ID 66467
Author
Hashimoto, Erika Faculty of Integrated Arts and Sciences, The University of Tokushima
Kimura, Kaori Faculty of Integrated Arts and Sciences, The University of Tokushima
Kawanai, Takuya Faculty of Integrated Arts and Sciences, The University of Tokushima
Nishimura, Yumiko Okayama University Dental School
Oyama, Yasuo Faculty of Integrated Arts and Sciences, The University of Tokushima Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Keywords
zinc
nitroprusside
cytotoxicity
nitric oxide
Content Type
Departmental Bulletin Paper
Description
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.
Journal Title
徳島大学総合科学部自然科学研究 = Natural Science Research, The University of Tokushima
ISSN
09146385
NCID
AN10065859
Publisher
徳島大学.総合科学部
Volume
24
Issue
2
Start Page
6
End Page
11
Sort Key
6
Published Date
2010-04
EDB ID
FullText File
language
eng
departments
Bioscience and Bioindustry