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Дата последнего поиска статьи во внешних источниках: 22 июля 2017 г.

Работа с статьей

[1] Comparison study of dna double-strand breaks formation in human peripheral blood lymphocytes exposed to high versus low dose-rate γ-radiation / M. V. Pustovalova, N. Y. Vorobyeva, E. Y. Arkhangelskaya et al. // Health Physics. — 2014. — Vol. 107, no. 1. — P. 48–48. Among various DNA lesions induced by ionizing radiation. DNA double-strand breaks (DSBs) are considered to be the most important due to their potential to cause cell death, mutagenesis and carcinogenesis. The goal of this study was to compare DSB formation in quiescent and stimulated to cell cycle division peripheral blood lymphocytes exposed to high versus low dose-rate y-radiation. The obtained results indicate significant differences in DSBs' induction and repair processes between quiescent (G0) and dividing lymphocytes after acute (irradiation time up to 2 min, dose-rate 1 Gy/min, dose 50, 100 and 200 cGy), as well as after continuous low dose-rate irradiation (irradiation time up to 72 h, dose-rate 0.5 mGy/min, dose 18. 72, 144 and 216 cGy). The dose rate decreasing to 0.5 mGy/min and proportionally the increasing of irradiation time up to 72 h significantly reduces the yield of DNA DSBs on the irradiation dose and changes the response character of quiescent and dividing lymphocytes to the irradiation. In the initial 24 h of irradiation in stimulated to cell cycle division lymphocytes, the yield of уH2АХ foci on the irradiation dose was approximately two times higher than in quiescent lymphocytes: after 48 h of irradiation, it was -1.5 times higher, and at the end of the irradiation period (72 h) the DSBs' amount in quiescent and dividing cells did not differ significantly. The character of dose-response curve for stimulated lymphocytes (the increase of the yH2AX foci amount in 24 h (72 cGy) and a “plateau" between 24 to 72 h (72-216 cGy)) points out that in dividing cells simultaneously to high yield of radiation induced DNA DSBs. The active repair processes of these damages occur also. At the same time in the quiescent cells, it pointed out a linear increase of DSBs with a dose/time of the low dose rate exposure (y=0.1+0.7x (R2=-0.98), where "y" is a number of yH2AX foci per cell and "x" is a dose in cGy), which indicates that with the low yield of radiation-induced DNA DSBs for these cells, the low efficiency of DSB repair is typical. That leads to accumulation of DNA breaks with the irradiation time/dose increasing. This process is accompanied with the increase of apoptotic cells percent and ROS production rate. This work was supported by the Russian Foundation for Basic Research grant #12-04-01-733-a.

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