[Role of topoisomerase II in the response of mammalian cells to the action of ionizing radiation. I. Change in the mitotic cell cycle of Chinese hamster CHO K1, irradiated with x-rays, after the action of novobiocin at a high concentration]. / Rol' topoizomerazy II v otvete kletok mlekopitaiushchikh na deistvie ioniziruiushchego izlucheniia. I. Izmenenie mitoticheskogo tsikla kletok kitaiskogo khomiachka CHO K1, obluchennykh rentogenovskimi luchami, posle deistviia novobiotsina v bol'shoi kontsentratsii.

Flow cytometry was used to study cell cycle recovery in X-irradiated Chinese hamster cells after action of novobiocin, an inhibitor of topoisomerase II. A prolonged treatment with 1 mM novobiocin (20-30 h) of intact cells results in the G2 + M delay. Novobiocin treatment of 5 Gy-irradiated cells results in a slight delay in cell exit from G1 into S phase and in a much longer G2-delay if compared with X-irradiated cells. These data allow to suggest an involvement of topoisomerase II in cell response to ionizing radiation.

[Effect of ionizing radiation on the mitotic cycle of rat embryonal cells, immortalized by oncogene E1A and transformed by oncogenes E1A and c-Ha-ras]. / Vliianie ioniziruiushchei radiatsii na mitoticheskii tsikly émbrional'nykh kletok krysy, immortalizovannykh onkogenom E1A i transformirovannykh onkogenami E1A i c-Ha-ras]

A comparative study of recovery of mitotic cycle in gamma-irradiated rat embryo fibroblast cells (intact, immortalized with oncogene E1A and transformed with two oncogens-E1A and c-Ha-Ras) was made to show eventually no difference in response to 5 Gy irradiation of intact and immortalized cells, and, on the other side, to demonstrate a great difference in response of immortalized and transformed cells. Cells transformed with the two oncogens E1A and c-Ha-Ras appeared to be much more resistant to ionizing radiation than intact cells and cells immortalized with one oncogene E1A. These data allow to suggest protein p53 tumor-suppressor functioning in transformed cells, but not in intact and immortalized cells.

[Changes in the mitotic cycle of Chinese hamster CHLV-79 RJK cells resistant to ethidium bromide after the action of ionizing radiation]. / Izmenenie mitoticheskogo tsikla kletok kitaiskogo khomiachka CHLV-79 RJK, ustoichivykh k bromistomy étidiiu, posle deistviia ioniziruiushchego izlucheniia.

A study was made of the effect of ionizing radiation on mitotic cycle and survival of the Chinese hamster cells of two clones-CHLV-79 RJK, and its derivative Vebr-30, resistant to ethidium bromide. Ethidium bromide resistant cells were more resistant to 1) lethal effects of gamma rays (by cell survival); 2) X-rays (by cell cycle recovery after irradiation of cells in a dose of 5 Gr); 3) colcemide treatment (by accumulation of cells in G2+M phase). These data may result from damaging a certain regulatory process, which may be involved in cell response to radiation damage and in repair of predominantly sublethal and partly lethal DNA lesions as well as of cell membrane structures.

[A comparative study of the effect of allopurinol and caffeine on mitotic cycle recovery in cells after x-ray irradiation]. / Sravnitel'noe issledovanie vliianiia allopurinola i kofeina na vosstanovlenie mitoticheskogo tsikla v kletkakh posle rentgenovskogo oblucheniia.

Alterations in the duration of mitotic cycle phases in X-irradiated HeLa cells after caffeine (CF) of allopurinol (AP) treatment are studied. Delays in S- and G2-phases, induced by 5 Gr of X-rays, are partially (1 mM) or completely (5 mM) decreased by both AP and CF. When the agent is removed from the medium, the delays are seen again. The data obtained enabled us to suggest a possible use of AP as a radiosensitizer in X-therapy of cancer transformations.

[The mitotic cycle and DNA repair in UV-irradiated murine neuroblastoma cells]. / Mitoticheskii tsikl i reparatsiia DNK v UF-obluchennykh kletkakh neiroblastomy myshei.

