Farm-grade chlorpyrifos (Durmet) is genotoxic in somatic and germ-line cells of Drosophila.

The mutagenic potential of Durmet, a farm-grade formulation of chlorpyrifos, was studied in the Drosophila wing mosaic and sex-linked recessive lethal tests. Larvae of the 2nd or 3rd instar carrying suitable recessive genetic markers on chromosome 3 were exposed to different concentrations of the insecticide and the frequency of induction of mutant mosaic spots on the wings was noted. The Basc technique was followed to study the induction of sex-linked recessive lethals. On the basis of the frequency of induction of mosaic wing spots and sex-linked recessive lethals, it is concluded that Durmet is genotoxic in somatic cells as well as germ cells of Drosophila.     

Genotoxicity of zineb detected through the somatic and germ-line mosaic assays and the sex-linked recessive-lethal test in Drosophila melanogaster

The genotoxicity of zineb, a carbamate fungicide, has been tested through eye, wing and female germ line mosaic assays and the sex-linked recessive-lethal test in Drosophila melanogaster. Larvae of different instars, heterozygous for appropriate recessive genetic markers, were exposed to the fungicide in food for different durations of time. The adult eyes and wings were screened for induction of mosaic spots and the eggs laid by the females were checked for induction of female germ-line mosaicism. It is concluded that zineb is genotoxic to both somatic and germ-line cells of Drosophila.     

Genotoxicity of ziram established through wing, eye and female germ-line mosaic assays and the sex-linked recessive lethal test in Drosophila melanogaster

The genotoxicity of ziram (zinc-dimethyl dithiocarbamate, CAS No. 137-30-4), a carbamate fungicide, is studied in the wing, eye and female germ-line mosaic assays and the sex-linked recessive lethal test in Drosophila melanogaster. First-, second- and third-instar larvae, carrying suitable recessive genetic markers on their first and third chromosomes, were exposed to ziram. Wings and eyes of adults were screened for the induction of mosaic spots and the eggs laid by adult females for germ-line mosaicism. The Basc method was used to detect sex-linked recessive lethals. Ziram is genotoxic to the somatic and germ cells of Drosophila melanogaster.     

Genotoxicity of Rogor studied in the sex-linked recessive lethal test and wing, eye and female germ-line mosaic assays in Drosophila melanogaster

The genotoxic potential of Rogor (dimethoate), an anticholinesterase organophosphate insecticide, has been studied in the sex-linked recessive lethal test and the wing, eye and female germ-line mosaic assays in Drosophila melanogaster. Larvae of different instars carrying suitable recessive genetic markers on their first and third chromosomes were exposed to the LD50 or half of this dose for the entire larval life. The Basc technique was followed for the detection of the induction of sex-linked recessive lethals. The wings and eyes of the adult flies and the eggs laid by the heterozygous females were checked for the induction of mosaicism. It is concluded that Rogor induces sex-linked recessive lethals in immature male germ cells and is recombinogenic and/or mutagenic in both the somatic and the germ-line cells of Drosophila.     

Acrylamide is genotoxic to the somatic and germ cells of Drosophila melanogaster

The genotoxic effects of acrylamide, a recently detected carcinogen, have been studied in the somatic (wing primordia) and germ cells of Drosophila melanogaster by the wing mosaic assay and the sex-linked recessive lethal test respectively. Larvae, 72 +/- 4 h old, were exposed to 6 different concentrations of acrylamide ranging between 0.25 mM and 5.0 mM in instant medium for 48 h. It is observed that acrylamide is both mutagenic and recombinogenic in the wing disc cells and induces sex-linked recessive lethals.     

Mutagenicity of hycanthone in Drosophila melanogaster

The schistosomicidal agent hycanthone was tested for mutagenicity in Drosophila melanogaster. The compound was administered either by injection into adult males or by larval feeding. The following types of genetic damage were measured:(1) complete and mosaic sex-linked recessive lethal mutations; (2) II–III translocations; and (3) dominant lethals.In postmeiotic germ cells, especially in late spermatids, a pronounced increase was found in the frequency of sex-linked recessive lethals, both completes and mosaics. By contrast, translocations and dominant lethals were not induced.     

