持续低剂量率照射后HepG2细胞的ATM磷酸化

目的 探讨持续低剂量率照射下HepG2细胞共济失调毛细血管扩张症突变基因(ATM)磷酸化的变化规律。方法 应用间接免疫荧光、Western blot技术检测持续低剂量率(8.28 cGy/h)照射下HepG2细胞ATM磷酸化蛋白的表达;采用集落形成法观察持续低剂量率照射对HepG2细胞增殖活性的影响。 结果持续低剂量率照射30 min后,ATM即已发生磷酸化,持续照射6 h时,ATM磷酸化蛋白表达量最多,以后逐渐减弱。使用Wortmannin抑制ATM磷酸化后,降低了持续低剂量率照射下肝癌细胞的存活分数。结论在持续低剂量率照射中后期ATM磷酸化减弱,提示持续低剂量率照射具有增加HepG2细胞辐射敏感性的潜能。

ATM phosphorylation in HepG2 cells following continuous low dose-rate irradiation

Objective To investigate the change of ATM phosphorylation in HepG2 cells following a condnuous low dose-rate irradiation.Methods Cells were pemistendy exposed to low dose-rate(8.28 cGy/h) irradiation.Indirect immunofluorescence and Western blot were used to detect the expression of ATM phosphorylated proteins.Colony forming assay Was used to observe the effect of a low dose-rate irradiation on HepG2 cell survival.Results After 30 min of low dose-rate irradiation.the phosphorylation of ATM occurred.After 6 h persistent irradiation,the expression of ATM phosphorylated protein reached the peak value,then gradually decreased.After ATM phosphorylation was inhibited with Wortmannin,the surviving fraction of HepG2 cells was lower than that of the irradiation alone group at each time point(P<0.05).Conclusions Continuous low dose-rate irradiation attenuated ATM phosphorylation.suggesting that continuous low dose-rate irradiation has a potential effect for increasing the radiosensitivity of HepG2 cells.