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Glutathione Depletion Promotes Aluminum-Mediated Cell Death of PC12 Cells
https://hokuriku.repo.nii.ac.jp/records/539
https://hokuriku.repo.nii.ac.jp/records/539370494dc-0f66-417b-ac39-72675b1a329f
名前 / ファイル | ライセンス | アクション |
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Biological & Pharmaceutical Bulletin 2005.06 (451.5 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||||||
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公開日 | 2018-07-18 | |||||||||
タイトル | ||||||||||
タイトル | Glutathione Depletion Promotes Aluminum-Mediated Cell Death of PC12 Cells | |||||||||
タイトル | ||||||||||
タイトル | Glutathione Depletion Promotes Aluminum-Mediated Cell Death of PC12 Cells | |||||||||
言語 | en | |||||||||
言語 | ||||||||||
言語 | eng | |||||||||
キーワード | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | aluminum | |||||||||
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言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | cell death | |||||||||
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言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | glutathione | |||||||||
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言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | oxidative stress | |||||||||
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言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | reactive oxygen species | |||||||||
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 | |||||||||
著者 |
Satoh, Eiko
× Satoh, Eiko× Okada , Morihiro× Takadera, Tsuneo
WEKO
316
× Ohyashiki , Takao× Okada , Morihiro |
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抄録 | ||||||||||
内容記述タイプ | Abstract | |||||||||
内容記述 | Exposure of rat phenochromocytoma cells (PC12 cells) to aluminum maltolate complex, Al(maltol)3, induced a decrease in intracellular glutathione (GSH) concentration, resulting in a facilitated release of lactate dehydrogenase (LDH) from the cell and an increase in trypan blue-stained cells. Similar phenomena were observed as the cells were treated with L-buthione-[S,R]-sulfoximine (BSO) in the presence of Al(maltol)3. On the other hand, treatment of PC 12 cells with BSO alone in the absence of Al(maltol)3 did not affect the cell viability. Pre-treatment of PC12 cells with N-acetylcysteine (NAC) for 30 min before a 48 h-exposure to Al(maltol)3 effectively protected the cells from Al(maltol)3 toxicity by increasing intracellular GSH concentration. NAC also effectively inhibited reactive oxygen species (ROS) generation induced by treatment of the cells with Al(maltol)3. However, several lipophilic radical scavengers such as α-tocopherol and 3(2)-tert-butyl-4-hydroxyanisole, and an iron chelator, desferrioxamine, did not prevent Al(maltol)3-mediated ROS production or the decrease of cell viability. Based on these results, we discussed the role of intracellular GSH against the onset of aluminum toxicity in the context of ROS production. | |||||||||
書誌情報 |
en : Biological & Pharmaceutical Bulletin 巻 28, 号 6, p. 941-946, 発行日 2005-06 |
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出版者 | ||||||||||
出版者 | 公益社団法人日本薬学会 | |||||||||
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収録物識別子タイプ | ISSN | |||||||||
収録物識別子 | 0918-6158 |