A correlation has been shown between a reduced rate of movement of UV-irradiated neuroblastoma cells from G1 into S phase, an essential increase of cells in S phase while progressing through the cell cycle, and a defect in free DNA synthesis on a damaged template. These indices may reflect one and the same cell response to the UV light.

[The effect of 3-aminobenzamide on the mitotic cycle of Chinese hamster cells cultured on a medium with 5-bromodeoxyuridine following ionizing radiation action]. / Vliianie 3-aminobenzamida na mitoticheskii tsikl kletok kitaiskogo khomiachka, kul'tiviruiumeykh na srede s 5-bromdezoksiuridinom, posle deistviia ioniziruiushchei radiatsii.

A specific inhibitor of poly(ADP-ribose)polymerase-3-aminobenzamide (6 mM) has been shown to: 1) reduce survival of non-irradiated CHO-K1 cells, cultivated in medium containing 5-bromodeoxyuridine (10 mkM, BDU cells), and increase their radiosensitivity; 2) induce G2 delay in BDU cells while progressing through the cell cycle as analysed by the DNA flow cytometry; 3) increase to a great degree G2 delay in X-irradiated BDU cells. 3-Aminobenzamide is primarily effective when it is present during the first or two first cell cycles after the initial addition of BDU. The above data confirm the involvement, presumably an indirect one, of ADP-ribosylation in the DNA repair through affecting the chromatin structure.

[The regulation of DNA repair processes in mammalian cells. III. The effect of epidermal growth factor on the postradiation recovery of the cell cycle in human A 431 cells and embryonic fibroblasts]. / Reguliatsiia protsessov reparatsii DNK v kletkakh mlekopitaiushchikh. III. Vliianie épidermal'nogo faktora rosta na postradiatsionnoe vosstanovlenie kletochnogo tsikla u kletok A 431 i émbrional'nykh fibroblastov cheloveka.

Recovery of the cell cycle in cells A 431 and in human embryo fibroblasts (EFH) differs much. Unlike EFH, A 431 cells have: 1) synchronized exit of cells from G1 into S phase after 5 Gr irradiation; 2) G2-block; 3) much less manifestation of these two phenomena in the presence of EGF; 4) a lesser effectiveness of the repair of DNA single-strand breaks. EGF stimulation of the repair of radiation-induced DNA lesions, SSB in particular, may be of great importance for the postirradiation cell cycle recovery.

[The recovery of the mitotic cycle and DNA repair in Chinese hamster cells cultured on a medium with 5-bromodeoxyuridine following the action of ionizing radiation]. / Vosstanovlenie mitoticheskogo tsikla i reparatsiia DNK kletok kitaiskogo khomiachka, kul'tiviruemykh na srede s 5-bromdezoksiuridinom, posle deistviia ioniziruiushchei radiatsii.

A correlation has been shown between a strong decrease in survival of X-irradiated CHO-K1 cells cultured with 5-BudR, a strong inhibition of recovery of DNA single-strand breaks, and an essential increase in G2-delay while progressing through the cell cycle. This strong correlation may point to the involvement of repair processes into the final radiation effect on the cell.

[The effect of inhibitors of ADP ribosylation on the restoration of the mitotic cycle and on DNA repair after the action of ionizing radiation in Chinese hamster cells]. / Vliianie ingibitorov ADF-ribozilirovaniia na vosstanovlenie mitoticheskogo tsikla i na reparatsiiu DNK posle deistviia ioniziruiushchei radiatsii v kletkakh kitaiskogo khomiachka.

Specific inhibitors of poly(ADP-ribose)polymerase-3-aminobenzamide and 3-metoxybenzamide (6, 12 mM) have been shown to: 1) reduce survival of X-irradiated CHO K1 cells to a slight degree; 2) increase S- and particularly G2-delays in X-irradiated cells, while progressing through the cell cycle as analysed by the DNA flow cytofluorimetry; 3) reduce effectiveness of DNA single-strand breaks repair. The above data suggest a definite role of ADP ribosylation in the cell repair activity.

[The effect of caffeine on the duration of the mitotic phase cycle in CHO-K1 Chinese hamster cells, irradiated with x-rays]. / Vliianie kofeina na dlitel'nost' faz mitoticheskogo tsikla u kletok kitaiskogo khomiachka CHO-K1, obluchennykh rentgenovskimi luchami.

