To provide further background data on the wing spot somatic mutation and recombination assay, 10 selected carcinogens (acetamide, acrylamide, benzo(a)pyrene, cyclophosphamide, diethylstilbestrol, 4-nitroquinoline N-oxide, propyleneimine, safrole, thiourea, and o-toluidine) were tested in this assay. 72-h-old third-instar larvae, trans-heterozygous for 2 recessive wing cell markers: multiple wing hairs (mwh) and flare3 (flr3) were fed with 3 concentrations of each carcinogen during the rest of their development until pupation, and the genotoxic effects were measured as significant increases in the appearance of visible mutant hair clones on the adult wing blade. Our results show that 6 of the carcinogens tested produce significant increases in wing spot frequency, at least at one of the concentrations assayed. Benzo(a)pyrene, diethylstilbestrol, safrole and thiourea were the compounds that did not increase the incidence of mutant clones.
The pyrethroid insecticide cypermethrin was tested for the induction of genetic damage in male germ cells of Drosophila melanogaster. Sex-linked recessive lethals, sex-chromosome loss and non-disjunction were studied following different routes of administration: adult feeding, injection and larval feeding. Our results show that, after adult injection and larval ingestion, cypermethrin induces a small but significant increase in the frequency of sex-linked recessive lethal mutations. However, no significant increases were observed in the frequency of sex chromosome loss or non-disjunction after exposure of male flies to cypermethrin at concentrations up to 20 p.p.m.
The induction of genetic damage in germ cells of Drosophila melanogaster by the pyrethroid insecticide fenvalerate was studied. Adult feeding, larval feeding and adult injection were the routes of administration used. Our results indicate that, under the conditions of testing, fenvalerate is unable to induce sex-linked recessive lethals, sex-chromosome losses and non-disjunction.
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