Testing the mutagenicity of malondialdehyde and formaldehyde by the Drosophila mosaic and the sex-linked recessive lethal tests

The mutagenicities of malondialdehyde and formaldehyde were tested by screening each for genetic mosaics of Drosophila melanogaster and by the Muller-5 test for sex-linked recessive lethal mutations. For comparison, the effects of X-rays were also assayed by the above technique. Malondialdehyde, a degradation product of polyunsaturated fatty acids, was found to be a weak mutagen by the above criteria; it induced point mutations and chromosome exchanges at low frequency, as proved by the mosaic test, but failed to induce detectable sex-linked lethality. Formaldehyde was more mutagenic than malondialdehyde; beside induction of mosaic spots it induced sex-linked recessive lethal mutations, but only in the larval testes of Drosophila. Formaldehyde also induced disintegration of the clones. Formaldehyde treatment (feeding larvae with formaldehyde-containing food for about 4 days) was 5 times more mutagenic than malondialdehyde treatment and 5 times less effective than irradiation by 1000 R of X-rays. Wing mosaicism offers a more sensitive way to detect mutagenesis as compared with eye mosaicism. It is suggested that aldehyde-induced mosaic spots derive from mitotic recombination and point mutations.     

Mechanism of inactivation and mutagenesis induced by ethyleneimine in Drosophila germ cells. V. Relation of complete and mosaic mutations during the supplementary action of high temperature]

Supplementary effect of high temperature (37 degrees C) an hour after the treatment of mature sperms of Drosophila with ethylene imine resulted in an increased level of the inactivation (the frequency of dominant lethal mutation). The frequency of complete mutations (recessive sex-linked lethal mutations) increased by the supplementary effect of high temperature at low doses of E1, and it did not change under a comparatively high dose of the mutagen. The frequency of mosaic mutations decreased under the effect of high temperature at both doses of E1. No effect of high temperature was observed in 4 and 24 h after the E1 treatment. The results obtained are discussed in connection with the proportion of inactivation and mutagenesis under the effect of chemical mutagens on Drosophila germ cells.     

Evidence for the absence of a mutagenic effect of methadone in germ cells of Drosophila melanogaster.

The compound, methadone, used as a modality in the treatment of heroin addiction, was tested for mutagenic activity in germ cells of Drosophila. Results were negative in tests for sex-linked recessive lethals using feeding and injection procedures. Similarly, results from tests for chromosome breakage and nondisjunction failed to provide evidence of a mutagenic effect.     

Effects of a chromosome-3 mutator gene on radiation-induced mutability in Drosophila melanogaster females

A series of X-irradiation experiments was carried out using Drosophila melanogaster females homozygous for a third chromosome mutator gene and females which had a similar genetic background except that the mutator-bearing third chromosomes were substituted by normal wild-type chromosomes. The mutator females had been previously shown by Gold and Green to manifest a higher level of radiation-induced mutability (as measured by the X-ray-induction of sex-linked recessive lethals) in their pre-meiotic germ cells compared to normal females at an exposure of 100 R. In the presence work, the sensitivity of the pre-meiotic germ cells of mutator and normal females to the X-ray induction (2000 R) of sex-linked recessive lethals was studied. In addition, experiments were conducted to examine the sensitivity of the immature (stage 7; prophase I of meiosis) oocytes of both kinds of females to the induction of dominant lethals, X-linked recessive lethals and X-chromosome losses. The result show that in pre-meiotic germ cells, the frequencies of radiation-induced recessive lethals are similar in both kinds of females. However, the proportion of these mutations that occur in clusters of size 3 and higher, is higher in mutator than in normal females. In stage-7 oocytes, the frequencies of radiation-induced dominant lethals and sex-linked recessive lethals were similar in both kinds of females. The X-loss frequencies however, were consistently higher in mutator females although statistical significance was obtained only at higher exposures (3000 and 3750 R) and not at lower ones (750-2250 R). Possible reasons for the discrepancy between the present results and those of Gold and Green with respect to pre-meiotic germ cells are discussed.     

