重イオンマイクロビームを用いた放射線誘発バイスタンダー効果の分子メカニズムの解析

Analysis of molecular mechanisms for radiation-induced bystander effects using heavy ion microbeams

松本 英樹*; 畑下 昌範*; 高橋 昭久*; 浜田 信行*; 和田 成一*; 舟山 知夫; 坂下 哲哉; 柿崎 竹彦; 小林 泰彦

Matsumoto, Hideki*; Hatashita, Masanori*; Takahashi, Akihisa*; Hamada, Nobuyuki*; Wada, Seiichi*; Funayama, Tomoo; Sakashita, Tetsuya; Kakizaki, Takehiko; Kobayashi, Yasuhiko

A classical paradigm of radiation biology asserts that all radiation effects on cells, tissues and organisms are due to the direct action of radiation. However, there has been a recent growth of interest in the indirect actions of radiation including the radiation-induced adaptive response, the bystander effect, low-dose hypersensitivity, and genomic instability, which are specific modes of stress exhibited in response to low-dose/low-dose rate radiation. However, mechanisms of these phenomena are not fully known. The objective of this project is to elucidate molecular mechanisms of the bystander effect using heavy ion microbeams in JAEA. We found that the foci of H2A.X were formed in the unirradiated cells in the target colony including the irradiated cell 30 min after irradiation with 260 MeV Ne beams and that this formation of the foci was almost completely suppressed by the addition of NO specific scavenger, c-PTIO. Also we found that the foci of H2A.X were formed in the unirradiated cells in the untargeted colonies 6 h after irradiation with 260 MeV Ne beams and that this formation of the foci was almost completely suppressed by the addition of c-PTIO. Our findings demonstrate that NO is an initiator/mediator for evoking heavy ion microbeam-induced bystander effects.