni(II) cellular uptake or metallothionein expression.
  • Resistant cells exhibited a high incidence of centromeric heterochromatic abnormalities.
  • Nickel resistance was stable over generations but decreased over time without selection, correlating with reduced centromeric fusions.

Conclusions:

  • Nickel resistance in BALB/c-3T3 cells is associated with significant heterochromatic abnormalities, particularly centromeric fusions.
  • These findings suggest that nickel-induced alterations in heterochromatin may play a role in the early stages of nickel-induced carcinogenesis.

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