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The study covered state of spermatogenic epithelium and dominant lethal mutations output in mice of BALB/c and CBA lines, subjected to total gamma-irradiation and in Wistar rats after intraperitoneal injection of potassium bichromate (K2Cr2,O7) in small and sublethal doses. The BALB/c line mice under low irradiation dose (0.25 Gy) demonstrated stimulation effect on spermatogenic epithelium, but in the CBA line mice no such effect was seen. Both mice lines under irradiation of 0.25 Gy and 1.0 Gy demonstrated increase in pathologic sperm counts and in percentage ofpreimplantation embryonal death. In rats, injection of potassium bichromate in doses of 0.028 mg/kg and 2.8 mg/kg increased number of micronuclear spermatids, larger pathologic sperm counts and percentage of postimplantation deaths. Thus, lower general embryonal deaths under radiation exposure is due to preimplantation embryonal deaths, under exposure to 6-valent chromium--is due to postimplantation losses.

A comparative study of the effects of gene mutations mus209, mus309, mei-41 and rad54 of Drosophila melanogaster on the sensitivity to low-level exposure of different duration was carried out. Taken into account was the survival rate at different stages of ontogeny, female fecundity, the frequency of dominant lethal mutations (DLM) and the DNA damage. mei-41 and rad-54 mutants were most sensitive to the action of low dose radiation (80 mGy) in terms of survival and DLM. However, at the level of DNA damage, an increased radiosensitivity is observed only at larger doses of low intensity irradiation. Based on these observations, we can conclude about the importance of repair and its genes in the formation of the effect of low level doses of ionizing radiation in Drosophila.

The dose-rate effect of acute and chronic irradiation in the dose of 0.2 Gy in Drosophila melanogaster repair (mei-41, mus209 [Russian character: see text] mus309) and free radicals detoxication (sod) mutant strains was investigated. Was shown the lack of dose rate effect on the rate of dominant lethal mutations in mei-41, mus209 and sod. However in mus309, that has defect in the main Drosophila pathway of the DNA double strand breack repair, the increase of the mutation rate after chronic irradiation was observed (inverse dose-rate effect). The obtained results suggest the main role of DNA double strand breack repair in dose-rate effect formation in Drosophila.

It was investigated the influence of the chronic gamma-irradiation in the dose rate of 0.17 sGy/h on the rate of genetic variability in the laboratory strains of Drosophila melanogaster with genotypic distinguishes in mobile genetic elements and defects in the DNA repair processes. It was shown that the rates of induction of recessive lethal mutations depended on genotype of investigated strains. In the different strains we have observed an increase as well as a decrease of the mutation rate. Also in was established that irradiation leads to the frequencies of the GD-sterility and mutability of the snw and h(w+) in the P-M and H-E dysgenic crosses. The obtained results suggest that mobile genetic elements play an important role in the forming of genetic effects in response to low dose irradiation.

Studies to analyze the genetic processes in natural populations of plants were started on the territory of the East-Ural Radioactive Trace (EURT) in 1962 and in the zone of the Chernobyl accident in May 1986. The main directions of the genetic studies in both radioactive areas were similar: 1) study of the mutation process intensity depending on the dose and dose rate and analysis of dose-effect relationships for different genetic changes (point mutations, chromosome aberrations in mitosis and meiosis) in irradiated plant populations; 2) study of the mutation process dynamics in generations of chronically (prolongly) irradiated populations of plants; 3) analysis of microevolutionary processes in irradiated plant populations. The report presents an analysis of observed dose-effect relationships under the action of radiation on populations of Arabidopsis thaliana, Pinus sylvestris and a number of other plant species. Analysis of the mutation processes dynamics in 8 Arabidopsis populations growing in the zone of the Chernobyl catastrophe has demonstrated that the level of the embryo lethal mutations 10 years after the accident in the irradiated populations significantly exceeds the control level. The following phenomena observed in chronically irradiated populations have also been considered: increased radioresistance of irradiated populations (radioadaptation), the appearance of abnormal karyotypes and selective markers upon chronic irradiation. The authors call attention to the high importance of monitoring of genetic processes in irradiated plant populations for understanding of the action of radiation on human populations.

