@misc{oai:repo.qst.go.jp:00070502,
 author = {Nenoi, Mitsuru and Vares, Guillaume and Bing, Wang and 根井 充 and Ｇｕｉｌｌａｕｍｅ Ｖａｒｅｓ and 王 冰},
 month = {Sep},
 note = {When pregnant ICR mice were irradiated with high doses of X-rays (4-5 Gy) on day 12 after fertilization (E12), only three living fetuses (out of 12) remained per dam on E18 which exhibited widespread malformations However, when the mice were pre-exposed to low dose of X-rays (0.3 Gy) on E11, the number of living fetuses significantly increased while the fraction of malformed fetuses dropped. In order to reveal the molecular mechanisms underlying this radioadaptive response (RAR), we analyzed the modulation of gene expression in irradiated mouse fetuses. Using DNA microarrays, several RAR-related target genes (such as Tead3 Äi0and Cacna1aÄi0) were identified, and their functional involvement in RAR was confirmed by RNA interference experiments using cultured fetal limb bud cells. Meanwhile, we also investigated RAR against the mutagenic effects of high-LET radiation in cultured lymphoblastoid cells. The cells were exposed to 0.02 Gy or 0.1 Gy priming X rays or high-LET heavy-ion radiation (C-ions at 20 keV/mum or 40 keV/mum and Ne-ions at 150 keV/mum), followed six hours later by a 1 Gy challenging dose of heavy-ion radiation. Reduced mutation frequencies at the HPRT Äi0gene locus were observed in cells pre-exposed to priming radiation, compared to cells exposed to challenging dose alone. Analysis of the gammaH2AX kinetics in irradiated cells indicated that increased DSB repair rates were observed in adapted cells, suggesting the functional involvement of an efficient DSB repair mechanism in RAR. 
The implication of molecular mechanisms underlying RAR in low-dose radiation risk will be discussed., 第１４回国際放射線会議（14th International Congress of Radiation)},
 title = {On the molecular mechanisms or radioadaptive responses},
 year = {2011}
}