@misc{oai:repo.qst.go.jp:00064048,
 author = {Suzuki, Masao and Tsuruoka, Chizuru and Konishi, Teruaki and Oikawa, Masakazu and Hua, Liu Cui and Kaneko, Yumiko and Furusawa, Yoshiya and 鈴木 雅雄 and 鶴岡 千鶴 and 小西 輝昭 and 及川 将一 and 劉 翠華 and 金子 由美子 and 古澤 佳也},
 month = {Sep},
 note = {Recently 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 fibroblasts induced by the 200kVp X-ray challenging dose (1.5Gy) was reduced at 0.15 times in cells pre-treated with low-dose-rate neutrons (1mSv/8h) as a priming dose compared to unpre-treated cells. Furthermore, the reduced mutation frequency was returned to the control level, when using a specific inhibitor of gap-junction mediated cell-cell communication (40µM lindane). We set up a hypothesis that recoiled protons emitted by the interaction between primary neutrons and surroundings near irradiated cells induce radio-adaptive response in irradiated cell population via gap-junction mediated bystander effect. To examine the hypothesis around 1.5% of total cells were irradiated with single 3.4MeV proton before irradiating the X-ray challenging dose using the microbeam irradiation system, Single Particle Irradiation system to Cell (SPICE) in National Institute of Radiological Sciences, Japan. The result clearly showed that the X-ray induced mutation frequency of hprt locus was suppressed in cells pre-treated with proton microbeams and returned to the control level, when using a specific inhibitor of gap-junction mediated cell-cell communication. The result suggests that neutron-induced adaptive response is caused by recoiled protons and gap-junction mediated bystander effect plays an important role to induce such cellular response., 56th Annual Meeting of Radiation Research Society},
 title = {Radio-adaptive response of hprt mutation in normal human fibroblasts induced by proton microbeams.},
 year = {2010}
}