ID 74530
Author
Harada, Soya Faculty of Integrated Arts and Sciences, The University of Tokushima
Kubota, Chiharu Faculty of Integrated Arts and Sciences, The University of Tokushima
Kitano, Natsuho Faculty of Integrated Arts and Sciences, The University of Tokushima
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 Tokushima University Educator and Researcher Directory KAKEN Search Researchers
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
Keywords
intracellular Zn2+
NOR-3
cytotoxicity
nitric oxide
glutathione
Content Type
Departmental Bulletin Paper
Description
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.
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
Volume
25
Issue
1
Start Page
1
End Page
6
Sort Key
1
Published Date
2011
EDB ID
FullText File
language
eng
departments
Bioscience and Bioindustry