Mutagenic effects of some water-soluble metal compounds in a somatic eye-color test system in Drosophila melanogaster

Rasmuson, Åsa

doi:10.1016/0165-1218(85)90111-9

Cited by 31 publications

(8 citation statements)

References 27 publications

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“…The average control frequency of mutant spots (0.26) was consistent with the normal background range reported by different authors [Frei and Würgler, 1995;Torres et al, 1998;Rizki et al, 2002]. Thus, in the wing spot test, CC does not appear to be genotoxic, which agrees with the only results previously reported in somatic cells of Drosophila using the zeste test [Rasmuson, 1985].…”

Section: Resultssupporting

confidence: 91%

“…Cadmium chloride (CC) has been the most commonly evaluated cadmium compound, inducing deletions and causing increases in the frequency of gene mutation, mitochondrial mutation, and intragene recombination in Saccharomyces cerevisiae [Brennan and Schiestl, 1996;Pesheva et al, 1997], although it does not induce gene mutation in Salmonella typhimurium [Pesheva et al, 1997]. In Drosophila melanogaster, CC increases the frequency of sex-linked recessive lethal mutations and dominant lethal mutations in germ cells [Pesheva et al, 1997]; however, it was negative in the unstable zeste test that measures somatic effects [Rasmuson, 1985].…”

Section: Introductionmentioning

confidence: 97%

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Genotoxicity modulation by cadmium treatment: Studies in the Drosophila wing spot test

Rizki

Kossatz

Creus

et al. 2004

Environ and Mol Mutagen

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The genotoxic activity of cadmium chloride (CC) has been evaluated in the somatic mutation and recombination test (SMART) in Drosophila melanogaster. In addition, its possible modulating effect on the genotoxicity of two known mutagenic agents, potassium dichromate (PDC) and ethyl methanesulfonate (EMS), was investigated. Three different types of combined treatments of CC with the two genotoxins were performed: pretreatment, cotreatment, and posttreatment. The SMART assay is based on the principle that loss of heterozygosity for the recessive markers, multiple wing hairs (mwh) and flare-3 (flr(3)), leads to the formation of mutant clones in the imaginal disks of larvae, which are expressed as mutant spots on the wings of adult flies. Thus, after adult emergence, the wings of the adult flies were scored for the presence of single and/or twin spots. Our results show that CC alone was not effective in increasing the frequency of any of the three categories of spots (small, large, and twin). In the cotreatment experiments, CC increased the genotoxicity of PDC but it decreased the genotoxicity of EMS. No effects of CC were observed in the pretreatment or posttreatment experiments; however, only low concentrations of CC, PDC, and EMS were tested in the pretreatment assays due to the high toxicity of the treatment. Although our results with PDC are consistent with the hypothesis that cadmium can interfere with repair mechanisms, the EMS data suggest that other modulating mechanisms are also involved in the genotoxicity of this metal.

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Section: Resultssupporting

confidence: 91%

Section: Introductionmentioning

confidence: 97%

Genotoxicity modulation by cadmium treatment: Studies in the Drosophila wing spot test

Rizki

Kossatz

Creus

et al. 2004

Environ and Mol Mutagen

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“…Results of in vivo mutagenicity studies have consistently shown positive results for chromium (VI) compounds (Rasmuson 1985, Knudsen 1980, Paschin, et al, 1982, Newton and Lilly 1986, Bigaliev, et al, 1978, Wild 1978, DiPaolo and Castro 1979, Bigaliev, et al, 1977and Sarto, et al, 1982 Bianchi and Levis 1985, EPA 1984a, Bonati, et al, 1976and Singh 1983. These results support the carcinogenicity findings in animal studies for chromium.…”

Section: L-36supporting

confidence: 78%

Tooele Army Depot - South Area Suspected Releases Units RCRA Facility Investigation - Phase II for SWMUs 1, 25, and 37. Appendices: D-M

