Relationship of HepG2 cell sensitivity to continuous low dose-rate irradiation with ataxia-telangiectasia mutated phosphorylation / 南方医科大学学报

ABSTRACT

<p><b>OBJECTIVE</b>To 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.</p><p><b>METHODS</b>HepG(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.</p><p><b>RESULTS</b>The 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).</p><p><b>CONCLUSION</b>Continuous 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.</p>