徳島大学 教育・研究者情報データベース(EDB)

1. 徳島大学.大学院ソシオ・アーツ・アンド・サイエンス研究部.創生科学研究部門.環境共生科学分野(2009年4月1日〜2016年3月31日)

1. (英) Hashimoto Erika / (日) 橋本 恵里香 / (読) はしもと えりか

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2. (英) Kimura Kaori / (日) 木村 香織 / (読) きむら かおり

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3. (英) Kawanai Takuya / (日) 河内 琢也 / (読) かわない たくや

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4. (英) Nishimura Yumiko

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5. 小山 保夫

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(英) Nitroprusside increases intracellular Zn2+ concentration without affecting cellular thiol content: A model experiment using rat thymocytes and FluoZin-3

(英) Nitric oxide (NO) is cytotoxic under some conditions although it has physiological roles. It is recently proposed that the cytotoxicity of NO is resulted from its interaction with glutathione and zinc. Since we have revealed that a decrease in cellular content of non-protein thiols, presumably glutathione, induces intracellular Zn2+ release, there is a possibility that the cytotoxicity of nitroprusside, a donor of NO, is resulted from the interaction of NO with cellular thiols, leading to an increase in intracellular Zn2+ concentration. To test the possibility, the effects of nitroprusside on cell lethality, intracellular thiol content, and intracellular Zn2+ concentration were examined in rat thymocytes by using a flow cytometer with propidium iodide and FluoZin-3. Nitroprusside at concentrations of 0.3 mM or more (up to 10 mM) significantly augmented FluoZin-3 fluorescence, indicating an increase in intracellular Zn2+ concentration. It was also the case under external Zn2+-free condition, suggesting nitroprusside-induced release of intracellular Zn2+. However, nitroprusside at 10 mM did not affect cell lethality and cellular thiol content. Thus, it can be concluded that nitroprusside-induced increase in intracellular Zn2+ concentration is not related to its cytotoxicity.