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Clustered gonocyte apoptosis in cultured fetal rat testes induced by accelerated heavy-ion-irradiations and its possible mechanisms

https://repo.qst.go.jp/records/62781
https://repo.qst.go.jp/records/62781
0d263495-2716-4485-ab51-259308ca600e
Item type 会議発表用資料 / Presentation(1)
公開日 2008-10-17
タイトル
タイトル Clustered gonocyte apoptosis in cultured fetal rat testes induced by accelerated heavy-ion-irradiations and its possible mechanisms
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_c94f
資源タイプ conference object
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Bing, Wang

× Bing, Wang

WEKO 620035

Bing, Wang

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Tanaka, Kaoru

× Tanaka, Kaoru

WEKO 620036

Tanaka, Kaoru

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Shang, Yi

× Shang, Yi

WEKO 620037

Shang, Yi

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Fujita, Kazuko

× Fujita, Kazuko

WEKO 620038

Fujita, Kazuko

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Noda, Yuko

× Noda, Yuko

WEKO 620039

Noda, Yuko

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Doi, Kazutaka

× Doi, Kazutaka

WEKO 620040

Doi, Kazutaka

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Ninomiya, Yasuharu

× Ninomiya, Yasuharu

WEKO 620041

Ninomiya, Yasuharu

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Morimoto, Yasuko

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WEKO 620042

Morimoto, Yasuko

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Moreno, Stephanie.G

× Moreno, Stephanie.G

WEKO 620043

Moreno, Stephanie.G

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Herve, Coffigny

× Herve, Coffigny

WEKO 620044

Herve, Coffigny

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Hayata, Isamu

× Hayata, Isamu

WEKO 620045

Hayata, Isamu

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Murakami, Masahiro

× Murakami, Masahiro

WEKO 620046

Murakami, Masahiro

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Eguchi-Kasai, Kiyomi

× Eguchi-Kasai, Kiyomi

WEKO 620047

Eguchi-Kasai, Kiyomi

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Nenoi, Mitsuru

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WEKO 620048

Nenoi, Mitsuru

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王 冰

× 王 冰

WEKO 620049

en 王 冰

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田中 薫

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WEKO 620050

en 田中 薫

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尚 奕

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WEKO 620051

en 尚 奕

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藤田 和子

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WEKO 620052

en 藤田 和子

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野田 攸子

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WEKO 620053

en 野田 攸子

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土居 主尚

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WEKO 620054

en 土居 主尚

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二宮 康晴

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WEKO 620055

en 二宮 康晴

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森本 泰子

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WEKO 620056

en 森本 泰子

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早田 勇

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WEKO 620057

en 早田 勇

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村上 正弘

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WEKO 620058

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笠井 清美

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WEKO 620059

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根井 充

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抄録
内容記述タイプ Abstract
内容記述 The increased clinical application of cancer radiotherapy and the human activities in space missions make the study on the biological effects from high-LET ionizing radiation a great concern for both public health and academic research. Investigations through the ground-based experiments using accelerated heavy ions are of critical importance to provide important scientific basis for radiation risk estimates and offer significant insight into the mechanisms regarding protection against radiation. In the previous France-Japan Workshop, we reported that heavy-ion irradiations on E15 generally induced markedly detrimental effects on prenatal gonads, postnatal testicular development and male breeding activity in Wistar rats. To explore the possible mechanisms underlying radiation-induced clustered gonocyte apoptosis in fetal gonads, which played a vital role in the fate of postnatal testis development, carbon and neon-ion irradiations (neon ions, beam energy 400MeV/nucleon, LET 30keV/microm; carbon ions, beam energy 290MeV/nucleon, LET 13keV/microm) of cultured fetal rat testes were applied to investigations ever after focusing on cellular and molecular events with or without inhibitors (administered 2h prior to irradiations) of p53 (pifithrin-alpha;100microM), gap junction (lindane, 40microM), or pan-caspase (Z-VAD-FMK, 100microM), or nitric oxide specific scavenger (cPTIO, 200microM). Results showed that, in addition to the clustered distribution, the time course and the percentage of apoptosis on E15 equivalent in vitro appeared similar to that in utero in response to carbon and neon-ion irradiations. Further study using accelerated carbon-ion irradiations showed that irradiations induced increased p53 expression and decreased expressions of p21 and Bcl-2 in a dose dependent manner. The pan-caspase inhibitor effectively inhibited apoptosis occurrence and reduced the extent of clustered distribution, while such effects were not observed with the presence of p53 or gap junction inhibitor, or nitric oxide specific scavenger. These findings indicated that irradiations of cultured fetal testes manifested pathologically similar gonocyte apoptosis to that in utero. The apoptosis was independent on p53, gap junction and nitric oxide. 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.
会議概要(会議名, 開催地, 会期, 主催者等)
内容記述タイプ Other
内容記述 The 7th Japan-France Workshop on Radiation Biology
発表年月日
日付 2008-10-16
日付タイプ Issued
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