The frequency of irradiation-induced recessive lethals has been studied in chromosomes 1 and 2 of Drosophila melanogaster. It supposed, that the higher level of mutability may be explained in destabilization of genotype. The essential part in induction of genotype destabilization replies the genome instability mechanisms.

In 1986-1994, genetic effects of radiation on males of wild mice caught in areas of radioactive contamination after the Chernobyl reactor accident were studied. The gamma-radiation dose rates on the soil surface in the areas varied from 0,02 to 200 mR/h. The frequency of reciprocal translocations in mouse spermatocytes was relatively low and increased linearly with increasing of the dose rate. The levels of recessive lethal mutations in mouse populations did not depend on the radiation dose rate in the areas and decreased with a time.

Purpose: Low doses of ionizing radiation reduce the growth rates of clones following irradiation of the progenitor cells. Such reductions of clone growth have been proven by means of measurements of clone size distributions. The medians of such distributions can be used to quantify the radiation damage. Prolongations of generation times and cell death as result of heritable lethal mutations have been discussed as causes for the reduction of clone growth., Material and Methods: The cell number of a clone of hypotetraploid CHO-cells was compared to the frequency of micronucleated binucleated cells in the same clone using the cytokinesis-block-micronucleus method. The dose dependent reduction of clone sizes is measured by the difference of the medians (after log transformation) of the clone size distributions., Results: At cytochalasin-B concentrations of 1 microgram/ml and after an incubation time of 16 h a yield of binucleated cells of about 50% was obtained. Median clone size differences as a measure of clonal radiation damage increased linearly with incubation times of 76, 100, 124, and 240 h following irradiation with 3, 5, 7, and 12 Gy. The frequency of binucleated clone cells with micronuclei strongly increased with decreasing clone size by a factor up to 20 following irradiation with 3, 5, and 7 Gy. The frequency of micronucleated binucleated clone cells was found to be independent of incubation time after irradiation., Conclusion: Radiation induced clone size reductions result from cell losses caused by intraclonal expression of micronuclei which have its origin in heritable lethal mutations. Measurements of clone size distributions can be done automatically. They can serve as predictive test for determination of median cell loss rates of surviving cell clones.

Single whole-body exposure of adult male rats Wistar in different stages of spermatogenesis to gamma-rays (doses from 0.25 to 5.00 Gy) resulted in violations of antenatal development of the first generation offsprings. The pronouncement of these violations depends on the spermatogenesis stage in the moment of irradiation and exposure dose.

There was a 30% increase in spermatozoids with microheads and a 3-fold increase in "young" spermatozoids at later times after irradiation of BALB/c mice a dose of 1.0 Gy. With radiation doses of 0.1-1.0 Gy, BALB/c and CBA mice (which differ in viability of spermatogenous cells, the number of Sertoli cells and total embryonal death rate) exhibited a significant increase in the preimplantation death at the stage of spermatogonia and stem cells. The results obtained indicate reduction of the fertilizing capacity of sperm which is probably realized as dominant lethal mutations.

Genetic study of rats showed the possibility of registration of the minor doses of the inside and outside irradiation. The postmiosis mutations, number of reciprocal translocations in spermatogonia may be used for indexation of the effects.

The biological effects of heavy charged particle (HZE) radiation are of particular interest to travellers and planners for long-duration space flights where exposure levels represent a potential health hazard. The unique feature of HZE radiation is the structured pattern of its energy deposition in targets. There are many consequences of this feature to biological endpoints when compared with effects of ionizing photons. Dose vs response and dose-rate kinetics may be modified, DNA and cellular repair systems may be altered in their abilities to cope with damage, and the qualitative features of damage may be unique for different ions. The nematode Caenorhabditis elegans is being used to address these and related questions associated with exposure to radiation. HZE-induced mutation, chromosome aberration, cell inactivation and altered organogenesis are discussed along with plans for radiobiological experiments in space.

