Translocations In Male Mice Research Articles

Dominant lethal mutations, heritable translocations, and unscheduled DNA synthesis induced in male mouse germ cells by glycidamide, a metabolite of acrylamide

The hypothesis that acrylamide induces dominant lethal mutations and heritable translocations in male mice, not through direct adduction, but by conversion to the reactive epoxide, glycidamide, was investigated. Three studies, namely, induction of dominant lethal mutations, heritable translocations, and unscheduled DNA synthesis in spermatids, which were conducted earlier in this laboratory for acrylamide, were also performed for glycidamide to determine its mutagenic properties and to compare responses. Results of these studies are consistent with the proposal that in vivo conversion to glycidamide is responsible for the mutagenicity of acrylamide in male mice.

Dominant lethal and heritable translocation tests with chlorambucil and melphalan in male mice

Chemicals used in the treatment of cancer include several that are potent mutagens in a range of in vitro and in vivo assays. For some, genetic effects have also been demonstrated in humans, detected as chromosomal aberrations in peripheral lymphocytes. Because (1) many of these agents are confirmed mutagens, (2) humans are exposed to them in relatively high doses, and (3) an increasing number of early cancer victims are surviving to reproductive age, it is important that information be available on the genetic and reproductive hazards associated with exposure to these agents. Chlorambucil and melphalan are structurally related chemicals that are included in our efforts to identify and assess such hazards among cancer chemotherapy agents. To date, both have been reported to induced specific locus mutations in germ cells of male mice (Russell et al., 1989; Russell et al., 1992b) and melphalan is one of very few chemicals shown to induced such mutations in spermatogonial stem cells. More recently, both chemicals were found to have strong reproductive effects in female mice (Bishop and Generoso, 1995, in preparation). In the present studies, these chemicals were tested for the induction of dominant lethal mutations and heritable translocations in male mice. Both chemicals were found to have reproductive effects attributable to cytotoxicity in specific male germ cell stages and to induce dominant lethal mutations and heritable translocations in postmeiotic germ cells, particularly in mid to early stage spermatids. Thus, relatively extensive data are now available for assessing the genetic and reproductive hazards that may result from therapeutic exposures to these chemicals.

Quantitative estimation of the genetic risk associated with the induction of heritable translocations at low‐dose exposure: Ethylene oxide as an example

This paper explores how quantitative risk assessment methods might be extended to analysis of risks to the human germ line. High inhalation exposures to ethylene oxide are reported to cause heritable translocations in male mice with a steep and nonlinear dose-response-curve. We explore quantitative estimation of risk to humans from low exposures based on these animal data, addressing questions of tissue dosimetry for this alkylating agent, expected equivalency of doses across species, germ-cell sensitivity, and extrapolation of dose-response relationship to low exposure levels. Various dose-response models are discussed in terms of their applicability to genetic end points and their ability to reflect the underlying basis of induced heritable translocations.

Studies of the induction of dominant lethals and translocations in male mice after chronic exposure to microwave radiation.

Male C3H mice were exposed to 100 W m-2 of 2.45 GHz continuous-wave microwave radiation for 6 h per day for a total of 120 h over an 8-week period. The exposure level was chosen so that the specific energy absorption rate (SAR) would be approximately equal to the level of 4 W kg-1 which is considered by a number of organizations to be a threshold for adverse biological effects. At the end of the treatment period the mice were mated with a different group of (C3H x 101) F1 hybrid females each week for the following 8 weeks. There was no significant reduction in pregnancy rate, preimplantation survival or postimplantation survival in the exposed group compared to sham-exposed controls. At the end of the mating period a cytogenetic analysis was carried out of meiotic chromosome preparations of testicular tissue, thus sampling cells that were stem cell spermatogonia during the treatment regime. The results showed no difference in the frequency of reciprocal translocations between the sham and treated groups, or in the frequency of cells with autosome or sex chromosome univalents. Low levels of fragments and exchanges were found in both groups. It is concluded that there is no evidence in this experiment to show that chronic exposure of male mice to 2.45 GHz microwave radiation induces a mutagenic response in male germ cells. This conclusion is in agreement with the observations of Berman et al. (1980), who reported a lack of male germ cell mutagenesis after repetitive or chronic exposure of rats to 2.45 GHz.

