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Biomedical subjects

O M Rozanova

Publications and source records attributed to O M Rozanova.

At least 19 recordsLinked to original sources
PubMed1999

[Correlation between the duration of radiation adaptive response in bone marrow cells of mice and the dose of gamma-irradiation in vivo].

The dependence between the adaptive response and adaptive dose was studied on the basis of cytogenetic damage in polychromatic erythrocytes of bone marrow cells in mice after a low dose gamma-irradiation in vivo. The adaptive response to doses of 0.1 and 0.2 Gy was found to be retained for at least two months after irradiation. However, the adaptive dose of 0.4 Gy did not induce prolonged adaptive response.

Adaptation, Biological↗
PubMed1998

[Action of low doses of gamma-radiation on cytogenetic damage in polychromatophilic erythrocytes of bone marrow in mice in vivo].

The frequency of micronuclei was estimated in bone marrow polychromatic erythrocytes (PCEs) of mice gamma-irradiated in vivo at doses of 5-50 cGy. The dose-effect curve was found to have a complex stepwise pattern with three consequent segments: (1) high radiosensitivity, (2) a significant decrease in radiosensitivity, and (3) an increase in radiosensitivity.

Animals↗
PubMed1997

Action of chronic irradiation on the cytogenetic damage of human lymphocyte culture.

The action of chronic irradiation (dose rate 2.9 Gy/day) on human lymphocyte culture was investigated. Whole blood was irradiated at 37 degrees C. Aliquots (0.2 ml) of whole blood were cultivated by the standard method. A medium containing phytohemagglutinin was added immediately after irradiation. All structural chromosome- and chromatid-type changes were recorded. The experimental data showed that the conditions of irradiation of lymphocytes affected neither the background level of chromosome damage nor their radiosensitivity. The obtained dose-response curve of chromosome aberrations was described by a linear regression, which then became a plateau. There is no statistically significant difference between the results for the low doses (10-50 cGy) of chronic and acute radiation.

Adult↗
PubMed1996

[Induction of cytogenetic damage in Chinese hamster cells after combined exposure to low doses of gamma-radiation and various chemical and physical agents].

Supersensitivity of Chinese hamster cells to low doses of gamma-radiation (dose range 5 to 50 cGy) was revealed by means of the cytokinesis-block micronucleus test. Treating these cells with caffeine (repair inhibitor) and mercaptoethylamine (radioprotector) and exposing them to secondary radiation emitted by protons with an energy of 70 GeV showed that this supersensitivity is associated with the absence of cytogenetic repair. When cells at the G2 phase received preliminary doses of 30 and 75 cGy before being irradiated at 150 cGy, the incidence of cytogenetic damage decreased, i.e., an adaptive cell response resulting from a radiation-induced mitotic delay was observed.

Adaptation, Physiological↗
PubMedDate not supplied

[Dependence of the cytogenetic adaptive response in the rat bone marrow cells on the dose of chronic gamma irradiation in vivo].

The induction of chromosome aberrations in bone marrow cells of rats exposed to chronic gamma-irradiation and subsequently to acute gamma-irradiation was studied. Adult male rats were exposed ot 3-40 cGy (2.9 cGy/day) of chronic gamma-irradiation (adaptive dose) and subsequently to 4 or 6 Gy of gamma-rays (47 cGy/min, challenge dose). The yield of chromosome aberrations in marrow cells induced by adaptive and challenge dose was lower than the sum of the yields separately induced by chronic and acute gamma-irradiation. The most effective dose for induction of the adaptive response was 0.4 Gy.

Adaptation, Physiological↗
PubMedDate not supplied

[Induction of cytogenetic damages by combined action of heavy metal salts, chronic and acute gamma irradiation in bone marrow cells of mice and rats].