Recent experimental evidence concerning the nature of radiosensitive targets in mouse immature (resting) oocytes has led to new experimental designs that permit measurement of radiation-induced genetic damage in these important cells. We have previously reported initial results of the detection of genetic damage in mouse immature oocytes using monoenergetic 0.43-MeV neutrons. Here we provide a full report of our data and compare the genetic sensitivity of immature oocytes with those measured by others for maturing oocytes. Until recently, all attempts to detect radiation-induced genetic damage in mouse immature oocytes had failed. This appears to have been because the radiation types and modes of dose delivery used in those studies did not sufficiently spare the hypersensitive lethality target (the plasma membrane) while at the same time deposit enough dose in DNA to produce detectable mutation. Recoil protons from 0.43-MeV neutrons produce short ionization tracks (2.6 micron mean) and can therefore deposit energy in the DNA without simultaneously traversing the plasma membrane. Using these particles, we have obtained dose-response relationships for both chromosome aberrations and dominant lethal mutations in oocytes from females irradiated 8-12 weeks earlier, when oocytes were immature. Results suggest that the intrinsic mutational sensitivity of mouse immature oocytes is not very different from that of maturing oocytes.

To develop a specific-locus test (SLT) system for environmental mutagenesis using vertebrate species other than the mouse, we first established a tester stock of the fish medaka (Oryzias latipes) that is homozygous recessive at three loci. The phenotypic expression of these loci can be easily recognized early in embryonic development by observation through the transparent egg membrane. We irradiated wild-type males with 137Cs gamma-rays to determine the dose-response relationships for dominant lethal and specific-locus mutations induced in sperm, spermatids, and spermatogonia. Through observation of 322,666 loci in control offspring and 374,026 loci in offspring obtained from 0.64-, 4.75-, or 9.50-Gy-irradiated gametes, specific-locus mutations were phenotypically detected during early development. These putative mutations, designated "total mutation," can be recognized only in embryos of oviparous animals. The developmental fate of these mutant embryos was precisely followed. During subsequent embryonic development, a large fraction died and thus was unavailable for test-crossing, which was used to identify "viable mutations." Our medaka SLT system demonstrates that the vast majority of total mutations is associated with dominant lethal mutations. Thus far only one spontaneous viable mutation has been observed, so that all doubling calculations involving this endpoint carry a large error. With these reservations, however, we conclude that the quantitative data so far obtained from the medaka SLT are quite comparable to those from the mouse SLT and, hence, indicate the validity of the medaka SLT as a possible nonmammalian test system.

The results of this study indicate the existence of a strong interaction between ethyl methanesulfonate (EMS) and ultraviolet light (UV) for cell killing in the yeast Saccharomyces cerevisiae. Conversely, mutation and gene conversion frequencies observed for the combined treatment of EMS and UV do not deviate significantly from that expected on the basis of simple additivity. Studies involving repair-deficient mutants (rad mutants) reveal that the synergistic interaction for cell killing depends on RAD52 function (recombinational repair), but not on RAD3 function (excision repair). On the basis of this analysis, the interaction between EMS and UV in S. cerevisiae might arise from the inhibition of double-strand break repair by one, or both agents.

The induction of mutations following combined treatment with acrylamide (AA) plus X-rays has been determined using the dominant lethal mutations test in Pzh:SFISS male mice. Combinations of a mutagenic dose of both agents (1.00 Gy, 125 mg/kg b.w.) and a non-mutagenic dose, i.e., a dose that alone does not produce dominant lethals (0.25 Gy, 25 mg/kg b.w.), were used. For the discussion of the effects of combined action of X-rays and acrylamide the term 'enhancement in risk' was used whenever the effects observed after combined exposure significantly exceeded the sum of the effects produced separately by the agents. Such an enhanced risk has been observed in late spermatids after combined action of X-rays and AA at non-mutagenic doses, and in spermatozoa, spermatids and late spermatocytes after exposure to mutagenic doses.

