Changes in the Number of Double-Strand DNA Breaks in Chinese Hamster V79 Cells Exposed to γ-Radiation with Different Dose Rates

被引:18
作者
Kotenko, Konstantin V. [1 ]
Bushmanov, Andrey Y. [1 ]
Ozerov, Ivan V. [1 ]
Guryev, Denis V. [1 ]
Anchishkina, Natalya A. [1 ]
Smetanina, Nadezhda M. [1 ]
Arkhangelskaya, Ekaterina Y. [1 ]
Vorobyeva, Natalya Y. [1 ]
Osipov, Andreyan N. [1 ]
机构
[1] Fed Med Biol Agcy SRC FMBC, Burnasyan Fed Med Biophys Ctr, State Res Ctr, Moscow 123098, Russia
来源
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2013年 / 14卷 / 07期
基金
俄罗斯基础研究基金会;
关键词
DNA double-strand breaks; gamma-H2AX foci; gamma-radiation; dose rate effect; V79; cells; RATE IRRADIATION; REPAIR; DAMAGE; FOCI; INDUCTION; RESPONSES; LESIONS; CANCER; CYCLE; MICE;
D O I
10.3390/ijms140713719
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A comparative investigation of the induction of double-strand DNA breaks (DSBs) in the Chinese hamster V79 cells by gamma-radiation at dose rates of 1, 10 and 400 mGy/min (doses ranged from 0.36 to 4.32 Gy) was performed. The acute radiation exposure at a dose rate of 400 mGy/min resulted in the linear dose-dependent increase of the gamma-H2AX foci formation. The dose-response curve for the acute exposure was well described by a linear function y = 1.22 + 19.7x, where "y" is an average number of gamma-H2AX foci per a cell and "x" is the absorbed dose (Gy). The dose rate reduction down to 10 mGy/min lead to a decreased number of gamma-H2AX foci, as well as to a change of the dose-response relationship. Thus, the foci number up to 1.44 Gy increased and reached the "plateau" area between 1.44 and 4.32 Gy. There was only a slight increase of the gamma-H2AX foci number (up to 7) in cells after the protracted exposure (up to 72 h) to ionizing radiation at a dose rate of 1 mGy/min. Similar effects of the varying dose rates were obtained when DNA damage was assessed using the comet assay. In general, our results show that the reduction of the radiation dose rate resulted in a significant decrease of DSBs per cell per an absorbed dose.
引用
收藏
页码:13719 / 13726
页数:8
相关论文
共 26 条
  • [1] Track structure, radiation quality and initial radiobiological events: Considerations based on the PARTRAC code experience
    Alloni, Daniele
    Campa, Alessandro
    Friedland, Werner
    Mariotti, Luca
    Ottolenghi, Andrea
    [J]. INTERNATIONAL JOURNAL OF RADIATION BIOLOGY, 2012, 88 (1-2) : 77 - 86
  • [2] Cellular responses to DNA double-strand breaks after low-dose γ-irradiation
    Asaithamby, Aroumougame
    Chen, David J.
    [J]. NUCLEIC ACIDS RESEARCH, 2009, 37 (12) : 3912 - 3923
  • [3] Residual γH2AX foci as an indication of lethal DNA lesions
    Banath, Judit P.
    Klokov, Dmitry
    MacPhail, Susan H.
    Banuelos, C. Adriana
    Olive, Peggy L.
    [J]. BMC CANCER, 2010, 10
  • [4] Evasion of early cellular response mechanisms following low level radiation-induced DNA damage
    Collis, SJ
    Schwaninger, JM
    Ntambi, AJ
    Keller, TW
    Nelson, WG
    Dillehay, LE
    DeWeese, TL
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (48) : 49624 - 49632
  • [5] The Repair and Signaling Responses to DNA Double-Strand Breaks
    Goodarzi, Aaron A.
    Jeggo, Penelope A.
    [J]. ADVANCES IN GENETICS, VOL 82, 2013, 82 : 1 - 45
  • [6] The influence of heterochromatin on DNA double strand break repair: Getting the strong, silent type to relax
    Goodarzi, Aaron A.
    Jeggo, Penny
    Lobrich, Markus
    [J]. DNA REPAIR, 2010, 9 (12) : 1273 - 1282
  • [7] Inducible response required for repair of low-dose radiation damage in human fibroblasts
    Grudzenski, Saskia
    Raths, Antonia
    Conrad, Sandro
    Ruebe, Claudia E.
    Loebrich, Markus
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2010, 107 (32) : 14205 - 14210
  • [8] An oncogene-induced DNA damage model for cancer development
    Halazonetis, Thanos D.
    Gorgoulis, Vassilis G.
    Bartek, Jiri
    [J]. SCIENCE, 2008, 319 (5868) : 1352 - 1355
  • [9] No induction of p53 phosphorylation and few focus formation of phosphorylated H2AX suggest efficient repair of DNA damage during chronic low-dose-rate irradiation in human cells
    Ishizaki, K
    Hayashi, Y
    Nakamura, H
    Yasui, Y
    Komatsu, K
    Tachibana, A
    [J]. JOURNAL OF RADIATION RESEARCH, 2004, 45 (04) : 521 - 525
  • [10] Contribution of DNA repair and cell cycle checkpoint arrest to the maintenance of genomic stability
    Jeggo, Penny A.
    Loebrich, Markus
    [J]. DNA REPAIR, 2006, 5 (9-10) : 1192 - 1198