The aim of the present work was to study the combined action of salts of heavy metals (lead and cadmium), and acute and chronic gamma-irradiation on the cytogenetic damage to bone marrow cells of rats and mice. It was shown that the chronic exposure of rats and mice in vivo to gamma-irradiation induced the adaptive response. The salts of heavy metals supplemented to the diet of rats enhanced the cytogenetic damage to the non-irradiated animals, slightly enhanced the effect of chronic and acute gamma-irradiation, decreased the cytogenetic adaptive response induced by chronic gamma-irradiation.

Adaptation, Physiological↗
PubMedDate not supplied

[Detection of genomic instability in offspring of male mice chronically exposed to gamma-radiation by the "adaptive response" test].

The genomic instability (GI) in somatic cells of the progeny (F1 generation) of male mice chronically exposed to low-dose gamma-radiation was studied by comparative analysis of chromosome damage. BALB/C male mice exposed to 0.1 Gy (0.01 Gy/day) and 0.5 Gy (0.01 and 0.05 Gy/day) were mated with unirradiated females 15 days after irradiation. For comparison of radiosensitivity, two-month-old males, the descendants of irradiated and unirradiated animals, were subjected to irradiation with a dose of 1.5 Gy (0.47 Gy/min) from a 60Co source. GI was revealed by the standard scheme of adaptive response. The experiments indicated that, by using the test "adaptive response", it is possible to detect the transition of gamma-radiation-induced genomic instability in sex cells of male parent into somatic cells of mice (F1 generation) either from changes in radiosensitivity or by the absence of the adaptive response induced by a standard scheme.

Adaptation, Physiological↗
PubMedDate not supplied

[Low doses of radiation decrease the level of spontaneous and gamma-induced chromosomal mutagenesis in bone marrow cells of mice in vivo].

Low doses of ionizing radiation are known to induce adaptive response (AR), which is characterized in most cases by temporary nature, though the possibility of long-term persistence of AR is not ruled out. In this investigation we studied the effect of low doses of gamma-radiation on both high-dose radiation-induced and spontaneous level of cytogenetic damage throughout the life of mice. SHK male mice 2 months old were used. Priming doses of 0.1 and 0.2 Gy (0.125 Gy/min, gamma-radiation from 60Co) were used. A challenging dose of 1.5 Gy (1 Gy/min) was used in the experiments using a routine AR experimental design. The frequency of micronucleated polychromatic erythrocytes in bone marrow cells of primed, primed and challenged, and control groups was assessed at various times of animal life span. It was shown that: a) single low-dose gamma-irradiation induces a cytogenetic AR which can be revealed at 1, 3, 6, 9, 12 months after priming; b) single low-dose gamma-irradiation decreases the cytogenetic damage to a level below the spontaneous rate at the end of lifetime (20 months) of animals; c) ability to induce adaptive response does not depend on the age of animals at the moment of priming irradiation. In conclusion, the mechanisms underlying AR not only protect from chromosome damage induced by high-dose irradiation but also may play a role in spontaneous mutagenesis during aging of animals.

Adaptation, Physiological↗
PubMedDate not supplied

[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.

Animals↗
PubMedDate not supplied

[Chromosome mutagenesis and cytogenetic monitoring].

A model of formation of radiation-induced cytogenetic damage is proposed on the basis of our own and literature data. The model postulates that localization of DNA damage and repair process play an important role in the final effect.

Animals↗
PubMedDate not supplied

[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.

Animals↗
PubMedDate not supplied

[Modeling, using nucleases, of the effect of radiation on Chinese hamster fibroblasts. On the role of single-stranded DNA breaks, induced by DNAase I, in the initiation of chromosome aberrations].

DNAase I injected to Chinese hamster fibroblast cells resulted in the chromosome aberration induction at all stages of the cell cycle and death of cells. Comparison of the effects of DNAase I and gamma-radiation on Chinese hamster cells showed that with close values of the induced DNA breaks there were close values of the cytogenetic damage and the number of DNA damages per aberrant cell.

Animals↗