A new mathematical approach to the description of interaction data (Ager and Haynes, 1987) is applied here to the interaction between heat and ultraviolet light (UV) in Saccharomyces cerevisiae. A strong synergism for cell killing is found to be associated with large increases in gene conversion (of up to 8-fold), and mutation (of up to 14-fold). Analysis of the interaction data for both wild-type and repair-deficient strains indicates that the heat-UV synergism arises via the inhibition of two different repair pathways. Unambiguous conclusions regarding the molecular mechanisms by which these repair processes are inhibited cannot be drawn on the basis of dose-response data alone. However, this approach does enable one to make well defined, empirical comparisons of the nature and kinetics of such interactions.

Genetic effects of irradiation in males of wild house mice which were caught in the region of Chernobyl Nuclear Power Station were studied. The dose rate on the ground surface varied from 0.04 to 200 mR/h of gamma-irradiation. The increasing yield of dominant lethal mutations was only observed in males from the most contaminated sector. Reciprocal translocations were observed in spermatocytes of mice at all the levels of contamination. The rate of reciprocal translocations was relatively low and increased linearly with the elevation of the dose rate. The extent of testis damages increased also, as the dose rate grew. The frequency of abnormal sperm heads, the yield of recessive lethal mutations, litter size and radiosensitivity of the first progeny were not changed, depending on the dose rate.

Two groups of lethal mutations that are expressed only in somatic cells were isolated using the gonosomic selective method. The mutations tend to be organized in clusters along the sex chromosome. Analysis of mutation expression allowed to characterize the degree of changes in genetic diversity of somatic and germ lines in development; it is minimal in the III instar larvae and prepupae and maximal in the I and II instar larvae and pupae.

The dilute (d) coat color locus of mouse chromosome 9 has been identified by more than 200 spontaneous and mutagen-induced recessive mutations. With the advent of molecular probes for this locus, the molecular lesion associated with different dilute alleles can be recognized and precisely defined. In this study, two dilute mutations, dilute-lethal20J (dl20J) and dilute prenatal lethal Aa2, have been examined. Using a dilute locus genomic probe in Southern blot analysis, we detected unique restriction fragments in dl20J and Aa2 DNA. Subsequent analysis of these fragments showed that they represented deletion breakpoint fusion fragments. DNA sequence analysis of each mutation-associated deletion breakpoint fusion fragment suggests that both genomic deletions were generated by nonhomologous recombination events. The spontaneous dl20J mutation is caused by an interstitial deletion that removes a single coding exon of the dilute gene. The correlation between this discrete deletion and the expression of all dilute-associated phenotypes in dl20J homozygotes defines the dl20J mutation as a functional null allele of the dilute gene. The radiation-induced Aa2 allele is a multilocus deletion that, by complementation analysis, affects both the dilute locus and the proximal prenatal lethal-3 (pl-3) functional unit. Molecular analysis of the Aa2 deletion breakpoint fusion fragment has provided access to a previously undefined gene proximal to d. Initial characterization of this new gene suggests that it may represent the genetically defined pl-3 functional unit.

A method of selective screening of recessive sex-linked lethal mutations, that are manifested only in somatic cells of D. melanogaster, has been developed. Lethals were induced with X-irradiation of X-chromosomes at the moment of their topographic segregation from embryonic somatic cells. Analysis of mutation expression confirmed the method selectivity.

Muller-5 males were irradiated with X-rays in nitrogen, in air or in oxygen (followed by nitrogen or oxygen post-treatments in the nitrogen and oxygen series) and were mated to females of a repair-proficient strain (mei+) or to those of a strain known to be deficient in excision repair of UV damage (in somatic cells). The latter strain, designated as mei-9a, is also known to be sensitive, in the larval stages, to the killing effects of UV, X-rays and to a number of chemical mutagens. The frequencies of sex-linked recessive lethals and autosomal translocations induced in the spermatozoa of males were determined and compared. The frequencies of sex-linked recessive lethals in the mei-9 control groups were consistently higher than in the mei+ groups. Irradiation in air or in nitrogen led to significantly higher yields of recessive lethals when the irradiated males were mated to mei-9 females, whereas, after irradiation in oxygen, the yields were similar with both kinds of female. No significant differences in the frequencies of reciprocal translocations were observed between the mei+ and mei-9 groups after irradiation of the males in nitrogen, in air or in oxygen. Likewise, no differential effects of the contrasting post-treatments (nitrogen versus oxygen), either for recessive lethals or for translocations, could be discerned. These results are considered to support the notion that the kinds of genetic damage induced in mature spermatozoa in air or in nitrogen are qualitatively similar (at least with respect to the component(s) that lead to the production of recessive lethal mutations), but clearly different when induced in an oxygen atmosphere. The enhanced yields of recessive lethals with mei-9 females (after irradiation of the males either in air or in nitrogen) has been interpreted on the assumption that the mei-9 mutant is also deficient for the repair of X-ray-induced, recessive lethal-generating premutational lesions. Possible reasons for the lack of differences between the mei+ and mei-9 groups with respect to translocation yields and for the absence of measurable differences in response between the contrasting post-treatments (after irradiation of the males in nitrogen) are discussed.

