Suppression of naphthylamine mutagenicity by Amaranth

Stoltz, D.R.; Stavrić, B.; Iverson, F.; Bendall, R.; Klassen, R.

doi:10.1016/0027-5107(79)90029-0

Cited by 20 publications

(4 citation statements)

References 8 publications

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“…However, these aromatic amines were poorly activated to bacterial mutagens by a rat liver 9,000 x g supernatant fraction (S9), whereas hamster liver S9 was highly effective in mediating the mutagenicity of these compounds [Stoltz et al, 1979;Dunkel, 19791. In the present studies, equivocal DNA repair responses were induced by both of these arylamines in rat hepatocytes, while clearly positive responses were produced in hamster hepatocytes, which roughly correlates with the mutagenicity data.…”

Section: Discussionmentioning

confidence: 99%

“…This step is believed to be important in the formation of mutagenic metabolites from this aromatic amine [Schut et al, 19781. Hamster hepatocytes also were shown to be much more effective than rat hepatocytes in mediating the bacterial mutagenicity of benzidine, although in this case the difference appeared to be largely due to the presence of an inhibitor of benzidine activation in rat liver cytosol [Prival and Mitchell, 19821. Previous testing of l-naphthylamine [Probst et al, 19811 and pararosaniline hydrochloride [Williams et al, 19821 in the rat HPC/DR assay yielded negative results. However, these aromatic amines were poorly activated to bacterial mutagens by a rat liver 9,000 x g supernatant fraction (S9), whereas hamster liver S9 was highly effective in mediating the mutagenicity of these compounds [Stoltz et al, 1979;Dunkel, 19791. In the present studies, equivocal DNA repair responses were induced by both of these arylamines in rat hepatocytes, while clearly positive responses were produced in hamster hepatocytes, which roughly correlates with the mutagenicity data. A negative response was previously obtained by McQueen et a1 [1983b] for 1naphthylamine in the hamster HPC/DR assay.…”

Section: Discussionmentioning

confidence: 99%

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Comparison of rat and hamster hepatocyte primary culture/DNA repair assays

Kornbrust

Barfknecht

1984

Environ. mutagen

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Previous studies have demonstrated marked differences in the capacity of hepatocytes from rats or hamsters to mediate the metabolic activation of chemical carcinogens to genotoxic (ie, mutagenic) products. Thus far, very few investigations of species differences in DNA repair have been performed. Therefore, a comparison of the relative extent of DNA repair elicited by various genotoxic chemicals in rat and hamster hepatocytes was conducted, using the hepatocyte primary culture/DNA repair (HPC/DR) assay. Of the 11 chemicals tested, eight were more potent in inducing DNA repair in hamster hepatocytes than in rat hepatocytes. Dimethylnitrosamine, diethylnitrosamine, 2-acetylaminofluorene, 9-aminoacridine, pararosaniline hydrochloride, 1-naphthylamine, benzidine and 1,2:3,4-diepoxybutane were all active in hamster hepatocytes at a concentration at least ten times less than the lowest effective concentration in rat hepatocytes. The direct-acting alkylating agent, methylmethane sulfonate, was equipotent in inducing DNA repair in both rat and hamster hepatocytes, indicating that the differences in DNA repair observed for the other chemicals were probably not a result of species differences in DNA repair capacities. In contrast, 1-nitropyrene produced a greater DNA repair response in rat hepatocytes than hamster hepatocytes, while the bacterial mutagen 3-(chloromethyl)pyridine hydrochloride was inactive in both hepatocyte systems. These studies demonstrate the feasibility of using hamster hepatocytes in the HPC/DR assay and illustrate the utility of performing the assay with hepatocytes from more than one species.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Comparison of rat and hamster hepatocyte primary culture/DNA repair assays

Kornbrust

Barfknecht

1984

Environ. mutagen

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“…The observation that genetic activity occurred with cycad flour containing cycasin is of some importance. Increasing consideration is being given to the detection of genetically active compounds that are contained in complex mixtures, and some results indicate that detection is not always possible (42). With judicious application of our method, it should be possible to test compounds that are normally ingested for their genetic hazard potential under conditions that more closely resemble the normal exposure conditions of the gastrointestinal tract.…”

Section: Discussionmentioning

confidence: 99%

Activation of cycasin to a mutagen for Saccharomyces cerevisiae by rat intestinal flora

Mayer¹,

Goin²

1983

Appl Environ Microbiol

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Genetic test systems involving microorganisms and liver enzyme preparations may be insufficient to detect compounds that require breakdown by enzymes provided by the microbial flora of the intestinal tract. A method is described for providing such activation and for simultaneously testing the potential genetic activity of breakdown products in an indicator organism. Parabiotic chambers containing Saccharomyces cerevisiae genetic test organisms in one chamber were separated by a membrane filter from rat cecal organisms and test chemical contained in the other chamber. The genetic activities of cycasin breakdown products for mutation, gene conversion, and mitotic crossing-over in samples incubated aerobically are reported. Samples containing cycasin alone had a small but clearly increased frequency of genetic damage. Samples containing rat cecal organisms without cycasin showed no increase in genetic activity. Anaerobic incubation resulted in no increase in genetic activity in any of the samples.

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“…The method has been used extensively for chemical and biological characterization of condensed tobacco smoke, 23 -9397 giving knowledge of the components that can be expected in the various fractions. 3.…”

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confidence: 99%