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1.
Radiats Biol Radioecol ; 43(2): 136-43, 2003.
Article in Russian | MEDLINE | ID: mdl-12754794

ABSTRACT

In the present work it is shown that the phenomenon of interphase chromosome centromeric region displacement, earlier revealed by the authors, is not realized in G0-lymphocytes with heterozygous BRCA1/2 gene mutations. The role of these genes in DNA double strand break (DSB) reparation is known. It is concluded that chromosome locus displacement is necessary for DSB repair, at least in the process of homologous recombination. In accordance with our data, some feature (pericentromeric cluster disintegration and displacement, the nucleus size increasing) characteristic for S- and G0-lymphocytes are observed in normal G0-lymphocytes treated with 3 and 10 cGy. However, the size of nucleus in G0-lymphocytes is restored through 6 hours after irradiation in opposite to the process in dividing cells. It was proposed that some typical for resting cell functions of G0-lymphocytes after inducing by adaptive doze of radiation are stopped as similarly as after stimulation of cells. Interestingly, that the process of the induced chromosome loci displacement is correlated with the decreasing of DNA reparation possibilities under UV-irradiation. The induced apoptosis level also decreases when chromosome loci are displaced. The possible mechanisms of the revealed phenomenon are discussed. This research supported by RFBR grant (No. 01-04-49180).


Subject(s)
DNA Damage , DNA Repair , DNA , Genes, BRCA1/radiation effects , Genes, BRCA2/radiation effects , Lymphocytes/radiation effects , Mutation , Animals , Apoptosis/radiation effects , Cell Nucleus/radiation effects , Centromere/radiation effects , DNA/radiation effects , DNA Damage/radiation effects , DNA Repair/radiation effects , Interphase/radiation effects , Lymphocytes/cytology , Mice , Multigene Family , Radiation Dosage , Time Factors , Ultraviolet Rays
2.
Radiats Biol Radioecol ; 40(5): 554-66, 2000.
Article in Russian | MEDLINE | ID: mdl-11252232

ABSTRACT

The mutation process has many stages. The information presented in this article suggest that a cell exposed to low LET radiation in the low-dose range (up to 1 cGy) must almost completely repair all spontaneous and radiation-induced DNA lesions. But reparation of DNA double-stranded breaks (DSB), which are the basis of genome instability has peculiarity. We have shown that the mechanisms of action of low doses (which initiate natural antimutagenic reactions of resting cells--an adaptive response) are associated with chromosome loci (centromere) movement in a cell nucleus. We suggest that the movement of chromosome loci in cell nucleus is the fundamental mechanism for repair of DSB and switching of the transcription of gene (it is known that in case of lymphoid cells Ikaros-complexes repressor is colocolizated with centromere loci); in particular, of nucleolar transcription activities because the latter is dependent on centromere arrangement. Because the movement of chromosome loci in both the mitotic cycle and under adapting dose on resting cells is much the same it could be assumed that in latter case the cells also lose their functional characteristic for differentiated resting cells. Under chronic exposure to low doses the functional changes can be the cause of organic changes if adapting dose affects the sufficient part of the cells. The role of cells of evolutional or ontogenetic reserve in mutation process is considered.


Subject(s)
Cell Nucleus/radiation effects , Cell Nucleus/ultrastructure , Chromosomes/radiation effects , Eukaryotic Cells/radiation effects , Mutation/radiation effects , Animals , DNA Damage , DNA Repair , Dose-Response Relationship, Radiation , Humans
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