No evidence found for induction of dominant lethal mutations and heritable translocations in male mice by calcium cyclamate

Calcium cyclamate, an artificial sweetener, was studied for its effectiveness in inducing transmissible chromosomal aberrations in germ cells of male mice. Both the dominant-lethal and the heritable translocation tests were carried out following daily treatment (on weekdays) of males by oral intubation with the maximum tolerated dose for 6 weeks. Calcium cyclamate is negative in both tests; therefore, there is no evidence of induced chromosome breakage and exchange.

Acrylamide: Induction of heritable translocations in male mice

Acrylamide (AA), known to induce dominant lethals in male rodents, was studied in the mouse heritable translocation test by using intraperitoneal injections on 5 consecutive days. Matings on days 7-10 following the last injection yielded a high frequency of translocation carriers in the F1 male population, which demonstrated that acrylamide is an effective inducer of translocations in postmeiotic germ cells. As an inducer of both dominant lethals and heritable translocations in late spermatids and early spermatozoa, AA is similar to alkylating agents such as ethylmethanesulfonate and ethylene oxide. However, AA's chemical structure, the nature of adducts formed with DNA, and it lack of mutagenicity in bacteria suggest a different mechanism as the basis for AA's germ cell mutagenicity.

Transmission of X-ray-induced reciprocal translocations in normal male mice and in male mice with a reduced sperm count due to translocation homozygosity

Normal (+/+) and translocation T(1;11.13S)70H homozygous (T/T) male mice received 2 × 2.5 Gy X-rays with a 24-h interval. After 120 days, the frequency of late diplotene-metaphase I spermatocytes with translocation multivalents was 14.1% for +/+ and 13.7% for T/T males, respectively, in one group of animals of each type. The difference is not significant. A second group was allowed to sire progeny for 60 days with 2 normal females per week. Reciprocal translocations detectable at diakinesis/metaphase I were observed in 2.5% of the 395 male progeny from the irradiated +/+ fathers, and in 2.9% of the 489 male progeny from the irradiated T/T fathers. This leads to a pooled estimated transmission of 0.81±0.19. Translocations induced in the long 11.13 1 metacentric chromosome were not transmitted with a different frequency. The rate of heritable induced translocations in this study was 5.4 × 10 −5 /rad/gamete. On the basis of the data of Generoso et al. (1984) for the frequency of the heritable spontaneous translocations in male mice, it is concluded that, because of their low doubling dose (3.3–4.6 rad), the spontaneous translocations are probably of postmeiotic origin.

239Plutonium-induced heritable translocations in male mice

This study was conducted to estimate the frequency of transmitted reciprocal translocations per rad of exposure to α particles from [ 239Pu]citrate. Data indicate that the rate of induction of heritable translocations is related linearly to the duration of spermatogonia stem cell exposure. The estimated increase in heritable translocations per rad of exposure of the stem cell to α particles is in the range of 1.45−2.91 × 10 −5/gamete.

Effect of saccharin on the induction of chromosomal translocations in male mice and their F 1 offspring

The dose-dependent effects of sodium saccharin on the fertility and the induction of chromosomal translocations in treated mice and their Fi males were examined. C3H x 101 mice were treated with saccharin for 2 successive weeks at doses of 200 and 500 mg/kg of body wt. Data from the fertility study showed that saccharin did not induce any significant effect on fertility. Cytological analysis of meiotic cells showed no chromosomal rearrangements. Semisterility and sterility were noted in f 1 males of saccharin-treated animals. In semi-sterile and sterile F 1 males of saccharin-treated animals chromosomal translocations were not found.

