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D M Spitkovskiĭ

Publications and source records attributed to D M Spitkovskiĭ.

79 records · Page 5Linked to original sources
PubMedDate not supplied

[The modelling of the initiation of genetic damages from low doses of ionizing radiation in eukaryotic cells based on the concept of the existence of evolutionary reserve cells].

The model predicting quantitatively a dose response for genetic lesions in low dose range is presented. The model is based on the concept of programmed initiation of the genetic damage in the subpopulation of specific cells of "evolutionary reserve" (CER). It is demonstrated that complex shape of dose-response curve results from superposition of processes in different subpopulations within exposed cell population, mainly in CER. The model allows us to explain the minimum observed in the dose-response curve at doses corresponding to one (on the average) event of energy deposition per CER with spontaneous aberrations. The equation for dose-response function for dicentrics describes satisfactory experimental observations. Advantage of proposed equation is that it does not deal with free parameters to fit the data. They are determined independently by using known physical and biological characteristics. The data described allow us to suggest that sensitive body for CER is a cell as a whole. Probably, programmed initiation of genetic lesions in CER requires both two hits at cell membrane and radiation effect on cell nucleus.

Animals↗
PubMedDate not supplied

[The characteristics of unscheduled DNA synthesis and of the changes in the structural parameters of human lymphocyte nuclei after the action of x-ray radiation in low doses and in combination with UV irradiation].

Effects of X-ray low doses (0.5-25 cGy) with following UV light (254 nm, 20 J/m2) on human peripheral blood lymphocytes were studied. Reparation response registered by unscheduled DNA synthesis (UDS) activity was demonstrated to be the most intensive after action of X-rays in dose ranges 2-3 cGy and 15-20 cGy, and least intensive after 10 cGy. In those cells where UV light was followed by X-rays, dose ranges 2-3 cGy and 15-20 cGy cause essential decrease of UDS as compared with UV-light action only. The most intensive UDS was in those UV-irradiated lymphocytes which where previously exposed to 10 cGy of X-rays. At the same time 10 cGy cause minimal reparation response without UV light. Possible mechanisms of discovered phenomena are discussed. In particular, reaction on 2-3 cGy might be a reorganization of genome for adaptive response or an evolution reserve cells response. From 10 cGy the reason of reaction might be a reparation, induced by radiation.

Cell Nucleus↗
PubMedDate not supplied

[Changes induced by low doses of ionizing radiation in the accessibility to DNA restriction enzymes of the ribosomal gene system of human lymphocytes].

Human lymphocytes were X-irradiated at doses 0-10(-2) Gy and allowed to repair for some time. Nuclei were prepared and digested with restriction endonuclease Rsa I to selectively release 28S RNA gene fragment fraction, containing the DNA-binding protein, Hpa II digestion of nuclei was used to investigate the methylation of the 28S RNA gene fragment. There was a differential enrichment of 28S RNA gene binding protein for different X-ray doses with maximum enrichment for dose 2-3 x 10(-2) Gy with following diminish to 10 x 10(-2). The enrichment of less methylated fractions of 28S RNA gene was observed during X-irradiation. This might be explained by a different X-ray-induced changes of methylated and unmethylated rDNA binding with nuclear proteins. The possible mechanism for this phenomena are discussed.

Blood Proteins↗