Role of ATM in repair of the DSBs induced by LDR radiation

Abstract

We have investigated effects of low-dose-rate radiation (LDR) on human cells immortalized by the hTERT gene. GI-phase-arrested cells were irradiated by LDR (0.3mGy/min) continuously for a maximum of 2 weeks or high-dose-rate radiation (HDR; 2Gy/min). In normal human cells, the survival after LDR radiation was significantly high, while the induction of micronuclei was significantly low, when compared to those after HDR irradiation. In contrast, in AT cells significant difference between LDR and HDR were not observed. Only few γH2AX foci formation was observed in LDR irradiated normal cells, while in AT cells significant number of γH2AX foci were induced after LDR irradiation. We have suggested that ATM played an important role in repairing the DSBs induced by LDR radiation. However, it is still not clear ATM function in repair of DNA damage induced by LDR radiation. We are now investigating the effects of LDR radiation on DSB repair deficient cells (Artemis, DNA Ligase IV and NBS) arrested in the G0/G1 phase.