Chromosomal changes in cell lines from mouse tumors induced by nickel sulfide and methylcholanthrene

Christie, Nelwyn T.; Tummolo, Donna M.; Biggart, Neal W.; Murphy, Edwin C.

doi:10.1007/bf00117770

Cited by 5 publications

(2 citation statements)

References 41 publications

(41 reference statements)

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“…Our data suggest that nickel acetate, and perhaps other carcinogenic nickel compounds, can cause DNA repair problems and that this activity may be one of the mechanisms responsible for their carcinogenic properties. Our suggestion is also consistent with the observation of chromosome abnormalities in mouse tumors induced by nickel compounds which are not clastogenic (39).…”

Section: Discussionsupporting

confidence: 92%

Toxicological interactions between nickel and radiation on chromosome damage and repair.

Heo²,

Chiewchanwit³

1994

Environ Health Perspect

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Carcinogenic nickel compounds are usually found to be weak mutagens; therefore these compounds may not exert their carcinogenic activity through conventional genotoxic mechanisms. On the other hand, the activities of many nickel compounds have not been adequately investigated. We evaluated the genotoxic activities of nickel acetate using conventional chromosome aberration and sister chromatid exchange assays and found that there was no increase of chromosome aberrations or sister chromatid exchanges, although the highest dose (1000 pM) caused mitotic inhibition. In addition,. we investigated its effect on DNA repair using our challenge assay. In this assay, lymphocytes were exposed to 0.1 to 100 pM nickel acetate for 1 hr during the GO phase of the cell cycle. The cells were washed free of the chemical and, 1.5 hr later, were irradiated with two doses of y-rays (75 cGy per dose separated by 60 min). A significant dose-dependent increase of chromosome translocations was observed (p<0.05). The increase is more than expected based on additive effects from exposure to nickel or trays individually. In contrast to the increase of chromosome translocations, there was no increase in chromosome deletions, although there was a nickel dose-dependent reduction of mitotic indices. Our data suggest that pretreatment with nickel interferes with the repair of radiation-induced DNA damage and potentially cause mistakes in DNA repair. Furthermore, we suggest that nickel-induced abnormal DNA repair may be a mechanism for its carcinogenic properties. The DNA repair problems that we observed after exposure to low doses of nickel may be viewed as a type of adaptive response. Contrary to some investigators who showed that adaptive responses may be beneficial, our data indicated that some responses may cause more problems than expected.-Environ Health Perspect 102(Suppl 9): 73-77 (1994)

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Section: Discussionsupporting

confidence: 92%

Toxicological interactions between nickel and radiation on chromosome damage and repair.

Heo²,

Chiewchanwit³

1994

Environ Health Perspect

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“…The clastogenic effect of nickel can be observed both in vivo and in vitro and in some cases it can be traced even after tumor formation. Thus, in one study, intramuscular injections of crystalline nickel sulfi de resulted in the appearance of rhabdomyosarcomas in mice [34]. Three cell lines established from these tumors were characterized by a rearranged marker chromosome that was present in a majority of the cells of each line.…”

Section: Genetic and Epigenetic Changes In Nickel-exposed Cellsmentioning

confidence: 99%

Nickel‐Dependent Gene Expression

Salnikow

Kasprzak

2007

Nickel and Its Surprising Impact in Nature

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Mutagenicity of soluble and insoluble nickel compounds at the gpt locus in G12 chinese hamster cells

Lee

Pons

Tummolo

et al. 1993

Environ and Mol Mutagen

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Nickel is an established human and animal carcinogen, but efforts to demonstrate its mutagenicity in a number of cell types have not been successful. In this report we describe the mutational response to nickel compounds in the G12 cell line, an hprt deficient V79 cell line containing a single copy of the E. coli gpt gene. This cell line has a low spontaneous background, making it suitable for assessment of mutagenic responses to environmental contaminants. When G12 cells were treated with insoluble particles of crystalline nickel sulfide < 5 microns in diameter, a strong, dose-dependent mutagenic response was observed up to 80 times the spontaneous background. Of 48 mutant gpt(-) clones isolated that were induced by insoluble nickel, all were capable of DNA amplification of the gpt sequences by polymerase chain reaction (PCR). The ability to produce full-length PCR products is an indication that large deletions of gene sequences have not occurred. When G12 cells were treated with soluble nickel sulfate, the mutational response was not significantly increased over the spontaneous background. This difference in mutagenic response reflects a large difference in the mutagenic potential of soluble and insoluble nickel compounds, which reflects the carcinogenic potential of these forms of nickel.

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Chromosomal changes in cell lines from mouse tumors induced by nickel sulfide and methylcholanthrene

Cited by 5 publications

References 41 publications

Toxicological interactions between nickel and radiation on chromosome damage and repair.

Toxicological interactions between nickel and radiation on chromosome damage and repair.

Nickel‐Dependent Gene Expression

Mutagenicity of soluble and insoluble nickel compounds at the gpt locus in G12 chinese hamster cells

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