Female mice were X-irradiated with 0.5-4.5 Gy 2 h before mating to unirradiated males of the same strain. The dominant lethal frequencies (DLF) were determined by growing the embryos in vitro from the two-cell stage and determining the relative rates of successful embryogenesis to the blastocyst stage and to the trophectoderm outgrowth with proliferated inner cell mass stage. The DLF increased with increasing dose, the two linear aspects having a breakpoint at about 1.5 Gy. The nature of embryo failure was also dose dependent. At doses less than 2.0 Gy embryos failed predominantly after blastocyst formation, but at higher doses the embryos failed both before and after blastocyst formation. Over the dose range tested, the frequency with which lesions leading to dominant lethality were induced [i.e., -ln(1 - DLF)] increased linearly with increasing dose.

The induction of dominant lethal mutations by doses of 100-400 rad X-rays in oocytes of the guinea-pig and golden hamster was studied using criteria of embryonic mortality. For both species higher yields were obtained from mature than from immature oocytes, in contrast to results for the mouse. Data on fertility indicated that in the golden hamster, as in the mouse, immature oocytes were more sensitive to killing by X-rays than mature oocytes but that the converse was true in the guinea-pig. The dose-response relationship for mutation to dominant lethals in pre-ovulatory oocytes of guinea-pig and golden hamsters was linear, both when based on pre- and post-implantation loss and when on post-implantation loss only. The rate per unit dose was higher for the golden hamster, and the old golden hamsters were possibly slightly more sensitive than young ones. The mutation rate data for mature oocytes of the mouse, using post-implantation loss alone, also fitted a linear dose-response relationship, except that the rate per unit dose was lower than for the other two species.

The modifying effect of dynamic space flight factors (DF) on radiation chromosomal damages in Drosophila oocytes of the 7-th and 14-th stages was studied. It has been found that the number of dominant lethal mutations increases under the simultaneous action of radiation and dynamic factors on oocytes-7. The magnitude of radiation effect on mature oocytes did not change upon additional action of DF. It is assumed that the modifying effect of DF on radiation damage may be a reason for discrepancy of flight experimental results.

2 groups of Wistar male rats (6-7 weeks old) were given ethanol, 15% in drinking water, for 5 days. The level of ethanol was gradually raised to 20 and 30% resp. Both groups received ethanol between 15 and 20% or 15 and 30% continuously during 35 days. Another group was given 30% ethanol for a period of 4 days before mating started. In addition to a control group, which received no treatment, a positive control group of rats exposed to 200 R X-rays, was used. After the treatments, individual males were paired with virgin Wistar females (10-12 weeks) at weekly intervals, and 8 sequential pairings were undertaken. Females were examined for uterine contents and corpora lutea, 10-11 days after their separation from the males. The females mated with irradiated males showed a high incidence of dead implantations and reduction of live implantations. No significant differences in the number of dead, live and total implantations at pre- and/or post-implantation levels were observed among the control and the ethanolic groups, showing that ethanol did not induce any dominant lethal mutations in these Wistar male rats. In the light of studies on alcoholics and other recent data, a need to investigate, independently, the potential mutagenic effects of ethanol and alcoholic beverages is discussed.

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.

