The analysis of chromosome lesions in peripheral blood lymphocytes of Hodgkin's lymphoma (HL) patients after chemotherapy and chemotherapy with the subsequent course of radiation therapy is carried out. Is shown, that the mean aberration frequency was significantly higher in HL patients after chemotherapy (7.20 +/- 0.58 per 100 metaphases) than in non-treated HL patients (4.80 +/- 0.54, p < 0.01). The subsequent carrying out of radiation therapy enlarges number of chromosome aberrations on 100 metaphases up to 46.7 +/- 10.7 (p < 0.05), of which chromosome-type aberrations (43.2 +/- 10.3 on 100 metaphases) averaged 92.5%. In lymphocytes of 37 out of 43 HL antitumoral treatment patients, we found, in addition to ordinary aberrant cells, a large number of multiaberrant (MA-cells) cells, i.e. metaphases carrying multiple (at least four) chromosome-type exchange aberrations. In 30 non-treated HL patients only one MA-cell was found. From 171 MA-cells which were in 43 HL patients after antitumoral treatment, 114 MA-cells were found at inspection of 9766 diploid metaphases, and the remaining 57 MA-cells were found at inspection of 196 polyploid metaphases. The carrying out after chemotherapy of radiation therapy enlarges in lymphocytes frequency of appearance of MA-cells. The analysis of MA-cells in diploid and polyploid metaphases shown, that the MA-cells could be formed both in vivo, and in vitro in absence of influence of clastogenic factors, and could survive at least two rounds of in vitro replication.

The lymphocytes of healthy donors were exposed to 60Co gamma-rays in doses ranging 0.5 to 6.0 Gy, and were incubated with PHA and 5-bromodeoxyuridine at 37 degrees C for 72 h. In the course of five consecutive in vitro divisions of cultured lymphocytes, the frequency of polyploid metaphases were determined, and chromosome structural aberrations in polyploid and diploid metaphases were analyzed. Dose dependence of polyploid formation was investigated, and patterns of polyploid cells were analyzed at various DNA replication cycles post exposure and 5-bromodeoxyuridine addition. Radiation is most effective induces of polyploid metaphase of the second and of the third mitotic divisions. In metaphases of the fourth mitotic divisions radiation does not enlarge authentically frequency of polyploid cells. In metaphases of the fifth divisions was not retrieved of polyploid cells. Was shown, that 84.8% of polyploid metaphases compound of tetraploids, while of octoploids and the cells with endoreduplicated chromosomes compound, accordingly, 8.4 and 6.8%. The analysis of chromosome aberrations have shown that the percentage of aberrant cells was higher in polyploid metaphases than in diploids, which indicated that chromosome lesions were involved in formation of polyploid metaphases.

The Chinese hamster cells V-79 were irradiated by y-rays in doses 0.5 Gy and 3 Gy at dose rate of 0.48 Gy/min (an acute irradiation) and in dose 0.5 Gy at dose rate of 0.0485 MGy/min (a prolonged irradiation). The acute and prolonged irradiation in a dose 0.5 Gy enlarges frequency of appearance of micronucleus. Subsequent cultivation of the irradiated cells during 20 generations enlarges frequency of micronucleus, and for a prolonged irradiation the boosted frequency of micronucleus is saved during 40-60 generations. After an acute irradiation the number of micronucleus starts to be reduced after 20 generations. An acute and prolonged irradiating in a dose 0.5 Gy enlarge frequency of chromosome aberrations at once after an irradiating, which is gradually reduced up to a control level to 20 generating. The irradiating in a dose 3 Gy enlarges frequency of chromosome aberrations at once after an irradiating, which is reduced up to a control level to 20 generating, then increases to 40-th generating and remains at this level before 60-th generating.

The radioprotective and antistressful activities of L-arginine and the "Pronumol" preparation, in which L-arginine is contained in the complex of proteins with nucleic acids, were studied. In mice repeated peroral intake of L-arginine and "Pronumol" partially prevented radiation-induced and stress-induced lipid peroxidation and DNA degradation in thymus, increased hemopoietic stem cell survival, and prevented an increase in chromosome aberration frequency in bone marrow cells of irradiated mice. When repeatedly administered per os before irradiation, "Pronumol" increased survival of intestinal stem cells in irradiated mice and prevented thymus cell devastation induced by radiation and stress.