Nonhomologous synapsis of the sex chromosomes in the heteromorphic bivalents of two X-7 translocations in male mice: R5 and R6.

Electron microscopy of pachytene nuclei of mice heterozygous for either of two reciprocal X-7 translocations (R5 or R6) revealed a high frequency of heteromorphic bivalents involving the translocated chromosomes. In both translocations the break was in the proximal third of the 7 and the distal third of the X, but the R5 breaks were closer to the 7 centromere and X telomere than the R6 breaks. In both translocations the 7 frequently synapsed nonhomologously with the X7. In R5 the part of the X to which the 7 synapsed may include a region that synapses with the Y in normal mice. However, in R6 the 7 synapsed with a portion of the X that never synapses with the Y (Synapsis was clearly in the "differentiated" region). In both translocations the Y synapsed maximally with the X portion of the 7X in those nuclei in which there was nonhomologous synapsis of the 7 with the X7. The Y occasionally synapsed nonhomologously with the 7 portion of the 7X. The behavior of the bivalents suggests that the autosomal portions of the 7X and X7 may alter the behavior of the sex-chromosome portions. Both the nonhomologous synapsis of the Y with the 7X and the timing of events during pachytene have led us to question the "homology" between the X and Y in this species.

Synaptonemal complex analysis of X-7 translocations in male mice: R2 and R6 quadrivalents

Synaptonemal complexes of surface-spread spermatocytes of mice heterozygous for reciprocal translocations R2 or R6 between the X-chromosome and chromosome 7 were examined by light and electron microscopy (EM). Measurements of the lengths of all chromosome axes involved in the translocation configurations and of the extent of synapsis were used to calculate the position of the break points of the two translocations. The breaks for R2 were determined to be at 62% of the 7 as measured from the centromere, and at 27% of the X. Quadrivalents were formed almost exclusively. The break points for R6 were calculated to be at 30% of the 7 as measured from the centromere, and at 75% of the X. Although in R6 the break in the X lies within the potential pairing region of the sex chromosomes, univalent Ys were rarely observed (6%). The EM sample of 76 nuclei contained: 42% quadrivalents, 52% heteromorphic bivalents, 4% trivalent plus Y univalent, and 2% X7-7 bivalent plus two univalents (7X and Y). Nonhomologous synapsis occurred in the quadrivalents of both R2 and R6. In R6 nonhomologous synapsis of the X portion of the 7X with the 7 involved up to 14% of the length of the 7. Methods are discussed for determining the position of the break points in the presence of nonhomologous synapsis. It is proposed that the high percentage of bivalents is due to premature desynapsis of the 7X from the 7 and that the X portion of the 7X axis confers its property of premature desynapsis on that portion of the 7 to which it is attached.

Synaptonemal complex analysis of X-7 translocations in male mice. I. R3 and R5 quadrivalents.

The synaptonemal complexes of surface-spread spermatocytes of mice heterozygous for one of two reciprocal translations (R3 and R5) between the X and chromosome 7 have been examined by light and electron microscopy (EM). The break points of R3 were determined to be at 70% of chromosome 7, as measured from the centromere, and at 22% of the X. Translocation quadrivalents were formed almost exclusively. The break points of R5 were at 21% of chromosome 7 as measured from the centromere, and at 83% of the X. There was little indication that the break in the X interfered with sex-chromosome synapsis between the 7X and Y. Univalent Y's were not observed in R3, and only seldom observed (8-14%) in R5. However, in contrast to R3, R5 formed quadrivalents relatively rarely (20% in the EM study of 100 nuclei), and heteromorphic bivalents of 7X-Y and X7-7 quite frequently (72%). Possible causes of this high bivalent frequency are discussed. Light-microscope (LM) analysis alone was found to be inadequate for interpreting synaptic configurations (quadrivalents vs. bivalents) in R5. The LM analysis was further complicated by the occurrence of nonhomologous synapsis in the heteromorphic bivalents of R5, a phenomenon easily recognized and interpreted in the EM portion of the study.

