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  1. 原著論文

Sodium orthovanadate (vanadate), a potent mitigator of radiation-induced damage to the hematopoietic system in mice.

https://repo.qst.go.jp/records/46612
https://repo.qst.go.jp/records/46612
58255b2e-ced4-4f4f-a102-cac89484e868
Item type 学術雑誌論文 / Journal Article(1)
公開日 2013-10-22
タイトル
タイトル Sodium orthovanadate (vanadate), a potent mitigator of radiation-induced damage to the hematopoietic system in mice.
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_6501
資源タイプ journal article
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 464666

Bing, Wang

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Tanaka, Kaoru

× Tanaka, Kaoru

WEKO 464667

Tanaka, Kaoru

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Morita, Akinori

× Morita, Akinori

WEKO 464668

Morita, Akinori

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Ninomiya, Yasuharu

× Ninomiya, Yasuharu

WEKO 464669

Ninomiya, Yasuharu

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Maruyama, Kouichi

× Maruyama, Kouichi

WEKO 464670

Maruyama, Kouichi

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Fujita, Kazuko

× Fujita, Kazuko

WEKO 464671

Fujita, Kazuko

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Hosoi, Yoshio

× Hosoi, Yoshio

WEKO 464672

Hosoi, Yoshio

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Nenoi, Mitsuru

× Nenoi, Mitsuru

WEKO 464673

Nenoi, Mitsuru

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王 冰

× 王 冰

WEKO 464674

en 王 冰

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田中 薫

× 田中 薫

WEKO 464675

en 田中 薫

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二宮 康晴

× 二宮 康晴

WEKO 464676

en 二宮 康晴

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丸山 耕一

× 丸山 耕一

WEKO 464677

en 丸山 耕一

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藤田 和子

× 藤田 和子

WEKO 464678

en 藤田 和子

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根井 充

× 根井 充

WEKO 464679

en 根井 充

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抄録
内容記述タイプ Abstract
内容記述 Previous in vitro and in vivo studies showed that sodium orthovanadate (vanadate), an inorganic vanadium compound, could effectively suppress radiation-induced p53-mediated apoptosis via both transcription-dependent and transcription-independent pathways. As a potent radiation protector administered at a dose of 20 mg/kg body weight (20 mg/kg) prior to total-body irradiation (TBI) by intra-peritoneal (ip) injection, it completely protected mice from hematopoietic syndrome and partially from the gastrointestinal syndrome. In the present study, radiation mitigation effects from vanadate were investigated by ip injection of vanadate after TBI in mice. Results showed that a single administration of vanadate at a dose of 20 mg/kg markedly improved the 30-day survival and the peripheral blood hemogram, relieved bone marrow aplasia and decreases occurrence of the bone marrow micronucleated erythrocytes in the surviving animals. The dose reduction factor was 1.2 when a single dose of 20 mg/kg was administrated 15 minutes after TBI in mice using the 30-day survival test as the endpoint. Results also showed that either doubling the vanadate dose (40 mg/kg) in a single administration or continuing the vanadate treatment (after a single administration at 20 mg/kg) from the following day at a dose of 5 mg/kg per day for 4 consecutive days would further significantly improved the efficacy for rescuing bone marrow failure in the 30-day survival test. Taken together, these findings indicate that vanadate would be a potent mitigator suppressing the acute lethality (hematopoietic syndrome) and minimizing the detrimental effects (anhematopoiesis and delayed genotoxic effects) induced by TBI in mice.
書誌情報 Journal of Radiation Research

巻 54, 号 4, p. 620-629, 発行日 2013-07
ISSN
収録物識別子タイプ ISSN
収録物識別子 0449-3060
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