@misc{oai:repo.qst.go.jp:00062645,
 author = {Bing, Wang and Tanaka, Kaoru and Shang, Yi and Fujita, Kazuko and Ninomiya, Yasuharu and Moreno, Stephanie.G and Herve, Coffigny and Hayata, Isamu and Murakami, Masahiro and Eguchi-Kasai, Kiyomi and Nenoi, Mitsuru and 王 冰 and 田中 薫 and 尚 奕 and 藤田 和子 and 二宮 康晴 and 早田 勇 and 村上 正弘 and 笠井 清美 and 根井 充},
 month = {Jul},
 note = {The increasing human activities in space missions make the study on effects from high-LET ionizing radiation an important issue to be addressed. We reported previously that prenatal irradiations with heavy-ion beams on gestation day 15 generally induced markedly detrimental effects on prenatal gonads, postnatal testicular development and male breeding activity in rats. To explore the mechanisms involved in radiation-induced gonocyte apoptosis in fetal gonads, which played a critical role in the fate of postnatal testis development, accelerated heavy-ion irradiations and organotypic culture of Wistar fetal rat testes were applied to investigations focused on cellular and molecular events after irradiations with or without chemical addition. Results showed that, in addition to the clustered distribution, both the time course and the percentage of apoptosis in gonocytes on gestation day 15 equivalent in vitro appeared similar to that in utero after exposure to either carbon-ion beams with a LET value of about 13 keV/mu m or neon-ion beams with a LET value of about 30 keV/mu m. Irradiations induced increased p53 expression in a dose dependent manner and decreased expressions of p21 and Bcl-2 by Western Blot examination. Administration of pan-caspase inhibitor prior to irradiations effectively inhibited apoptosis occurrence and reduced the extent of clustered apoptosis, while such effects were not observed with the presence of p53 inhibitor, gap junction inhibitor, or nitric oxide specific scavenger. These findings indicated that irradiations of cultured fetal rat testes manifested pathologically similar apoptosis induction in gonocytes to that in utero. P53 expression was possibly responsible for the response to radiation damage rather than induction of apoptosis. The syncytial organization of gonocytes played a key role in formation of the clustered apoptosis, an event that both gap junction inhibitor and nitric oxide specific scavenger were incapable of preventing., 37th COSPAR Scientific Assembly},
 title = {Induction of apoptosis by accelerated heavy-ion beams in cultured fetal rat testes and its modification},
 year = {2008}
}