Heritable translocation and dominant-lethal mutation induction with ethylene oxide in mice

Ethylene oxide was studied for induction of dominant-lethal mutations and heritable translocations in male mice. The chemical was prepared in water and injected intraperitoneally. The dominant-lethal study was conducted using a single injection of 150 mg/kg (maximum tolerated dose); in the heritable translocation study males were injected daily on weekdays for 5 weeks with 60 or 30 mg/kg dose per day. Results clearly showed that ethylene oxide is effective in inducing dominant-lethal mutations and that the 4 stocks of untreated females used do not differ or may differ only slightly in the ability of their eggs to repair ethylene oxide-induced lesions in male germ cells. Increases in the frequencies of heritable translocations were also observed at the 2-dose levels. These frequencies did not deviate significantly from those expected on the basis of dose-square kinetics.

Strategies for detecting heritable translocations in male mice by fertility testing

Data from a heritable translocation test were analysed to estimate the best rule for classification of F 1 males in normals or partially sterile translocation carriers according to litter size or numbers of live and dead implants per mating. Six rules were com[ared for classification with up to three litter sizes per F 1 male observed. The results indicate that a translocation rate of 2%, or at best of 1%, can be detected with reasonable cost.

Some Primary Considerations in the Interpretation of the Dominant-Lethal Assay

Research ArticleOpen AccessSome primary considerations in the interpretation of the dominant-lethal assay. V A Ray, and M L Hyneck V A Ray Search for more papers by this author and M L Hyneck Search for more papers by this author Published:1 December 1973https://doi.org/10.1289/ehp.730627Cited by:16AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InRedditEmail FiguresReferencesRelatedDetailsCited By Bagri P, Kumar V and Sikka A (2014) An in vivo assay of the mutagenic potential of imidacloprid using sperm head abnormality test and dominant lethal test , Drug and Chemical Toxicology, 10.3109/01480545.2014.966832, 38:3, (342-348), Online publication date: 3-Jul-2015. Zhu S, Zhang J, Liu C, He Q, Vijayalaxmi , Prihoda T, Tong J and Cao Y (2015) Dominant lethal mutation test in male mice exposed to 900MHz radiofrequency fields, Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 10.1016/j.mrgentox.2015.07.004, 792, (53-57), Online publication date: 1-Oct-2015. Ashby J and Clapp M (1995) The rodent dominant lethal assay: a proposed format for data presentation that alerts to pseudo-dominant lethal effects, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(95)00041-G, 330:1-2, (209-218), Online publication date: 1-Aug-1995. Saunders R, Kowalczuk C, Beechey C and Dunford R (2009) Studies of the Induction of Dominant Lethals and Translocations in Male Mice after Chronic Exposure to Microwave Radiation, International Journal of Radiation Biology, 10.1080/09553008814551341, 53:6, (983-992), Online publication date: 1-Jan-1988. Ray V, Kier L, Kannan K, Haas R, Auletta A, Wassom J, Nesnow S and Waters M (1987) An approach to identifying specialized batteries of bioassays for specific classes of chemicals: Class analysis