The irradiation with mixed gamma-neutron radiation was carried out at the pulse nuclear reactor on fast neutrons BARS-6 in a regimen of one pulse (100 micros) and in a regimen of continuous irradiation during 60 minutes. Was shown, that the irradiation of mice with pulse radiation was 1.3-1.8 times more effective in the induction of the chromosome aberrations in bone marrow cells in comparison with the continuous regimen of irradiation. At the same time, other biological tests (yield of chromosome aberrations in human lymphocytes, decreasing the number of cells in thymus) demonstrated that pulsed and continuous regimens have almost equal biological effectiveness.

The V-79 Chinese hamster cells were irradiated by gamma-rays in dose of 0.5 Gy at powers of doses 0.48 Gy/min (an acute irradiation) and 0.0485 MGy/min (a prolonged irradiation). The acute and prolonged irradiation in a dose of 0.5 Gy enlarges frequency of the appearance of micronucleus (MN). Subsequent cultivation of the irradiated cells during 20 generations enlarges frequency of MN, and for prolonged an irradiation the boosted frequency of MN, is saved during 40-60 generations. After an acute irradiation the number of MN starts to reduce after 20 doublings.

Human peripheral blood lymphocytes were exposed to 60Co gamma-rays (a dose of 3 Gy) and cultivated during seven days in the presence of PHA and BrdU. It was shown that the metaphases of the first and second mitosises occurred during cultivation of the irradiated and unirradiated lymphocytes, being evidence about of irregularity of the coming into division of various fractions of lymphocytes. The time of cultivation did not influence a rate of aberrations in metaphases of the first and second mitosises of the irradiated lymphocytes. During the first and the subsequent mitosises the number of exchange chromosome aberrations decreased and reached a control level in metaphases of the fourth and fifth mitosises. The number of paired fragments at second and third mitosises increased a little and started to decrease only in metaphases of the fourth and fifth mitosises. The decrease in chromosome aberrations with prolongation of the cultivation of lymphocytes after irradiating is a consequence of elimination of cells with chromosome damages during sequential mitotic divisions.

Human lymphocytes from 16 healthy donors were exposed in vitro to an adapting dose of γ-rays (0.05 Gy) at G0, or G1, or G1/S stage of the cell cycle and subsequently to a challenging dose of γ-rays at G1, or G1/S, or S (1 Gy), or G2 (0.5 Gy) stage. Frequencies and distributions of the induced chromosome aberrations were analyzed in first-division metaphases. The data averaged over the donors revealed the protective action of the adapting exposure under the irradiation schemes with the challenging dose delivered at S or G2 stage. The majority of aberrations induced at these stages belonged to the chromatid type, and their yield was significantly higher in G2-exposed cells than in S-exposed cells. However, the relative reduction of the challenging dose effect (about 34%) in the adapted cells did not depend on the magnitude of this effect, and its value remained the same (within the experimental error) if aberrations were subdivided into chromosome and chromatid types or grouped as total deletions and total fragments. The adaptive response was not revealed under the schemes with the challenging dose delivered at G1 or G1/S stage. Analysis of the individual results showed that, in one and the same donor, the adaptive response could be observed under one irradiation scheme and not observed under other schemes, the most effective schemes being those with the challenging dose delivered at G2 stage. Four donors, however, did not show the adaptive response even under such schemes. Data on aberration distributions suggested that different repair processes, rather than a unique one, may underlie the adaptive response.

Irradiation by an adaptive dose 0.05 Gy at the G0 stage decreased the number of chromosome aberrations induced in lymphocytes by a challenge dose 0.5 Gy at the G2 stage. Adaptive response was not observed at the G1 stage, when the cells were exposed to adaptive dose 0.05 Gy and challenge dose 1.0 Gy respectively after 24 h and 29 h incubation with PHA. In lymphocytes exposed to 1.0 Gy at the G1 stage, cellular distribution of chromosomal aberrations followed the Poisson distribution, while in lymphocytes exposed to 0.5 Gy at the G2 stage, the distribution of aberrations differed from the Poisson distribution and was nearer to the degenerated Poisson distribution. The adaptive dose 0.05 Gy did not alter the distribution of chromosome aberrations induced by the challenge dose at the G1 or the G2 stages. The role of independent and whole-cellular repair in the formation of chromosome and chromatid aberration is discussed.

The adaptive response was studied in peripheral lymphocytes of healthy donors residing at territories with various levels of radioactive contamination. For donors from a clean territory (the town of Obninsk), the adaptive response depended on the cell cycle stage at which lymphocytes had been exposed to adaptive and challenge doses. The most expressed adaptive response was observed if lymphocytes had been exposed to the adaptive dose 0.05 Gy at G0 or G1 stage and to the challenge dose 0.5 Gy at G2 stage. Lymphocytes of donors from a contaminated territory (the town of Novozybkov) did not show an adaptive response in the conditions described above.