Jun 6, 1994

Molecular mechanisms of nickel carcinogenesis

The Science of the Total Environment
Max CostaK Salnikow

Abstract

Nickel treatment of intact cultured cells oxidized dichlorofluorescin to a fluorescent product indicating that nickel elevated the level of oxidants in cells. Nickel also caused an increase in crosslinking of amino acids to DNA and these complexes did not appear to involve the direct participation of Ni2+. Histidine, cysteine and tyrosine were prominent among the amino acids crosslinked to DNA. Nickel selectively damaged heterochromatin and this resulted in deletions of heterochromatic regions during nickel carcinogenesis. Thrombospondin was one of the genes expressed in normal cells that was not expressed in nickel-transformed cells. Other aspects of the molecular mechanism of nickel carcinogenesis are discussed.

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References

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Citations

Mentioned in this Paper

Histidine
Amino Acids, I.V. solution additive
Complex (molecular entity)
Dichlorofluorescin
Nickel
Chinese Hamster Ovary Cell
Gene Deletion
2',7'-difluorofluorescein
Plasma Protein Binding Capacity
Tetraiodofluorescein

About this Paper

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