The lethal and mutagenic effects and the nature of mutations induced by 90Sr-90Y and 89Sr in cells of the yeast Saccharomyces cerevisiae were studied. The lethal efficiency was determined for 89Sr as (7,6 +/- 1,05) X 10(-5) decay-1, for 90Sr-90Y-(3,3 +/- 1,6) X 10(-4) decay-1. The mutagenic efficiency for ade1 and ade2 genes was determined for 89Sr as (8,3 +/- 2,5) X 10(-9) decay-1, for 90Sr-90Y-(2,9 +/- 1,5) X 10(-8) decay-1. For ade2 locus, the spectrum of mutations induced by 89Sr was a follows: one deletion, 17% of frameshifts and 83% of base pair substitutions--51% of transversions, 22% of GC-AT transitions and 10% of AT-GC transitions. The data of the present work suggest that 90Sr-90Y and 89Sr are very efficient physical mutagens. The relative mutagenic efficiency (RME) was estimated for radionuclides studied.

Interaction between mutagenic effects of strong homogeneous magnetic fields and fission neutron-plus-gamma radiation was investigated, using the sex-linked, recessive, lethal test in Drosophila melanogaster. Drosophila males were exposed chronically, for seven days, to a 37,000-G homogeneous magnetic field and/or 3 doses of neutron-plus gamma radiation. Mutations in spermatozoa, spermatids, and spermatocytes were scored. There was no evidence of interaction between the effects of the two types of exposure in causing genetic damage in any of the three cell types. Dose-response relations for the radiation doses were linear for spermatozoa and spermatids for all three doses and for spermatocytes, up to 300 rads. Spermatozoa appear to be most sensitive to neutron-radiation-induced, recessive lethal mutations.

The mutagenic potential of 125I was studied using dominant lethal (DL) and testicular uptake studies. Dominant lethality (DL) represents embryonic death resulting from the chromosomal breakage in gametes of parents. When compared to controls, mice treated with different doses of 125I showed significant levels of induced DL. Significant pre-implantation losses were observed and variations in live implantations indicated total losses by the isotope. Dead implantations per pregnant female in the isotope treated groups showed a significant increase from controls indicating induced levels of post-implantation losses. All the stages of spermatogenesis, i.e., spermatozoa, spermatid, spermatocyte and spermatogonia were found to be sensitive to the induction of post-implantation losses, the spermatid stage being the most sensitive. Testicular uptake was measured from 1/2 hour to 72 hours after injection and maximum uptake was recorded at 1/2 hour, indicating the permeability of the blood/testis barrier.

A study was made of the protective effect of some radioprotective agents against dominant lethal mutations (DLM) in postspermatogonial stages and reciprocal translocations (RT) in spermatogonia induced by gamma-radiation. Among the radioprotective agents used, cystaphos, a combination of cystamine and 5-MOT and a mixture of 6 components proved to be most effective against DLM, and cystaphos, gammaphos and cystamine combined with 5-MOT proved effective against RT. The degree of radioprotective efficacy was relatively low. The efficacy of cystamine in protecting against RT was higher with exposure of gonocytes of 18.5-day embryos than spermatogonia of pubertal animals. The degree of the radioprotective effect varied depending on the stage of spermatogenesis, and, in all cases, it was lower than that observed in studies of protection against lethal effects of ionizing radiation.

Adult male mice had the lower halves of their bodies exposed in a waveguide system to 2.45 GHz microwave radiation for 30 min. The half body dose-rate of 43 W kg-1 had been shown in a previous study [7] to deplete severely the heat-sensitive stages of sperm production. The males were mated at intervals to adult hybrid females over the following 8-10 weeks. There was no significant reduction in post-implantation survival, suggesting that the microwave exposure did not have a mutagenic effect on the male germ cells. However, pregnancy rate was significantly reduced in weeks 3, 4, 5 and 6; reaching a minimum of about 10% of the control value in weeks 4 and 5. The occurrence of low values in weeks 4 and 5 correlated well with the expected reductions in sperm count due to the pattern of depletion of the spermatogenic epithelium of the testes. Thus it was concluded that the reduced pregnancy rate resulted from reduced male fertility. Pre-implantation survival can also be affected by reduced sperm count [8] and was significantly reduced in this study but it correlated less well with the anticipated heat response. A further study is in progress looking at the contribution of sperm count and sperm abnormality to the results.

