@misc{oai:repo.qst.go.jp:00067444, author = {Furusawa, Yoshiya and Shao, Chunlin and Aoki, Mizuho and Kobayashi, Yasuhiko and Funayama, Tomoo and Wada, Seiichi and Ando, Koichi and 古澤 佳也 and 青木 瑞穂 and 小林 泰彦 and 舟山 知夫 and 安藤 興一}, month = {Aug}, note = {The chemical factor involved in bystander effect and its transfer pathway were investigated in a confluent human fibroblast cell (AG1522) population. Micronuclei (MN) and G1-phase arrest were detected in cells irradiated by carbon (~100 keV/um) ions at HIMAC. A very low dose irradiation showed a high effectiveness in producing MN, suggesting a bystander effect. This effectiveness was enhanced by 8-Br-cAMP treatment that increases gap junctional intercellular communication (GJIC). On the other hand, the effect was reduced by 5% DMSO treatment, which reduce the reactive oxygen species (ROS), and suppressed by 100 mM lindane treatment, an inhibitor of GJIC. In addition, the radiation-induced G1-phase arrest was also enhanced by cAMP, and reduced or suppressed by DMSO or lindane. A microbeam device (JAERI) was also used for these studies. It was found that exposing one single cell in a confluent cell population to exactly one argon (~1260 keV/um) or neon (~430 keV/um) ion, additional MN could be detected in many other unirradiated cells. The yield of MN increased with the number of irradiated cells. However, there was no significant difference in the MN induction when the cells were irradiated by increasing number of particles. MN induction by bystander effect was partly reduced by DMSO, and effectively suppressed by lindane. Our results obtained from both random irradiation and precise numbered irradiation indicate that both GJIC and ROS contributed to the radiation-induced bystander effect, but the cell gap junction channels likely play an essential role in the release and transfer of radiation-induced chemical factors., 12th International Congress of Radiation Research}, title = {Bystander Effects through Gap Junction Channels by Heavy-ion Microbeam}, year = {2003} }