부산대학교 도서관

It is well known that high-LET heavy ion is more effective for lethal effect than low LET radiation. It is considered that this high effectiveness is caused by heavy ion-induced clustered DNA damages, which are thought to be non-repairable or difficult to be repaired. However, much less is known about difficultly of clustered DNA damages repair in DNA repair process. The major DNA repair pathway in mammalian cells is non-homologous end joining (NHEJ). In this study we investigated NHEJ pathway by analyzing responses of Ku to DNA damage induced by high-LET heavy ions. pGFP and pGFP-Ku80 were transfected into Ku80-defective xrs-5 cells. Cells were irradiated with 7.2 MeV /u Ar13+beams (LET=1610 keV/μm) at TIARA JAEA-Takasaki. Sensitivity of Xrs5-GFP-Ku80 cells and xrs5-GFP cells to Ar13+was comparable. This result indicates that DNA damage induced by Ar13+is difficult to be repaired. To evaluate the response of Ku80 to DNA damage induced by heavy ions, GFP and γH2AX foci in the nuclei were observed. These foci were co-localized at 10 min after irradiation, while GFP foci were not clear and co-localized signal were not observed at 20 min. it was inferred that Ku proteins recognized DNA damage induced by Ar ions and dissociate from DNA ends without repair.