Abstract
We have investigated effects of low-dose-rate radiation (LDR) on cells derived form normal human and patients of ataxia-telagiectasia (AT), NBS and Artemis deficient. Non-proliferative cells were irradiated by LDR (0.3 mGy/min) continuously up to 2 weeks or high-dose-rate radiation (HDR; 1 Gy/min). While the survival in normal cells after LDR radiation was significantly higher than that of HDR radiation, AT cells showed almost similar survival after both LDR and HDR. In contrast, the survival in Artemis deficient cells after LDR radiation was resistance than that in AT cells. Surprisingly, the survivals in NBS cells after LDR radiation showed almost similar resistance to that of normal cells. Although only few γH2AX foci was observed in LDR-irradiated normal cells, in AT cells significant numbers of γH2AX foci remained after LDR irradiation. However, in Artemis deficient cells numbers of γH2AX foci after LDR irradiation were about 50% of those in AT cells. In contrast, only a few γH2AX foci was observed in LDR irradiated NBS cells. These results suggest that ATM played an important role in repairing the double-strand break (DSB) induced by LDR radiation. Moreover, it is suggested that ATM might activate not only Artemis but also other factors in DSB-repair pathway after LDR radiation. On the other hand, function of NBS in cells irradiated with LDR might be differ to that HDR-radiated.
