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ID 111982
Author
Kanemoto-Kataoka, Yumiko Kitasato University|Tokushima University|Bayer Yakuhin, Ltd.
Oyama, Keisuke Kitasato University|Tokushima University|Osaka University
Oyama, Tomohiro M. Kitasato University|Tokushima University|Nishikumamoto Hospital
Ishibashi, Hitoshi Kitasato University|Tokushima University
Oyama, Yasuo Kitasato University|Tokushima University KAKEN Search Researchers
Keywords
Ziram
Lymphocytes
Cytoprotective action
Oxidative stress
Flow cytometer
Content Type
Journal Article
Description
Ziram, a dithiocarbamate fungicide, protects various vegetables and fruits against infections by fungus. Recently, there have been increasing anxieties about the risks in the use of dithiocarbamate fungicides. Our previous studies showed that Zn2+ was a determinant of Ziram cytotoxicity. In addition, Zn2+ is linked to H2O2 cytotoxicity. Therefore, in this study, we aimed to test the hypothesis that Ziram could augment the cytotoxicity of H2O2 by examining the changes induced by Ziram in some cellular parameters in rat thymic lymphocytes subjected to H2O2-induced oxidative stress using flow-cytometric methods with fluorescent dyes. Ziram significantly attenuated H2O2-induced cell death at sublethal concentrations. However, in the cells under oxidative stress elicited by H2O2, Ziram promoted the changing over from intact cells to living cells with exposed phosphatidylserine (PS) on plasma membranes, whereas it inhibited the transition from PS-exposed living cells to dead cells. Ziram significantly augmented H2O2 actions, including reduction of cellular glutathione levels and elevation of intracellular Zn2+ concentrations. Conversely, it attenuated H2O2-induced depolarization of mitochondrial membrane potential. Ziram at sublethal concentrations seems to exhibit promotive and suppressive actions on the process of cell death caused by H2O2. Ziram increased the number of living cells with exposed PS, a phenomenon characteristic of early stages of apoptosis. Thus, it is concluded that Ziram exhibits pseudo-cytoprotective actions against H2O2- induced oxidative stress.
Journal Title
Environmental Research
ISSN
00139351
NCID
AA12311499
AA11532415
Publisher
Elsevier
Volume
160
Start Page
232
End Page
238
Published Date
2017-10-10
Rights
© 2017. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Author
departments
Bioscience and Bioindustry