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Acute kidney injury model established by systemic glutathione depletion in mice
http://hdl.handle.net/2237/00030674
http://hdl.handle.net/2237/0003067446d3a049-0ced-41e2-bb49-c97d8d69026b
名前 / ファイル | ライセンス | アクション |
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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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× Oda, Shingo× Jia, Ru× Yokoi, Tsuyoshi |
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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 |
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著者版フラグ | ||||||
値 | author |