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PubMed1991

The genetic basis of resistance to ionising radiation damage in cultured mammalian cells.

To test the genetic similarity of independently-isolated hamster cell mutants sensitive to ionising radiation, these were fused in pairs and the hybrids exposed to X-rays. Some mutants (irs1, irs3, xrs-1, XR-1, BLM2) were found to complement all others tested for radiosensitivity in hybrids, and are therefore in separate genetic groups. The mutants irs2 and V-E5, both isolated from V79 cells, did not complement and therefore belong to the same group. Another pair, EM7 and irs1SF, formed hybrids with intermediate levels of survival between mutant and wild-type. However, the parental cells fused to irs1SF also showed intermediate sensitivity, suggesting a semi-dominant mutant phenotype rather than a lack of complementation. Crosses of some of these hamster mutants to the radiosensitive mouse mutant M10 showed clear complementation (irs1 x M10, irs2 x M10) but for others the complementation did not greatly exceed the sensitivity of one (irs3 x M10) or both mutants (XR-1 x M10). Taken with our previously-published data, these results show that there are at least 8 genetic groups determining resistance to ionising radiation damage in rodent cells.

Animals↗
PubMedDate not supplied

[Universal character of induction of cytogenetic aberrations by low intensity radiation, and estimation of genetic risk].

The analysis of contemporary state of the problem in quantitative estimation of cytogenetic effects within the low dose range is given. Experimentally derived modern data led to a conclusion that the relationship between radiation induced cytogenetic damage and dose within the low dose range is non-linear and universal (concerning test-objects) in nature. Consequences of the received results for biological dosimetry and the estimation of genetic and carcinogenic risk of low dose exposure are discussed.

Animals↗
PubMed1975

[The effect of cystamine on the outcome of dominant lethal mutations and reciprocal translocations in sex cells of mice subjected to gamma-irradiation in different doses].

Protective effect of cystamine (150 mg/kg) against genetic damages induced by gamma-irradiation in germ cells of male mice of CBA strain (at doses of 100, 300, 600 r) was studied. The application of cystamine decreased the frequency of dominant lethal mutations induced by radiation in sperms, spermatids and spermatocytes. The degree of the protective effect of cystamine depended on a radiation dose. The protective effect of cystamine was the highest at the radiation dose of 300 r. It was negligible at the radiation dose of 100 r and was completely absent at the dose of 600 r. Cystamine did not affect the rate of induced reciprocal translocations in the spermatogonia at all the radiation doses used.

Animals↗
PubMed1963

THE RELATION BETWEEN DNA SYNTHESIS AND CHROMOSOME STRUCTURE AS RESOLVED BY X-RAY DAMAGE.

Vicia faba root tip cells were treated for short periods with tritiated thymidine, either immediately before or after exposure of roots to x-rays, and autoradiograph preparations were analysed in an attempt to test the hypothesis that chromatid type (B') aberrations are induced only in those chromosome regions that have synthesized DNA prior to x-irradiation, whereas chromosome type (B'') aberrations are induced only in unduplicated chromosome regions. Studying the relation between presence or absence of label at loci involved in aberrations, in cells irradiated at different development stages, and the pattern of labelling in cells carrying both types of aberration leads to the conclusion that B'' aberrations are induced only in unreplicated chromosome regions. Following replication, only B' aberrations are induced, but these aberrations are also induced in chromosome regions preparing to incorporate DNA. It is suggested that the doubled response of the chromosome to x-rays prior to DNA incorporation might reflect a physical separation of replicating units prior to replication. The aberration yields in damaged cells which were irradiated in G(1)S, and early G(2) were in the ratio of 1.0:2.0:3.2. The data indicate that the increased yield of B' in early G(2) relative to S cells may be a consequence of changes in the spatial distribution of the chromosomes within the nucleus.

Chromatids↗