Relationship of HepG2 cell sensitivity to continuous low dose-rate irradiation with ataxia-telangiectasia mutated phosphorylation.
- Author:
Que-lin MEI
1
;
Jian-yong YANG
;
Duan-ming DU
;
Zai-zhong CHEN
;
Peng-cheng LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Ataxia Telangiectasia Mutated Proteins; Cell Cycle Proteins; metabolism; Cell Line, Tumor; Cell Survival; radiation effects; DNA-Binding Proteins; metabolism; Dose-Response Relationship, Radiation; Humans; Mice; Phosphorylation; radiation effects; Protein-Serine-Threonine Kinases; metabolism; Radiation Tolerance; radiation effects; Time Factors; Tumor Suppressor Proteins; metabolism
- From: Journal of Southern Medical University 2007;27(9):1391-1395
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the changes of ataxia-telangiectasia mutated (ATM) phosphorylation in HepG(2) cells in relation to HepG(2) cell survival under continuous low dose-rate irradiation.
METHODSHepG(2) cells were exposed to equivalent irradiation doses delivered at either a continuous low dose-rate (7.76 cGy/h) or a high dose-rate (4500 cGy/h), and the phosphorylated ATM proteins and surviving fraction of HepG(2) cells after the exposures were compared.
RESULTSThe phosphorylation of ATM protein was maximal at 0.5 Gy irradiation delivered at either a high doserate or a continuous low doserate. As the radiation dose increased, ATM protein phosphorylation decreased under continuous low dose-rate irradiation, but remained stable under high dose-rate irradiation. With comparable ATM protein phosphorylation induced by continuous low dose-rate irradiation and high dose-rate irradiation, there was no significant difference in the surviving fraction of HepG(2) cells (P>0.05), but at a significantly lower ATM protein phosphorylation level than that induced by high dose-rate irradiation, continuous low dose-rate irradiation resulted in increased cell killing (P<0.01).
CONCLUSIONContinuous low dose-rate irradiation increases HepG(2) cells radiosensitivity as compared with high dose-rate irradiation. Increased cell killing following continuous low dose-rate irradiation is associated with reduced phosphorylated ATM protein, and inhibition of ATM phosphorylation may increase the radiosensitivity of HepG(2) cells.