Mutagenicity of four hair dyes in Drosophila melanogaster.

The hair dye constituents p-phenylenediamine, 2,4-diaminoanisole sulfate, 2,4-diaminotoluene and 4-nitro-0-phenylenediamine were tested for mutagenicity in Drosophila melanogaster. The compounds were given orally to adult males. The induction of sex-linked recessive lethal mutation was used as a measure of mutagenicity. All four of the dyes tested were mutagenic with a peak mutagenic activity in metabolically active germ cells (spermatids and spermatocytes).     

Recessive lethals induced by ethyl methanesulfonate and diethyl sulfate in Drosophila melanogaster post-meiotic male cells pre-treated with butylated hydroxytoluene

The response of Drosophila melanogaster male germ cells to the induction of mutation by ethyl methanesulfonate (EMS) and diethyl sulfate (DES) and the influence of pre-treatments with butylated hydroxytoluene (BHT) were studied. Careful sampling of cell stages revealed that fully mature motile sperm were less sensitive to the induction of sex-linked recessive lethals by EMS than late spermatids, and that the remaining cell stages presented a fairly homogeneous response to the mutagen. The frequency of lethals induced by DES could be grouped into two plateaus: the first one, with a higher mutation rate, comprised motile and immotile sperm and late spermatids, the second one, medium and early spermatids. No sparing action of BHT was detected in any of the developing germ cells treated with EMS or DES, whereas an increase in sex-linked recessive lethal frequency was observed in some experiments in early spermatids. The enhancement of damage is attributed to impairment of repair achieved through the ability of BHT to modify enzymic activity.     

Production of mosaic lethals in different germ cell stages of drosophila by N-methyl-N'-nitro-N-nitrosoguanidine.

The delayed effect of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was studied in Drosophila melanogaster by the proportion of mosaic progeny produced after this treatment. Following injection of the chemical into wild type males, complete and mosaic sex-linked recessive lethals were scored by the Muller-5 method, in five successive broods representing the different stages of spermatogenesis. All broods showed significant increase over the control in the frequencies of complete lethals with gradual decrease in mutation rate from the post-meiotic stages to the pre-meiotic ones. In the case of mosaic lethals, too, the post-meiotic stages were generally more sensitive; but the increase over the control was significant only for the mature spermatozoa. The extension of the experiment to F4 generation showed that a mosaic F1 female may produce further mosaic progeny. The production of lethal mutations in successive generations after treatment with MNNG supports the view that chemically induced instabilities can be transmitted as such over several generations.     

Mutagenicity of sumithion tested in Drosophila somatic and germ cells

Sumithion, a broad-spectrum insecticide, was tested for its mutagenicity in the Drosophila wing-spot test and sex-linked recessive lethal test. Strains carrying the recessive mutant markers mwh and flr3 in their third chromosomes, expressed phenotypically as multiple trichomes or thickened and misshapen wing hairs in the adult wings, were used in the wing-spot test. Larvae transheterozygous for these markers were exposed to the insecticide in instant food and the sex-linked recessive lethal test was performed by the standard technique using the Basc strain. The compound is mutagenic in the wing primordial cells and induces recombination at high doses. Further, the frequency of induction of sex-linked recessive lethals is significant only at high treatment doses.     

The mutational spectrum of procarbazine in Drosophila melanogaster.

The antineoplastic agent Procarbazine was tested for the induction of genetic damage in Drosophila melanogaster. The compound was administered to adult males by oral application. The following types of genetic damage were measured: (1) sex-linked recessive lethals; (2) dominant lethals; (3) total and partial sex-chromosome loss; and (4) translocations. Procarbazine is highly mutagenic in causing recessive lethal mutations in all stages of spermatogenesis. In sperm a clear-cut concentration-effect relationship is not apparent, but in spermatids such a relationship is obtained for mutation induction at low levels of procarbazine exposure, while at high concentrations the induction of recessive lethals is not a function of concentration. A low induction of total sex-chromosome loss (X,Y) and dominant lethals was observed in metabolically active germ cells (spermatids), but procarbazine failed to produce well-defined breakage events, such as partial sex-chromosome loss (YL,YS) and II-III translocations. The results obtained in Drosophila melanogaster are discussed and compared with the mutational pattern reported in the mouse after procarbazine treatment.     

