@misc{oai:repo.qst.go.jp:00070497,
 author = {Suzuki, Masao and Tsuruoka, Chizuru and Hua, Liu Cui and Konishi, Teruaki and Oikawa, Masakazu and Autsavapromporn, Narongchai and 鈴木 雅雄 and 鶴岡 千鶴 and 劉 翠華 and 小西 輝昭 and 及川 将一 and アッサワプロンポーン ナロンチャイ},
 month = {Sep},
 note = {INTRODUCTION:  A central paradigm in radiation biology has been that only cells "hit" by a track of radiation would be affected to induce radiobiological consequences, and cells "not hi" should not be. However, it recently has been challenged by so called non-targeted effects, such as genomic instability, adaptive response and bystander effect, and such radiation-induced non-targeted effects may have important implications for low-dose-radiation induced biological effects. In this study we have examined cellular responses, such as bystander effect and radio-adaptive response, in normal human cells induced by low-fluence-proton irradiation using proton microbeams.   
\nMATERIALS AND METHODS: We have investigated that the mutation frequency at the hypoxanthine-guanine phosphoribosyltransferase (hprt) locus, which was detected with measuring 6-thioguanine resistant clones, in normal human skin fibroblas t! s induced by the 200kVp X-ray challenging dose was lower at 0.15 times in cells pre-treated with low-dose-rate neutrons (1mSv/8h) emitted from 241Am-Be source as a priming dose than that in untreated control cells. Furthermore, the reduced mutation frequency was returned to the control level when using a specific inhibitor of gap-junction mediated cell-cell communication (40microM lindane). Here we set up the hypothesis that recoiled protons emitted by the interaction between primary neutrons and surroundings near irradiated cells induce radio-adaptive response in a irradiated and unirradiated mixed cell population via gap-junction mediated bystander effect. To prove the hypothesis around 1.5% cells of total cell population were irradiated with single 3.4MeV proton using the microbeam irradiation system, Single Particle Irradiation system to Cell (SPICE) in National Institute of Radiological Sciences (NIRS) before irradiating the X-ray challenging dose.
\nRESULTS: The data of the hprt mutation induction clearly showed that the X-ray induced mutation frequency was suppressed in cells pre-treated with proton microbeams and returned to the control level when using a gap-junction inhibitor.
\nCONCLUSION: The result suggests that neutron-induced adaptive response is caused by protons and gap-junction mediated bystander effect plays an important role to induce such cellular response., 14th International Congress of radiation Research},
 title = {Radio-adaptive response for hprt mutation via bystander effect in normal human fibroblasts induced by proton microbeams},
 year = {2011}
}