VA¹

1995

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“…Oral treatment was weakly positive with the highest effect recorded at 12 mM. Rasmuson (1985) screened Ni salts, NiCl 2 and Ni(NO 3 ) 2 , for mutagenicity using a sensitive somatic eye-colour test system in Drosophila melanogaster. Larval feeding with 0.14 mM Ni(NO 3 ) 2 and 0.21 mM NiCl 2 did not cause somatic mutations above the control level.…”

Section: Gene Mutationsmentioning

confidence: 99%

Scientific Opinion on the risks to public health related to the presence of nickel in food and drinking water

Publication¹

2015

EFS2

119

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EFSA received a request from the Hellenic Food Authority (EFET) for a scientific opinion on the risk to human health from the presence of nickel (Ni) in food, particularly in vegetables. The EFSA Panel on Contaminants in the Food Chain (CONTAM Panel) decided to extend the risk assessment also to drinking water. The reproductive and developmental toxicity in experimental animals was selected as the critical effect for the assessment of chronic effects of Ni. A tolerable daily intake of 2.8 µg Ni/kg body weight (b.w.) per day was derived from a lower 95 % confidence limit for a benchmark dose at 10 % extra risk (BMDL 10 ) of 0.28 mg/kg b.w. for post-implantation fetal loss in rats. The current dietary exposure to Ni raises concern when considering the mean and 95th percentile chronic exposure levels for all different age groups. The systemic contact dermatitis (SCD) elicited in Ni-sensitive humans after oral exposure to Ni was selected as the critical effect suitable for the assessment of acute effects of Ni. A lowest BMDL 10 of 1.1 µg Ni/kg b.w. was derived for the incidence of SCD following oral exposure to Ni of human volunteers. The CONTAM Panel applied a margin of exposure (MOE) approach and considered an MOE of 10 to be indicative of a low health concern. The MOEs calculated considering the estimated mean and the 95th percentile acute exposure levels were considerably below 10 for all age groups. Overall, the CONTAM Panel concluded that, at the current levels of acute dietary exposure to Ni, there is a concern that Ni-sensitized individuals may develop eczematous flare-up skin reactions. The CONTAM Panel noted the need for mechanistic studies to assess the human relevance of the effects on reproduction and development observed in experimental animals and for additional studies on human absorption of nickel from food, for example in combination with duplicate diet studies. Following a call for data on Ni levels in food and drinking water (water intended for human consumption and mineral waters), a total of 18 885 food samples and 25 700 drinking water samples were available in the final dataset to estimate dietary exposure to nickel. No speciation data were provided. Samples were collected between 2003 and 2012 in 15 different European countries, with almost 80 % of the total collected in one Member State. The most reported analytical methods were inductively coupled plasma-mass spectrometry (ICP-MS) and atomic absorption spectrometry (AAS), that represented 54 % and 42 % of the methods reported, respectively. The highest sensitivity was reported for the analysis of drinking water with a limit of quantification (LOQ) of 0.001 µg/L (for both ICP-MS and AAS). In food, ICP-MS showed the lowest LOQ for the analysis of 'Alcoholic beverages' (0.002 µg/kg) while the lowest LOQ reported with AAS was 1 µg/kg for samples of 'Fish and seafood' and 'Sugar and confectionery'. In the final dataset, left-censored data represented 66 % of the analytical results, with 35 % in food samples and 89 % in drinking water sa...

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Mutagenic effects of some water-soluble metal compounds in a somatic eye-color test system in Drosophila melanogaster

Cited by 31 publications

References 27 publications

Genotoxicity modulation by cadmium treatment: Studies in the Drosophila wing spot test

Genotoxicity modulation by cadmium treatment: Studies in the Drosophila wing spot test

Tooele Army Depot - South Area Suspected Releases Units RCRA Facility Investigation - Phase II for SWMUs 1, 25, and 37. Appendices: D-M

Scientific Opinion on the risks to public health related to the presence of nickel in food and drinking water

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