Toxicology : Effects of Oxidative Stress Caused by tert-Butylhydroquinone on Cytotoxicity in MDCK Cells
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- SHIBUYA Naoko
- Laboratory of Animal Nutrition, School of Veterinary Medicine, Kitasato University, Aomori 034-8628, Japan
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- KOBAYASHI Shigeki
- Laboratory of Animal Nutrition, School of Veterinary Medicine, Kitasato University, Aomori 034-8628, Japan
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- YOSHIKAWA Yasunaga
- Laboratory of Veterinary Biochemistry, School of Veterinary Medicine, Kitasato University, Aomori 034-8628, Japan
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- WATANABE Kiyotaka
- Laboratory of Veterinary Biochemistry, School of Veterinary Medicine, Kitasato University, Aomori 034-8628, Japan
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- ORINO Koichi
- Laboratory of Veterinary Biochemistry, School of Veterinary Medicine, Kitasato University, Aomori 034-8628, Japan
書誌事項
- タイトル別名
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- Effects of Oxidative Stress Caused by <i>tert</i>-Butylhydroquinone on Cytotoxicity in MDCK Cells
- Effects of oxidative stress caused by tert-butylhydroquinone on cytotoxicity in MDCK cells
この論文をさがす
抄録
Antioxidant and oxidative stress effects of prooxidants are generally dose-dependent, and these effects depend on the prooxidant species and cell type. However, the cellular response to oxidant challenge is a complicated interplay of events involving cellular expression of phase II detoxification enzymes and cellular metal metabolism. This study demonstrates the effect of tert-butylhydroquinone (t-BHQ)-induced oxidative stress on MDCK cells. Cell toxicity tests were carried out using the crystal violet (CV) assay with the following prooxidants: t-BHQ, diethyl maleate (DEM), hydrogen peroxide (H2O2), diquat (DQ) and β-naphthoflavone (β-NF). Except for β-NF, these prooxidants showed dose-dependent cytotoxicity besides the most potent t-BHQ cytotoxicity. Only t-BHQ and DEM caused significant time-dependent expression of ferritin protein as an antioxidant, which segregates Fe2+, causing the Fenton reaction. t-BHQ and DEM increased formation of lipid peroxidation, but DQ showed a tendency to decrease lipid peroxidation levels. In XTT assay, even when substantial cell death was observed in the CV assay, t-BHQ appeared to increase cell viability by enhancing XTT reduction, likely through the production of NADPH. Although curcumin, which induces cytoprotective phase II enzymes and chelates metal irons, decreased cell viability, it inhibited t-BHQ cytotoxicity. These results indicate that t-BHQ exhibits strong cytotoxicity against MDCK cells, an effect mitigated by curcumin, and that t-BHQ-induced oxidative stress activates the pentose phosphate pathway.
収録刊行物
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- The Journal of Veterinary Medical Science
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The Journal of Veterinary Medical Science 74 (5), 583-589, 2012
公益社団法人 日本獣医学会
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詳細情報 詳細情報について
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- CRID
- 1390282681404511232
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- NII論文ID
- 130001879875
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- NII書誌ID
- AA10796138
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- COI
- 1:STN:280:DC%2BC38zptFersA%3D%3D
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- ISSN
- 13477439
- 09167250
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- NDL書誌ID
- 023806736
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- PubMed
- 22185773
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可