Evaluation of propylene oxide for mutagenic activity in 3 in vivo test systems

Propylene oxide (CAS No. 75-56-9) was tested for mutagenic activity following vapor exposure using 3 in vivo test systems. Rat dominant lethal and mouse sperm-head morphology assays were conducted using males exposed to propylene oxide at 300 ppm in a dynamic exposure chamber for 7 h per day on 5 consecutive days. A sex-linked recessive lethal test in Drosophila melanogaster employed a 24-h static exposure to propylene oxide at 645 ppm. Male mice were killed 1, 3, 5, 7, and 9 weeks post-exposure for evaluation of sperm-head morphology. Propylene oxide exposure did not result in an increase in abnormal forms. Male rats were mated with 2 virgin females per week for 6 weeks following exposure. A statistically significant increase in preimplantation losses and a statistically significant reduction in the number of living implants in the first post-exposure week did not appear to be treatment related. A highly significant increase in sex-linked recessive lethal mutations was observed in two germ cell stages (mature sperm and developing spermatocytes). These results warrant continued caution in potential human exposure to propylene oxide.     

Sensitivity of individual Drosophila to the mutagenic action of ethyl methanesulfonate

The genetic effect of some factors is generally evaluated as an average response of all individuals, without taking into account their potential differences. The presence of individual sensitivity in separate Drosophila organisms to the mutagenic influence of ethyl methanesulfonate was shown when analysing recessive sex-linked lethal mutations in germ cells of males. Different sensitivity of separate individuals to mutagens reflects the existence of cryptic genetic variability in Drosophila strains on a large scale. It is advisable to take into account individual sensitivity of organisms to mutagenic factors, when conducting mutation research and studying genetic consequences of biosphere pollution.     

Mutagenicity studies in Drosophila melanogaster with Lannate 20

Lannate 20 a carbamate pesticide was evaluated for its mutagenicity in Drosophila melanogaster by the sex-linked recessive lethals and chromosome II-III translocation tests by continuous larval feeding. The 3 sublethal doses of 0.2, 0.4 and 0.6 microliter of Lannate per 100 ml of the food medium induced a significant (P less than 0.01) increase in the number of sex-linked recessive lethals over the controls. However, no translocations were observed either in the treated or the control series.     

The influence of electrostatic and magnetic fields on mutation in Drosophila melanogaster spermatozoa.

Canton-S Drosophila melanogaster males were exposed to electrostatic and magnetic fields for 24 h to determine the influence of low energy fields on the production of sex-linked recessive lethal mutations in the mature, motile sperm. To detect sex-linked recessive lethal production in mature sperm the standard Muller-5 test was done. Exposure of the males to the magnetic field or the electrostatic field did not significantly affect the mutation frequency in mature sperm.     

Mutation Induction in the Male Recombination Strains of DROSOPHILA MELANOGASTER

One group of the second chromosome lines isolated from a southern Texas population of Drosophila melanogaster, which has been known to show relatively high frequencies of male recombinations, was found to increase the frequency of sex-linked recessive lethal mutations from a control frequency of 0.18% to 1.63%. The second group, which showed a very much reduced frequency of male recombinations, was found to cause a slight increase to 0.48%, although it was not statistically significant. The first group was also tested for the recessive lethal mutation frequency in the second chromosome; the frequency increased from a control frequency of 0.28% to 2.82%. Mapping of a portion of the sex-linked lethals indicated a distribution along the entire X chromosome, although there was a tendency of clustering towards the tip of the X chromosome. One sex-linked lethal line so far tested was found to be associated with an inversion (approximate breakpoints, 14A-18A). It was suggested that the element causing male recombination might be similar to the hi mutator gene studied earlier by Ives (1950).