Estimation of genetic effects of chronic exposure to low-dose rate gamma-radiation by cytogenetic methods and DNA-comet assay

The study of genetic effects in CBA/lac mice exposed for 1 year to constant low dose-rate gamma-radiation at a dose-rate 63 cGy/year has been carried out. We have shown the significant increase in the DNA breaks' level in spleen lymphocytes by comet-assay beginning from the total absorbed dose of 20 cGy. It is possible that the DNA breaks' level increase resulted from the structural rearrangement of chromatin or induction of lymphocyte proliferation. The results obtained by micronucleus test have proved that the mutagenic effect of chronic low dose-rate gamma-radiation depends on cell type and respectively on cell proliferation rate, cell differentiation, etc. So, by the end of experiment the significant increase in the frequency of PCE with micronuclei (MN) was observed. However, in contrast, the frequency of NCE with MN was not increased. No significant increase in the percent of lung cells with MN was registered.     

Nuclease-aided simulation of the action of radiation on Chinese hamster fibroblasts. The role of double-stranded DNA breaks induced by restrictases in initiating chromosomal disorders

Comparison was made between the effectiveness of restrictases inducing double-strand DNA breaks with blunt (Hae III and Eco RV) and cohesive (Hind III and Sal I) ends and that of gamma-radiation on the initiation of chromosome aberrations. The analysis of the spectrum of chromosome aberrations induced in the presence or absence of DNA repair inhibitors, as well as the study of the pattern of cell distribution by the number of DNA breaks per cell showed that the decisive role in the initiation of chromosome mutagenesis is played by the localization of the break in certain sequences of target DNA rather than the type of the break.     

Influence of low-dose-rate red and near-infrared radiations on the level of reactive oxygen species,the genetic apparatus and the tumor growth in mice in vivo

The effect of low-dose-rate red and near-infrared radiations from the matrix of light emitted diode (650 nm and 850 nm) and a He-Ne laser (633 nm) on activation of the reserve of a natural defense system in the mice exposed to radiation in vivo was studied by the level of reactive oxygen species (ROS) production in blood cells, the induction of cytogenetic adaptive response in bone marrow cells, thymus and spleen, and the rate of Ehrlich ascites carcinoma growth in a solid form. As a positive control animals were irradiated with X-rays by the scheme of the radiation-induced adaptive response (0.1 Gy + 1.5 Gy). The levels of ROS production was assessed in whole blood by luminol-dependent chemiluminescence, of cytogenetic damage — by the “micronucleus test” in the bone marrow, the weight of the thymus and spleen — by index of organ, and the rate of tumor growth — according to its size for 30 days after inoculation. Adaptogenic and anticarcinogenic effects of studied radiations were revealed. The values of these effects were not different from those in animals pre-irradiated with the X-rays. The relationship between the level of ROS production and adaptive response induction in the mice under the influence of non-ionizing radiation was first ascertained. The experimental data obtained may indicate a similar mechanism of induction of protective responses to ionizing and non-ionizing radiations in mice in vivo.     

The possibility for modification of the cytogenetic action of secondary radiation with 70-GeV protons on Chinese hamster fibroblasts

As estimated by the cytogenetic injury induced in Chinese hamster cells by secondary 70-GeV proton radiation, phenylmethylsulfonyl fluoride, an inhibitor of chromatin proteinases, has a radioprotective effect. The poly(ADP)-ribosylation-independent participation of the inhibitor in radiation cytogenetic mutagenesis has been shown.     

The role of irreparable DNA damage in initiating chromosomal mutagenesis in Chinese hamster cells irradiated with gamma and secondary proton radiation with an energy of 70 GeV

The study on the kinetics of DNA injury repair in Chinese hamster cells exposed to gamma and secondary proton radiation (70 GeV) has demonstrated the absence of distinctions in the kinetics of repair of rapidly repaired damages, a decreased rate of repair of slowly repaired lesions, and an increased residual irreparable damage induced by secondary radiation that reliably correlates with the RBE value estimated by the cytogenetic effect.     

The characteristics of the realization of cytogenetic damage in mammalian and plant cells exposed to low doses of radiation]

A complicated character of the cytogenetic injury dependence upon radiation dose was revealed after low-level gamma irradiation of Vicia faba seedlings and Chinese hamster fibroblasts. The dependence was linear with low-level secondary exposure to 70 GeV protons. The authors discuss a threshold nature of induction of the cytogenetic damage repair responsible for a high outcome of damages under the effect of low-level gamma radiation.     

Transgenerational genomic instability in the first generation offspring of mice exposed to low-intensity red and near-infrared irradiation in vivo

Transgenerational genomic instability in the first generation offspring of mice exposed to lowintensity infrared laser (632.8 nm) and light-emitting-diode infrared irradiation (850 nm) was investigated in vivo. It was found that the level of spontaneous damage in bone marrow according to the micronucleus test, the level of reactive oxygen species in whole blood, and the mass index of lymphoid organs in all of the descendants of irradiated mice did not increase. After additional X-ray exposure of the progeny at a dose rate of 1.5 Gy, a decrease in the level of damage and the absence of an adaptive response were revealed upon testing according to “radiosensitivity” and the radiation-induced adaptive-response scheme (0.1 + 1.5 Gy), respectively, compared to the descendants of nonirradiated mice. The rate of tumor growth in the offspring of irradiated mice did not differ from that in the descendants of nonirradiated mice, although inhibition of the tumor growth rate was observed in their irradiated parents. The survival rate after irradiation at a dose rate of 6.5 Gy did not differ from both the parents and the control.