using mutagenicity and carcinogenicity relationships and phylogenetic concordance and discordance patterns 1. composition and analysis of the overall data base a report of phase II of the U.S. environmental protection agency gene-tox program (MTR 07213), Mutation Research/Reviews in Genetic Toxicology, 10.1016/0165-1110(87)90018-2, 185:3, (197-241), Online publication date: 1-May-1987. Russell L and Hunsicker P (1987) Study of the base analog 6-mercaptopurine in the mouse specific-locus test, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(87)90251-X, 176:1, (47-52), Online publication date: 1-Jan-1987. Ehrenberg L (1984) ASPECTS OF STATISTICAL INFERENCE IN TESTING FOR GENETIC TOXICITY Handbook of Mutagenicity Test Procedures, 10.1016/B978-0-444-80519-5.50042-0, (775-822), . Sheu C and Moreland F (2008) Detection of Dominant Lethal Mutation in Mice After Repeated Low-Dose Administration of 6-Mercaptopurine, Drug and Chemical Toxicology, 10.3109/01480548309072463, 6:1, (83-92), Online publication date: 1-Jan-1983. Oakberg E, Crosthwait C and Raymer G (1982) Spermatogenic stage sensitivity to 6-mercaptopurine in the mouse, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(82)90179-8, 94:1, (165-178), Online publication date: 1-May-1982. Moreland F, Sheu C, Springer J and Green S (1981) Effects of prolonged chemical treatment with cyclophosphamide and 6-mercaptopurine in the dominant lethal test system, Mutation Research/Genetic Toxicology, 10.1016/0165-1218(81)90082-3, 90:2, (193-199), Online publication date: 1-Oct-1981. Sykora I, Gandalovičovǎ D and Řezábek K (1979) Absence of noxious effects of selected neuroleptics in dominant-lethal mutagenesis assay, Mutation Research/Genetic Toxicology, 10.1016/0165-1218(79)90090-9, 66:3, (291-299), Online publication date: 1-Mar-1979. Anderson D, McGregor D, Purchase I, Hodge M and Cuthbert J (1977) Dominant-lethal test results with known mutagens in two laboratories, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(77)90007-0, 43:2, (231-246), Online publication date: 1-May-1977. Anderson D, Hodge M and Purchase I (2018) Dominant lethal studies with the halogenated olefins vinyl chloride and vinylidene dichloride in male CD-1 mice, Environmental Health Perspectives, 21, (71-78), Online publication date: 1-Dec-1977. Anderson D, Hodge M and Purchase I (1976) Vinyl chloride: Dominant lethal studies in male CD-1 mice, Mutation Research/Genetic Toxicology, 10.1016/0165-1218(76)90034-3, 40:4, (359-370), Online publication date: 1-Nov-1976. Brewen J (1976) Practical evaluation of mutagenicity data in mammals for estimating human risk, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(76)90070-1, 41:1, (15-24), Online publication date: 1-Nov-1976. Generoso W, Preston R and Brewen J (1975) 6-Mercaptopurine, an inducer of cytogenetic and dominant-lethal effects in premeiotic and early meiotic germ cells of male mice, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(75)90237-7, 28:3, (437-447), Online publication date: 1-Jun-1975. Vol. 6December 1973Metrics About Article Metrics Publication History Originally published1 December 1973Published in print1 December 1973 Financial disclosures License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Some primary considerations in the interpretation of the dominant-lethal assay.