Male CBA mice were exposed to 14.5 MeV neutron, either in an acute (150 or 250 rad) or a chronic dose (250 rad) and the genetic effects of the irradiations were compared. No detectable difference in the rate of mutations existed between acute and chronic exposure, with these neutrons.

Fertility and frequency of gamma-induced dominant lethals in female oocytes have been studied in a strain of Drosophila melanogaster carrying rad(2)201G1 mutation and in the wild type strain. It was shown that oocytes of the mutant strain exhibited the higher sensitivity during the whole period of oogenesis, as compared to those of the wild type flies. The strongest influence of rad(2)201G1 mutation on the frequency of dominant lethals and fertility was observed.

The frequency of dominant lethal mutations (DLM) in the germ cells of male mice exposed to either THO- or gamma-irradiation of 137Cs at the dose of 0.5-3.7 Gr was studied. The distribution of the number of dead embryos in females from the control group as well as that at a dose of irradiation less than 1 Gr, corresponds to the Poisson rule. Spermatids appeared to be more radiosensitive than spermatocytes and spermatozoa. The rate of the effect caused by irradiation of both spermatocytes and spermatids did not depend on the dose rate of gamma-irradiation ranging from 1.10(-3) to 1.7 Gr per min. The linear quadratic formula of aD+bD2 describes the relation of the DLM frequency to the doses of either beta- or gamma-irradiation. The THO RBE increases with the decrease of the dose reaching 2.5 at the D less than 0.1 Gr.

Young and old hybrid female mice were given 0.5 Gy or 2 Gy acute x-irradiation, followed by (i) in utero examination for dominant lethal mutations, or (ii) examination of metaphase I oocytes for chromosome aberrations 2-3 weeks after the irradiation. Some of the old females had been mated when young to males of a specific locus stock. Others were left unmated until after the irradiation when they, and the young females, were mated to the same specific locus stock and allowed to have 1 (if given 2 Gy) or 2 (if given 0.5 Gy) litters before the dominant lethal test. In both the 0.5-Gy and 2-Gy series, mean sizes of first litters in the old late-mated group were markedly lower than in the old early-mated or young groups, the differences being significant at the 2-Gy level. The intrauterine examinations showed that this difference was largely the result of a reduced ovulation rate in the old late-mated females. Preimplantation loss tended to be higher in all the old females than in the young ones, but differences between the groups in postimplantation lethality were less pronounced. In the chromosome studies, only about half as many oocytes were recovered from the ovaries of old females than from young ones. At both the 0.5-Gy and 2-Gy dose levels interchange frequencies were non-significantly higher in old than in young females (with no clear-cut effect of mating status), while the overall frequency of aberrations (interchanges + fragments) was significantly higher in oocytes of old than young females after 2 Gy X-rays (35.5% against 12.5%). No specific locus mutations were found in 5616 offspring of unirradiated females.

The radiation-resistant free-living nematode Panagrellus redivivus was used to study mutation rates in oocytes, following gamma, proton and neutron irradiation in the dose range 45-225 grays. gamma-Radiation produced approximately 0.001 lethal X-chromosomes per gray over the range tested. Proton or neutron irradiation produced approximately 0.003 lethal X-chromosomes per gray at lower doses, with the mutation rate dropping to 0.001 lethal X-chromosome per gray at the higher doses. These results suggest a dose-dependent mutation-repair system. Cell lethality was also examined. gamma-Radiation produced the greatest amount of cell lethality at all doses, while neutron irradiation had no cell lethal effect at any of the doses examined.

