NOR-3, a donor of nitric oxide, increases intracellular Zn²⁺ concentration and decreases cellular thiol content : A model experiment using rat thymocytes, FluoZin-3, and 5-chloromethylfluorescein NOR-3, a donor of nitric oxide, increases intracellular Zn^<2+> concentration and decreases cellular thiol content : A model experiment using rat thymocytes, FluoZin-3, and 5-chloromethylfluorescein

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著者

    • Kawanai Takuya
    • Faculty of Integrated Arts and Sciences, The University of Tokushima
    • Koizumi Kazuki
    • Faculty of Integrated Arts and Sciences, The University of Tokushima
    • Oyama Yasuo
    • Faculty of Integrated Arts and Sciences, The University of Tokushima
    • Kinazaki Akio
    • Department of Pharmaceutical Care and Clinical Pharmacy, Faculty of Pharmaceutical Sciences, Tokushima Bunri University
    • Ishida Shiro
    • Department of Pharmaceutical Care and Clinical Pharmacy, Faculty of Pharmaceutical Sciences, Tokushima Bunri University
    • Okano Yoshiro
    • Department of Pharmaceutical Care and Clinical Pharmacy, Faculty of Pharmaceutical Sciences, Tokushima Bunri University

抄録

Our previous study showed that nitroprusside, a donor of nitric oxide (NO), increased intracellular Zn2+ concentration without affecting cellular content of glutathione (GSH) although it has been proposed that the cytotoxicity of NO is resulted from its interaction with glutathione and zinc. Nitroprusside releases not only NO but also cyanides (Fe(II)CN and Fe(III)CN), CN-, Fe2+, and Fe3+. Therefore, such decomposition products may mask NO-induced action on cellular GSH content. In this study, we used NOR-3 as a donor of NO to reveal the effects of NO on intracellular Zn2+ concentration and cellular GSH content in a cytometric manner with fluorescent probes, FluoZin-3-AM and 5-chloromethylfluorescein diacetate. NOR-3 at 1-3 mM significantly increased intracellular Zn2+ concentration and decreased cellular GSH content. After the removal of extracellular Zn2+ by diethylenetriamine-N,N,N',N",N"-pentaacetic acid (DTPA, a chelator for Zn2+), the increase in intracellular Zn2+ concentration by NOR-3 was still observed although DTPA significantly attenuated the increase in intracellular Zn2+ concentration by NOR-3. Results suggest an involvement of both intracellular Zn2+ release and increase in membrane Zn2+ permeability. It is likely that NO induces oxidative stress, leading to an increase in intracellular Zn2+ concentration.

収録刊行物

  • 徳島大学総合科学部自然科学研究

    徳島大学総合科学部自然科学研究 25, 1-6, 2011

    徳島大学

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各種コード

  • NII論文ID(NAID)
    110008761209
  • NII書誌ID(NCID)
    AN10065859
  • 本文言語コード
    ENG
  • 資料種別
    Departmental Bulletin Paper
  • 雑誌種別
    大学紀要
  • ISSN
    09146385
  • NDL 記事登録ID
    023447810
  • NDL 請求記号
    Z14-1395
  • データ提供元
    CJP引用  NDL  NII-ELS  IR 
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