Abstract
Our previous study suggested that the DNA damage induced by very low X-ray doses are largely due to bystander effects. The aim of this study was to verify whether DNA damage created by radiation-induced bystander effects are likely to be repaired. We examined the generation of DNA damage in cells by enumeration of phosphorylated ataxia telangiectasia mutated (ATM) foci, which are correlated with DNA damage repair, in normal human fibroblast cells (MRC-5) after X-irradiation at doses ranging from 1 to 1000 mGy. At 24 h after irradiation, 100% (1.2 mGy), 58% (20 mGy), 12% (200 mGy) and 8.5% (1000 mGy) of the initial number of phosphorylated ATM foci were detected. The number of phosphorylated ATM foci in MRC-5 treated with lindane, an inhibitor of radiation-induced bystander effects, prior to X-irradiation was assessed; phosphorylated ATM foci were not observed at 5 h (20 mGy) or 24 h (200 mGy) post-irradiation. We also counted the number of phosphorylated ATM foci in MRC-5 co-cultured with 20-mGy-irradiated MRC-5. After 48 h of co-culture, 81% of the initial numbers of phosphorylated ATM foci remained. These findings suggest that DNA damage by the radiation-induced bystander effect persist for long periods, whereas DNA damage induced by direct radiation effects are repaired relatively quickly.
