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  1. C100 医学部/医学系研究科
  2. C100a 雑誌掲載論文
  3. 学術雑誌

Acute kidney injury model established by systemic glutathione depletion in mice

http://hdl.handle.net/2237/00030674
http://hdl.handle.net/2237/00030674
46d3a049-0ced-41e2-bb49-c97d8d69026b
名前 / ファイル ライセンス アクション
appendPDF.pdf appendPDF (4.6 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2019-09-11
タイトル
タイトル Acute kidney injury model established by systemic glutathione depletion in mice
言語 en
著者 Matsubara, Akiko

× Matsubara, Akiko

WEKO 93365

en Matsubara, Akiko

Search repository
Oda, Shingo

× Oda, Shingo

WEKO 93366

en Oda, Shingo

Search repository
Jia, Ru

× Jia, Ru

WEKO 93367

en Jia, Ru

Search repository
Yokoi, Tsuyoshi

× Yokoi, Tsuyoshi

WEKO 93368

en Yokoi, Tsuyoshi

Search repository
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利
言語 en
権利情報 This is the peer reviewed version of the following article: [Matsubara, A, Oda, S, Jia, R, Yokoi, T. Acute kidney injury model established by systemic glutathione depletion in mice. J Appl Toxicol. 2019; 39: 919– 930. https://doi.org/10.1002/jat.3780], which has been published in final form at [https://doi.org/10.1002/jat.3780]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.
キーワード
主題Scheme Other
主題 acute kidney injury
キーワード
主題Scheme Other
主題 animal model
キーワード
主題Scheme Other
主題 BSO
キーワード
主題Scheme Other
主題 glutathione
キーワード
主題Scheme Other
主題 myoglobin
抄録
内容記述 Glutathione (GSH) is one of the most extensively studied tripeptides. The roles for GSH in redox signaling, detoxification of xenobiotics and antioxidant defense have been investigated. A drug‐induced rhabdomyolysis mouse model was recently established in L‐buthionine‐(S,R)‐sulfoximine (BSO; a GSH synthesis inhibitor)‐treated normal mice by co‐administration of antibacterial drug and statin. In these models, mild kidney injury was observed in the BSO only‐treated mice. Therefore, in this study, we studied kidney injury in the GSH‐depleted mouse. BSO was intraperitoneally administered twice a day for 7 days to normal mice. The maximum level of plasma creatine phosphokinase (351 487 ± 53 815 U/L) was shown on day 8, and that of aspartate aminotransferase was shown on day 6. Increased levels of blood urea nitrogen, plasma creatinine, urinary kidney injury molecule‐1 and urinary creatinine were observed. An increase of mRNA expression level of renal lipocalin 2/neutrophil gelatinase‐associated lipocalin was observed. Degeneration and necrosis in the skeletal muscle and high concentrations of myoglobin (Mb) in blood (347‐203 925 ng/mL) and urine (2.5‐68 583 ng/mL) with large interindividual variability were shown from day 5 of BSO administration. Mb‐stained regions in the renal tubule and renal cast were histologically observed. In this study, the GSH‐depletion treatment established an acute kidney injury mouse model due to Mb release from the damaged skeletal muscle. This mouse model would be useful for predicting potential acute kidney injury risks in non‐clinical drug development.
言語 en
内容記述タイプ Abstract
内容記述
内容記述 ファイル公開:2020-06-01
言語 ja
内容記述タイプ Other
出版者
言語 en
出版者 Wiley
言語
言語 eng
資源タイプ
資源タイプresource http://purl.org/coar/resource_type/c_6501
タイプ journal article
出版タイプ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 https://doi.org/10.1002/jat.3780
ISSN(print)
収録物識別子タイプ PISSN
収録物識別子 0260-437X
書誌情報 en : Journal of Applied Toxicology

巻 39, 号 6, p. 919-930, 発行日 2019-06
著者版フラグ
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