Selection responses of the laboratory stock Berlin wild (+60, +K) of Drosophila melanogaster to the mutagenic effects of high, accumulated exposures of X-rays were studied in several sub-populations with long irradiation histories. Interest was focussed on adaptive adjustments of mutation rates. In samples from the populations, radiosensitivities of immature oocytes were tested, by using dominant lethals (A), X-chromosome losses (B) and sex-linked recessive lethals (C) as end-points of genetic radiation damage. Populations RO II and RO V are similar to the previously studied population RO I and were exposed to 2100 R/generation, delivered to oocyte stages 6-14, mature sperm, and spermatids. RO II (first tests after 160 generations) is radioresistant relative to +60 (control). The resistance was characterized by dose-reduction factors (DRFs) of 1.72 (with respect to end-points A, B) and 1.53 (C), and these were similar to those previously obtained for RO I. The resistance of RO II was inherited semidominantly as was that of RO I, and the radiosensitivity of the hybrids RO I/RO II was similar to that of RO I and RO II with respect to end-points A and B. RO V did not become resistant within 25 generations of irradiation history (A). Populations RO III (6000 R/generation) and RO IV (7000 R/generation) have histories of irradiations given to oogonia and spermatogonia. Radiosensitivities of immature oocytes of RO III did not differ from those of +K after 55 generations, but after 105 and 135 generations of irradiation history, DRFs of 1.2 (A) and 1.44 (B) were observed. RO IV was characterized in generations 55-135 by DRFs of 1.31 (A) and 1.72 (B). Selection for relative radioresistance of immature oocytes was found (1) to be reproducible (RO II-RO IV), (2) not to require genetic pre-adaptation (RO V), and (3) to be, in part, also achieved by 'indirect' selection (RO III, RO IV). It is concluded that mutation rates in populations are selectively adjusted to evolutionary requirements.

The genetic effects of gonadal burdens of 238Pu after single injection were studied in male mice. The activity of plutonium was 7 to 1850 Bk/g. The average doses of accumulated alpha-particles in testis varied from 2 to 96 Gy.10(-2), the dose rate being 0.004 to 1 Gy.10(-2) per day. The genetic end points are: the dominant lethal mutation rate; the frequency of reciprocal translocations; the recessive lethal mutation rate and frequency of abnormal sperm head morphology. For all tests used, no linear dependence of the effect on the alpha-dose was observed. The RBE value of alpha-irradiation was 10-20 relative to chronic gamma-irradiation.

The sensitivity of oocytes of Drosophila melanogaster to the damages induced by ionizing radiation was studied in the strain carrying rad(2)201G1 mutation and in the wild-type strain 3.4. Three days old females of these strains were treated with 1500 r of gamma-rays. Then the fertility of flies and dominant lethals in laid eggs were recorded during nine days. In addition, the number of oocytes and the frequency of their resorption in ovaries of females were counted. It has been shown that mutant females display stage-specific radiosensitivity in comparison with wild-type flies. The fertility of irradiated mutant flies has been decreased because of the delay of the development and the resorption of oocytes. Early stages of generative cells, from oogonia to oocytes-7 exhibit increased sensitivity to the resorption. Mutant egg chambers in the stages 1-7 also demonstrate a high frequency of induced dominant lethality which reaches the maximum in the oocytes 6-7. It is supposed that radiation-induced dominant lethality and resorption of immature mutant oocytes are the result of the same damages in nuclear genetical structures.

Large-scale radiation-genetic studies on bacterial cells (E. coli) and Drosophila (D. melanogaster) using methods like an analysis of mutations of some structural genes and assessment of the frequency of mutations with relation to survival have shown for the first time that the efficacy of neutrons (E = 0.85 MeV) in the induction of gene mutations in Pro- and Eukaryotae is much lower than that of weak ionizing radiation with the same survival. Some features of radiation mutagenesis in a Drosophila mutant c(3)G defective in genetic recombination were described. A low level of the frequency of radiation-induced mutations typical of this mutant was also characteristic for some E. coli rec--mutants. A fact earlier reported for bacteria consisting in a higher (than one could expect extrapolation of lethal-sublethal irradiation doses to small ones) frequency of gene mutations in the range of relatively small absorbed doses of gamma-irradiation (the survival rate being not lower than 80%) was also first established for Drosophila. The importance of these entirely new facts for the theory of mutations in radiation genetics are briefly discussed.