Research ArticleOpen AccessSome primary considerations in the interpretation of the dominant-lethal assay. V A Ray, and M L Hyneck V A Ray Search for more papers by this author and M L Hyneck Search for more papers by this author Published:1 December 1973https://doi.org/10.1289/ehp.730627Cited by:16AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit FiguresReferencesRelatedDetailsCited by Bagri P, Kumar V and Sikka A (2014) An in vivo assay of the mutagenic potential of imidacloprid using sperm head abnormality test and dominant lethal test , Drug and Chemical Toxicology, 10.3109/01480545.2014.966832, 38:3, (342-348), Online publication date: 3-Jul-2015. Zhu S, Zhang J, Liu C, He Q, Vijayalaxmi , Prihoda T, Tong J and Cao Y (2015) Dominant lethal mutation test in male mice exposed to 900MHz radiofrequency fields, Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 10.1016/j.mrgentox.2015.07.004, 792, (53-57), Online publication date: 1-Oct-2015. Ashby J and Clapp M (1995) The rodent dominant lethal assay: a proposed format for data presentation that alerts to pseudo-dominant lethal effects, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(95)00041-G, 330:1-2, (209-218), Online publication date: 1-Aug-1995. Saunders R, Kowalczuk C, Beechey C and Dunford R (2009) Studies of the Induction of Dominant Lethals and Translocations in Male Mice after Chronic Exposure to Microwave Radiation, International Journal of Radiation Biology, 10.1080/09553008814551341, 53:6, (983-992), Online publication date: 1-Jan-1988. Ray V, Kier L, Kannan K, Haas R, Auletta A, Wassom J, Nesnow S and Waters M (1987) An approach to identifying specialized batteries of bioassays for specific classes of chemicals: Class analysis using mutagenicity and carcinogenicity relationships and phylogenetic concordance and discordance patterns 1. composition and analysis of the overall data base a report of phase II of the U.S. environmental protection agency gene-tox program (MTR 07213), Mutation Research/Reviews in Genetic Toxicology, 10.1016/0165-1110(87)90018-2, 185:3, (197-241), Online publication date: 1-May-1987. Russell L and Hunsicker P (1987) Study of the base analog 6-mercaptopurine in the mouse specific-locus test, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(87)90251-X, 176:1, (47-52), Online publication date: 1-Jan-1987. Ehrenberg L (1984) ASPECTS OF STATISTICAL INFERENCE IN TESTING FOR GENETIC TOXICITY Handbook of Mutagenicity Test Procedures, 10.1016/B978-0-444-80519-5.50042-0, (775-822), . Sheu C and Moreland F (2008) Detection of Dominant Lethal Mutation in Mice After Repeated Low-Dose Administration of 6-Mercaptopurine, Drug and Chemical Toxicology, 10.3109/01480548309072463, 6:1, (83-92), Online publication date: 1-Jan-1983. Oakberg E, Crosthwait C and Raymer G (1982) Spermatogenic stage sensitivity to 6-mercaptopurine in the mouse, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(82)90179-8, 94:1, (165-178), Online publication date: 1-May-1982. Moreland F, Sheu C, Springer J and Green S (1981) Effects of prolonged chemical treatment with cyclophosphamide and 6-mercaptopurine in the dominant lethal test system, Mutation Research/Genetic Toxicology, 10.1016/0165-1218(81)90082-3, 90:2, (193-199), Online publication date: 1-Oct-1981. Sykora I, Gandalovičovǎ D and Řezábek K (1979) Absence of noxious effects of selected neuroleptics in dominant-lethal mutagenesis assay, Mutation Research/Genetic Toxicology, 10.1016/0165-1218(79)90090-9, 66:3, (291-299), Online publication date: 1-Mar-1979. Anderson D, McGregor D, Purchase I, Hodge M and Cuthbert J (1977) Dominant-lethal test results with known mutagens in two laboratories, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(77)90007-0, 43:2, (231-246), Online publication date: 1-May-1977. Anderson D, Hodge M and Purchase I (2018) Dominant lethal studies with the halogenated olefins vinyl chloride and vinylidene dichloride in male CD-1 mice, Environmental Health Perspectives, 21, (71-78), Online publication date: 1-Dec-1977. Anderson D, Hodge M and Purchase I (1976) Vinyl chloride: Dominant lethal studies in male CD-1 mice, Mutation Research/Genetic Toxicology, 10.1016/0165-1218(76)90034-3, 40:4, (359-370), Online publication date: 1-Nov-1976. Brewen J (1976) Practical evaluation of mutagenicity data in mammals for estimating human risk, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(76)90070-1, 41:1, (15-24), Online publication date: 1-Nov-1976. Generoso W, Preston R and Brewen J (1975) 6-Mercaptopurine, an inducer of cytogenetic and dominant-lethal effects in premeiotic and early meiotic germ cells of male mice, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(75)90237-7, 28:3, (437-447), Online publication date: 1-Jun-1975. Vol. 6December 1973Metrics About Article Metrics Publication History Originally published1 December 1973Published in print1 December 1973 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Evaluation of Chromosome Aberration Effects of Chemicals on Mouse Germ Cells

