Non-disjunction induction by mutagenic agents in male cells of the Northern vole Microtus oeconomus

Non-disjunction induction by mutagenic agents in male cells of the Northern vole Microtus oeconomus

273 When compared to the effect of X-rays (100 rad, treatment at pre-leptotene) the non-disjunction inducing capacity of MMS seems to be about ~ and E...

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273 When compared to the effect of X-rays (100 rad, treatment at pre-leptotene) the non-disjunction inducing capacity of MMS seems to be about ~ and EMS ½ of that of X-rays. The genetic hazards of mutagen exposure during spermatogenesis are discussed.

2O7 Tates, A.D., Department of Radiation Genetics and Chemical Mutagenesis, University of Leiden (The Netherlands)

Non-disjunction induction by mutagenic agents in male cells of the Northern vole M i c r o t u s o e c o n o m u s Results from non
274 (50 mg/kg). The latter c o m p o u n d induced significant numbers of aberrant haploid and diploid gametes in early primary spermatocytes. The frequencies were about the same as those obtained after 50 R of X-rays. 1 A . D . T a t e s , P.L. Pearson and J.P.M. Geraedts. J. R e p r o d . F e r t . , 4 2 ( 1 9 7 5 ) 1 9 5 - - 1 9 8 .

2O8 Taylor, A.M.R., Department of Cancer Studies, Medical School, Birmingham B15 2TJ (U.K.) Unrepaired single and double DNA strand breaks shown cytogenetically following X-irradiation of lymphocytes from patients with ataxia telangiectasia Many reports have speculated on the possibility of interpreting chromosome aberrations in terms of damage incurred at the DNA molecular level, but the relationship between the two levels has been difficult to demonstrate experimentally. Cells from patients with classical xeroderma pigmentosum show sensitivity to UV light and 4-NQO as demonstrated by reduced cell survival, an increased level of chromosome aberrations and a defect in excision repair of damaged DNA. In another syndrome, ataxia telangiectasia (AT) we have been able to show that cells from all patients so far examined are radiosensitive at both the cellular and chromosomal levels. Other work has shown that there is a reduced level of 7-ray induced repair replication in some cell strains. Using sucrosegradient techniques it has not been possible to detect any significant differences in either single or double strand break production or repair, between normals and AT patients. Unrepaired or misrepaired DNA single or double strand breaks might be the basic lesions leading to the typical chromosome aberrations seen after Xirradiation of either normal or AT cells. It is suggested here that the unusually high level of radiation induced chromosome and chromatid type aberrations in AT cells compared with normals (Taylor et al., Nature (London), 260 (1976) 441--443) is due to a significantly increased fraction of unrepaired double and single strand breaks. The observed frequency of aberrations arising from single and double strand breaks at both Go and G2 can be accounted for by the presence of only a small fraction of breaks remaining unrepaired in AT cells. These may not be easily demonstrable using conventional sucrose-gradient techniques. An inability to repair all strand breaks may therefore be an important basic defect in AT repair.

209 Tazima, Y., National Institute of Genetics, Misima (Japan)

Low dose-rate experiment with tritiated thymidine as a simulator of chemical mutagens using silkworm oocyte system