@misc{oai:repo.qst.go.jp:00060401,
 author = {Bing, Wang and Ohyama, Harumi and Tanaka, Kaoru and Morimoto, Yasuko and Aizawa, Shirou and Yukawa, Osami and Hayata, Isamu and 王 冰 and 大山 ハルミ and 田中 薫 and 森本 泰子 and 相澤 志郎 and 湯川 修身 and 早田 勇},
 month = {Jun},
 note = {The limb developing system is a suitable model to study the teratogenetic effect of radiation in fetal mice. We found that radiation-induced apoptosis in the predigital regions of fetal limb buds was responsible for digital defects. In ICR and C57BL/6J mice, and C57BL/6J mice with different Trp53 gene status susceptibility to the radiation-induced apoptosis and digital defects was depending on the strain as well as Trp53 gene status and radiation dose. C57BL/6J mice were more radiosensitive than ICR mice. Trp53 wild-type C57BL/6J mice appeared to be the most radiosensitive and Trp53 knockout C57BL/6J mice the most radioresistant. An adaptive response (reduction of both fetal death and malformation) was demonstrated in fetal mice induced by priming low dose radiation prior to a high dose irradiation. Suppression of the digital defects was correlated to the inhibition of apoptosis. The priming dose was mouse strain-related. Both Trp53 alleles were essential for induction of the adaptive response. Furthermore, existence of the dose-rate effect was verified in both radiation-induced teratogenetic effect and adaptive response. The results indicate that Trp53-dependent apoptosis mediates radiation-induced digital defects and the Trp53 involves in the adaptive response in late organogenesis. Radiation-induced teratogenetic effect and adaptive response are due to a complex interplay between dose, dose rate and animal factors such as the strain, developmental stage, and gene background., The Fifth Japan-France Workshop on Radiobiology and Medical Imaging},
 title = {Radiation-Induced Teratogenetic Effect and Adaptive Response in Late Organogenesis in Mice},
 year = {2004}
}