抄録
DNA double strand breaks (DSBs) induced by ionizing radiation, are repaired by several pathways, such as non-homologus end joining (NHEJ), single-strand annealing (SSA), and homologous recombination (HR). Recently, it has been shown that ionizing radiation induces genomic instability, which is transmitted over many generations after irradiation through the progeny of surviving cells. This indicates that abnormal rejoining of DSB causes lesion, which persists as a radiation signature. Here we applied phosphorylation of histone H2AX induced by DSB as a marker of DNA lesion, and tried to establish a bio-dosimetry system, by which radiation signature on chromosome in irradiated nomal human diploid cells can be detected. We found that a number of phosphorylated H2AX foci per chromosome increased in a dose-dependent manner, and the foci colocalized at the site of chromosome aberrations. Interestingly, phosphorylated H2AX foci was also present even on chromosome which aberration was not left. Number of foci increased with dose dependent manner and it was about 11 times more than the number of chromosome aberrations. From these results, we concluded that phosphorylated H2AX foci could be a suitable marker for detection of radiation signature.
