@article{oai:repo.qst.go.jp:00082286,
 author = {Ryoichi, Hirayama and Atsushi, Ito and Akiko, Uzawa and Yoshitaka, Matsumoto and Miho, Noguchi and Li, Huizi and Motofumi, Suzuki and Koichi, Ando and Ryuichi, Okayasu and Sumitaka, Hasegawa and Yoshiya, Furusawa and Ryoichi, Hirayama and Atsushi, Ito and Akiko, Uzawa and Yoshitaka, Matsumoto and Miho, Noguchi and Li, Huizi and Motofumi, Suzuki and Koichi, Ando and Ryuichi, Okayasu and Sumitaka, Hasegawa and Yoshiya, Furusawa},
 issue = {5},
 journal = {Radiation Research},
 month = {Mar},
 note = {We examined lethal damages of X-rays induced by direct and indirect actions, in terms of DSB repair susceptibility using two kinds of repair deficient Chinese hamster ovary (CHO) cell lines.  These CHO mutants (51D1 and xrs6) are genetically deficient in one of the two important DNA repair pathways after genotoxic injury (homologous recombination (HR) and non-homologous end binding (NHEJ) pathways, respectively).  The contribution of indirect action on cell killing can be estimated by applying the maximum level of DMSO to get rid of OH radicals.  To control the proportion of direct and indirect actions in lethal damage, we irradiated CHO mutant cells under aerobic and anoxic conditions.  The contributions of indirect action on HR-defective 51D1 cells were 76% and 57% under aerobic and anoxic conditions, respectively.  Interestingly, these percentages were similar to those of the wild-type cells even if the radiosensitivity was different.  However, the contributions of indirect action to cell killing on NHEJ-defective xrs6 cells were 52% and 33% under aerobic and anoxic conditions, respectively.  Cell killing by indirect action was significantly affected by the oxygen concentration and the DSB repair pathways but was not correlated with radiosensitivity.  These results imply that the lethal damage induced by direct action is mostly repaired by NHEJ repair pathway since killing of NHEJ-defective cells has significantly higher contribution by the direct action. In other words, HR repair pathway may not effectively repair the DSB by direct action in place of NHEJ repair pathway.  We conclude that the type of DSB produced by direct action is different from that of DSB induced by indirect action.},
 pages = {441--451},
 title = {Lethal DNA lesions caused by direct and indirect actions of X-rays are repaired via different DSB repair pathways under aerobic and anoxic conditions},
 volume = {195},
 year = {2021}
}