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A Kh Akhmadieva

Publications and source records attributed to A Kh Akhmadieva.

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↗
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↗
PubMed1985

[Capacity of bone marrow cells to restore thrombocytopoiesis in lethally irradiated animals].

A study was made of the kinetics of thrombocytopoiesis restoration in lethally irradiated mice after transplantation to them of the donor marrow cells. In the initial period, the thrombocytopoiesis restoration is provided by transite cells-precursors of megakaryocytes present in the transplanted bone marrow; the subsequent restoration is due to cells of the self-maintaining population. The level of restoration does not correlate with the number of polypotent cells that form macrocolonies in the spleen of irradiated recipients.

Animals↗
PubMed1984

[Comparison of 2 methods of studying polypotent hematopoietic cells].

The cells giving rise to colonies in the spleen of a lethally irradiated recipient after their transplantation (exogenous CFUs) have a higher self-maintaining ability than those that repopulate their own hemopoietic territory after irradiation, due to the migration of these cells from screened territories (endogenous CFUs). The number of exogenous CFUs and their self-maintaining ability do not change with animals ageing.

Aging↗
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

[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.

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↗