Research ArticleOpen AccessEvaluation of chromosome aberration effects of chemicals on mouse germ cells. W M Generoso W M Generoso Search for more papers by this author Published:1 December 1973https://doi.org/10.1289/ehp.730613Cited by:15AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InRedditEmail FiguresReferencesRelatedDetailsCited By Garcia-Sagredo J (2008) Fifty years of cytogenetics: A parallel view of the evolution of cytogenetics and genotoxicology, Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms, 10.1016/j.bbagrm.2008.05.003, 1779:6-7, (363-375), Online publication date: 1-Jun-2008. Lockhart A, Piegorsch W and Bishop J (1992) Assessing overdispersion and dose-response in the male dominant lethal assay, Mutation Research/Environmental Mutagenesis and Related Subjects, 10.1016/0165-1161(92)90007-9, 272:1, (35-58), Online publication date: 1-Aug-1992. Kligerman A (1982) Fishes as Biological Detectors of the Effects of Genotoxic Agents Mutagenicity, 10.1016/B978-0-12-336180-6.50020-X, (435-456), . Brusick D, Matheson D, Jagannath D, Braude M, Brockman H and Hung C (2008) Genetic Screening of Compounds used in Drug Abuse Treatment. II. Methadone, Drug and Chemical Toxicology, 10.3109/01480548109066368, 4:1, (1-18), Online publication date: 1-Jan-1981. Sykora I, Gandalovičovǎ D and Řezábek K (1979) Absence of noxious effects of selected neuroleptics in dominant-lethal mutagenesis assay, Mutation Research/Genetic Toxicology, 10.1016/0165-1218(79)90090-9, 66:3, (291-299), Online publication date: 1-Mar-1979. Reddy C, Chan P and Hayes A (1978) Teratogenic and dominant lethal studies of patulin in mice, Toxicology, 10.1016/S0300-483X(78)91339-2, 11, (219-223), Online publication date: 1-Jan-1978. Ong T (1978) Genetic activities of hycanthone and some other antischistosomal drugs, Mutation Research/Reviews in Genetic Toxicology, 10.1016/0165-1110(78)90012-X, 55:1, (43-70), Online publication date: 1-Jan-1978. Wiemann H and Lang R (1978) Strategies for detecting heritable translocations in male mice by fertility testing, Mutation Research/Environmental Mutagenesis and Related Subjects, 10.1016/0165-1161(78)90004-3, 53:3, (317-326), Online publication date: 1-Jun-1978. Brusick D, Matheson D, Jagannath D, Braude M and Brockman H (2008) Genetic Screening of Compounds Used in Drug Abuse Treatment I. Naltrexone Hydrochloride, Drug and Chemical Toxicology, 10.3109/01480547809034430, 1:2, (103-135), Online publication date: 1-Jan-1978. Sheu C, Moreland F, Oswald E, Green S and Flamm W (1978) Heritable translocation test on random-bred mice after prolonged triethylenemelamine treatment, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(78)90028-3, 50:2, (241-250), Online publication date: 1-May-1978. Brusick D (2018) Alteractions of germ cells leading to mutagenesis and their detection, Environmental Health Perspectives, 24, (105-112), Online publication date: 1-Jun-1978.Epler J, Larimer F, Rao T, Nix C and Ho T (2018) Energy-related pollutants in the environment: Use of short-term tests for mutagenicity in the isolation and identification of biohazards, Environmental Health Perspectives, 27, (11-20), Online publication date: 1-Dec-1978. Matter B (1976) Problems of testing drugs for potential mutagenicity, Mutation Research/Environmental Mutagenesis and Related Subjects, 10.1016/0165-1161(76)90149-7, 38:4, (243-258), Online publication date: 1-Aug-1976. Kalter H (1975) Some relations between teratogenesis and mutagenesis, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/0027-5107(75)90041-X, 33:1, (29-36), Online publication date: 1-Nov-1975. Flamm W (1974) A tier system approach to mutagen testing, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 10.1016/S0027-5107(74)80030-8, 26:4, (329-333), Online publication date: 1-Aug-1974. Vol. 6December 1973Metrics About Article Metrics Publication History Originally published1 December 1973Published in print1 December 1973 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.