Alterations in the duration of mitotic cycle phases in X-irradiated Chinese hamster cells CHO K1 after caffeine (CF) treatment are studied. Delays in S- and G2-phases, induced by 1 and 5 Gr of X-irradiation, are partially or completely decreased by 1 mM or 5 mM CF, respectively. When CF is removed from the medium after irradiation, delays in S- and G2-phases are seen again, however long (0-12 hours) CF remains in the medium. The data obtained allow to suggest that since CF results in a radioresistant DNA synthesis, it may also postpone delays in S- and G2-phases, while cells are progressing through the cell cycle.

[Changes in the mitotic cycle of Chinese hamster cells and the repair of radiation damage in cells following the action of ionizing radiation]. / Izmenenie mitoticheskogo tsikla kletok kitaiskogo khomiachka i reparatsiia radiatsionnykh povrezhdenii kletok posle deistviia ioniziruiushchego izlucheniia.

Using DNA flow cytofluorimetry technique, the effect of ionizing and gamma irradiation on cell cycle in Chinese hamster cells of clone CHO K1 773 and of its derivative EBR-30 resistant to ethidium bromide was examined. Irradiation in doses of 1 and 5.5 Gr leads to a reduced rate of cell passing from G1 into S phase, to a prolonged S phase and to a larger postsynthetic block in EBR-30 cells than in 773 cells. Our data correlate with some delay in repair of gamma-induced (200 Gr) DNA single-strand breaks in the EBR-30 clone. Clones under investigation are not distinguished in their survival. Our results may arise from deficiency in some regulatory process usually involved in cell response to radiation-induced lesions.

[Effect of UV irradiation on the mitotic cycle of Chinese hamster cells with varying UV sensitivity. II. The temporal relations in blocked cell division]. / Vliianie UF oblucheniia na mitoticheskii tsikl kletok kitaiskogo khomiachka s razlichnoi UF-chuvstvitel'nost'iu. II. Vremennýe zavisimosti pri blokirovanom delenii kletok.

Analysis of cell distribution through phases of the cell cycle by the method of DNA flow cytofluorimetry has been utilized to investigate effects of UV light on the first cycle after irradiation in asynchronous Chinese hamster cells with different UV-sensitivity: V79 cell line (UV resistant cells) and UV-sensitive clones CHS2 and XII. Immediately after irradiation colcemid was added to the cultures to prevent mitosis and re-entering the cell cycle. UV irradiation did not affect the rate of cell passing from G1 into S phase in UV resistant cells. In UV irradiated cultures of UV-sensitive cells, a large portion of cells was arrested in G1, the effect increasing with UV dose. Besides, a portion of cells in S phase increased and the number of cells entering the G2+M compartment was essentially reduced in UV irradiated cultures of UV-sensitive cells much more than in V79 cells. The results may point to an inhibition of replicon initiation, and a larger DNA chain elongation in UV-sensitive clones after UV irradiation.

[Effect of UV irradiation on the mitotic cycle of Chinese hamster cells with varying UV sensitivity. I. The time ratios after irradiation of the cells with UV light]. / Vliianie UF obucheniia na mitoticheskii tsikl kletok kitaiskogo khomiachka s razlichnoi UF-chuvstvitel'nost'iu. I. Vremennýe zavisimosti posle oblucheniia kletok UF svetom.

The distribution of cells through the phases of the cell cycle by DNA flow cytofluorimetry was analysed to investigate the effects of UV irradiation on cell cycle progression in asynchronous Chinese hamster cells with different UV-sensitivity: cell line V79 (UV-resistant cells), and UV-sensitive clones: B6, CHS1, CHS2 and XII. The UV-irradiated cultures show a large accumulation of cells in S phase, the effect increasing with UV dose increase, which may point to an inhibition of the DNA chain elongation. UV-sensitive clones show a larger and more prolongated increase in the proportion of cells in S phase after irradiation with smaller dose than UV-resistant cells. Besides, the UV-sensitive clone XII shows an inhibition of movement of irradiated cells from G1 into S phase, that may testify to an inhibition of replicon initiation. These results suggest that there is a correlation in UV-irradiated Chinese hamster cells between alteration in cell cycle progression and UV-sensitivity of cells.