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
Author(s) -
Kanji Ishizaki,
Yuko Hayashi,
Hideaki Nakamura,
Yoshihiro Yasui,
Kenshi Komatsu,
Akira Tachibana
Publication year - 2004
Publication title -
journal of radiation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.643
H-Index - 60
eISSN - 1349-9157
pISSN - 0449-3060
DOI - 10.1269/jrr.45.521
Subject(s) - irradiation , dna damage , phosphorylation , dose rate , dna repair , microbiology and biotechnology , ionizing radiation , dna , cancer research , chemistry , biology , radiochemistry , biochemistry , physics , nuclear physics
Human fibroblast cells obtained from a normal individual and immortalized by introduction of the hTERT gene were irradiated with 0 to 5 Gy of acute high-dose-rate radiation (1.8 Gy/min) or chronic low-dose-rate radiation (0.3 mGy/min) in the G0 phase, and p53 activation was studied. After high-dose-rate irradiation, a dose-dependent induction of Ser15 phosphorylation was observed, whereas after low-dose-rate irradiation almost none was observed. Then we analyzed the focus formation of phosphorylated histone H2AX protein, which is closely correlated with the induction of double-strand breaks. High-dose-rate radiation induced a significant number of foci in a dose-dependent manner, whereas, low-dose-rate radiation could induce only a few foci even at the highest dose. These results strongly suggest that DNA damage induced by low-dose-rate radiation such as a double-strand break is efficiently repaired during chronic irradiation.
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