Chemical mutagenesis testing in <i>Drosophila</i>. VII. Results of 22 coded compounds tested in larval feeding experiments

Zimmering, S.; Mason, James; Valencia, R.

doi:10.1002/em.2850140406

Cited by 55 publications

(19 citation statements)

References 12 publications

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“…These variations in the experimental procedures utilized in the two studies may be responsible for the different results. The importance of larval treatment in mutagen screening was realized by Zimmering et al [1989], but the method was not pursued further since some of the tested chemicals did not respond. Our results indicate that larval treatment may still be valuable in environmental mutagen testing.…”

Section: Drosophila Melanogasteflmentioning

confidence: 99%

Mutagenicity testing of nine herbicides and pesticides currently used in agriculture

Kale

Petty

Walker

et al. 1995

Environ and Mol Mutagen

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Nine herbicides and pesticides were tested for their mutagenicity using the Drosophila sex-linked recessive lethal mutation assay. These are Ambush, Treflan, Blazer, Roundup, 2,4-D Amine, Crossbow, Galecron, Pramitol, and Pondmaster. All of these are in wide use at present. Unlike adult feeding and injection assays, the larvae were allowed to grow in medium with the test chemical, thereby providing long and chronic exposure to the sensitive and dividing diploid cells, i.e., mitotically active spermatogonia and sensitive spermatocytes. All chemicals induced significant numbers of mutations in at least one of the cell types tested. Some of these compounds were found to be negative in earlier studies. An explanation for the difference in results is provided. It is probable that different germ cell stages and treatment regimens are suitable for different types of chemicals. larval treatment may still be valuable and can complement adult treatment in environmental mutagen testing.

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Section: Drosophila Melanogasteflmentioning

confidence: 99%

Mutagenicity testing of nine herbicides and pesticides currently used in agriculture

Kale

Petty

Walker

et al. 1995

Environ and Mol Mutagen

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“…The toxic effects of methacrylonitrile have also been attributed to the in vivo release of cyanide and depletion of glutathione (Hartung 1982). There are few mutagenicity studies on methacrylonitrile; however, the available evidence indicates that the chemical is not genotoxic (Knaap et al 1985;NTP 2000;Zeiger et al 1987;Zimmering et al 1989).…”

mentioning

confidence: 99%

Characterization of the toxicity, mutagenicity, and carcinogenicity of methacrylonitrile in F344 Rats and B6C3F1 mice

Nyska

Ghanayem

2003

Arch Toxicol

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Methacrylonitrile is an unsaturated aliphatic nitrile. It is widely used in the preparation of homopolymers and copolymers, elastomers, and plastics, and as a chemical intermediate in the preparation of acids, amides, amines, esters, and other nitriles. Methacrylonitrile was nominated for study by the National Cancer Institute (USA) because of the potential for human exposure, structural similarity to the known carcinogen acrylonitrile, and a lack of toxicity and carcinogenicity data. Doses selected for the 2-year study were based on the results of the 13-week gavage studies. Groups of 50 male and 50 female animals were exposed by gavage to 0, 3, 10, or 30 mg/kg in F344 rats, and 0, 1.5, 3 or 6 mg/kg in B6C3F1 mice, 5 days per week for 2 years. Urinary excretion of N-acetyl- S-(2-cyanopropyl)- l-cysteine (NACPC) and N-acetyl- S-(2-hydroxypropyl)- l-cysteine (NAHPC) were measured as markers of exposure at various time points after methacrylonitrile administration, and demonstrated that exposure of animals to methacrylonitrile occurred as intended. Urinary excretion of NACPC and NAHPC increased in rats and mice in a dose-dependent manner. In contrast to observations in rats, the ratios of NACPC/creatinine were generally higher in female than in male mice. Further, the ratios of NAHPC/creatinine in rats were significantly greater at all time points and all doses than the corresponding ratios of NACPC/creatinine in male and female mice. In both rats and mice, survival was not affected by treatment. In rats, mean body weights of the 30 mg/kg groups were less than those of the vehicle controls after weeks 21 and 37 for males and females, respectively. No treatment-related effect on body weight was seen in mice. There were no neoplasms (in either species) or non-neoplastic lesions (mice only) that were attributed to methacrylonitrile administration. In rats, the incidences of olfactory epithelial atrophy and metaplasia of the nose were significantly greater in 30 mg/kg males and females than those in the vehicle controls. Increased incidences of cytoplasmic vacuolation occurred in the liver of males and females. Testing methacrylonitrile in a battery of short-term in vitro and in vivo tests showed no evidence of genotoxicity. In conclusion, under the conditions of these 2-year gavage studies, there was no evidence of a carcinogenic activity of methacrylonitrile in male or female F344/N rats or B6C3F1 mice. Methacrylonitrile-related non-neoplastic lesions were seen in the nose and liver of rats.

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“…Other in vivo studies have not demonstrated any genotoxic potential. Thus, GA did not induce gender-linked recessive lethal mutations in male Drosophila melanogaster treated as either larvae (Zimmering et al, 1989) or adults (Yoon et al, 1985). Peroral dosing with GA did not induce dominant lethal mutation in mice (Tamada et al, 1978) or unscheduled DNA synthesis (UDS) in male rat hepatocytes (Mirsalis et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Genetic toxicology studies with glutaraldehyde

Vergnes¹,

Ballantyne

2002

J of Applied Toxicology

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Glutaraldehyde (GA; CAS no. 111-30-8) has a wide spectrum of industrial, scientific and biomedical applications, with a potential for human exposure particularly in its biocidal applications. The likelihood for genotoxic effects was investigated in vitro and in vivo. A Salmonella typhimurium reverse mutation assay showed no evidence for mutagenic activity with strains TA98, TA1535, TA1537 and TA1538, with or without metabolic activation. However, there was a weak mutagenic response (1.9-2.3-fold at the highest non-toxic concentration) with TA100 in the presence of metabolic activation. In a Chinese hamster ovary (CHO) forward gene mutation assay (HGPRT locus) there were no consistent, statistically significant, reproducible or dosage-related increases in the frequency of 6-thioguanine resistant cells. There were no reproducible or dosage-related increases in sister chromatid exchanges in an in vitro test in CHO cells. An in vitro cytogenetics study in CHO cells showed no evidence for an increase in chromosomal aberrations on treatment with GA, either in the presence or absence of metabolic activation. In vivo, a mouse peripheral blood micronucleus test showed no increase in micronucleated polychromatophils at sampling times of 30, 48 and 72 h after acute gavage dosing with GA at 40, 80 and 125 mg kg(-1) (corresponding to 25, 50 and 85% of the LD(50)). The absence of an in vivo clastogenic potential was confirmed by no increase in chromosomal aberrations in a rat bone marrow cytogenetics study with sampling at 12, 24 and 48 h after acute gavage dosing with GA (12.5, 30 or 60 mg kg(-1) with males, and 7.5, 20 or 40 mg kg(-1) with females). Thus, in this series of tests, GA produced genotoxic effects in vitro only in a bacterial reverse mutation assay with no evidence for in vivo genotoxicity.

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Chemical mutagenesis testing in Drosophila. VII. Results of 22 coded compounds tested in larval feeding experiments

Cited by 55 publications

References 12 publications

Mutagenicity testing of nine herbicides and pesticides currently used in agriculture

Mutagenicity testing of nine herbicides and pesticides currently used in agriculture

Characterization of the toxicity, mutagenicity, and carcinogenicity of methacrylonitrile in F344 Rats and B6C3F1 mice

Genetic toxicology studies with glutaraldehyde

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