@inproceedings{oai:repo.qst.go.jp:00053235,
 author = {Bing, Wang and Ohyama, Harumi and Nose, Masako and Yukawa, Osami and Yamada, Takeshi and Hayata, Isamu and 王 冰 and 大山 ハルミ and 能勢 正子 and 湯川 修身 and 山田 武 and 早田 勇},
 book = {Molecular Mechanisms for Radiation-Induced Cellular Response and Cancer Development : Proceeding of the International Symposium on Biological Effects of Low Dose Radiation},
 month = {},
 note = {In the past 5 years, a series of study was done at our institute to
investigate radiation effects on the embryogenesis in mice with an emphasis
on mechanisms involved in the radiation-induced adaptive response and the
role of radiation-induced apoptosis played in teratogenesis in the late
period of organogenesis. Using the limb bud system, we first found that
radiation-induced apoptosis is involved in malformations, namely,
radiation-induced apoptosis in the predigital regions of embryonic limb buds
is responsible for digital defects in ICR mice. Examination of embryonic
C57BL/6J mice with different p53 status led to further finding that
susceptibility to the radiation-induced apoptosis and digital defects
depends on both the p53 status and the radiation dose. p53 wild-type mice
appeared to be the most sensitive, while p53 knockout mice were the most
resistant. These results indicate that p53-dependent apoptosis mediates
radiation-induced digital defects. The existence of a radioadaptive response
in fetuses, i.e., the priming dose significantly decreases the apoptosis
induction, prenatal death, and digital defects in the living fetuses induced
by the challenging dose, was found first in ICR strain mice and later
confirmed again in C57BL/6J mice. p53 heterozygous embryos did not show the
radioadaptive response, indicating the involvement of p53 in the
radioadaptive response.},
 pages = {191--194},
 publisher = {Institute for Environmental Science},
 title = {Radioactive Response and radiation-Induced Teratogenesis in the Late Period of Organogenesis in Mice: Involvement of p53-Dependent Apoptosis},
 year = {2002}
}