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Your search keyword '"Oyama, Tomohiro M."' showing total 38 results
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38 results on '"Oyama, Tomohiro M."'

24. Cell death process induced by hydrogen peroxide is accelerated by clioquinol in rat thymocytes

Author

Oyama, Tomohiro M., Fukunaga, Eri, and Oyama, Yasuo

Subjects
cytotoxicity, hydrogen peroxide, clioquinol, lymphocyte
Abstract

We examined the effect of clioquinol on the process of cell death induced by hydrogen peroxide (H2O2) using a flow cytometric technique with propidium iodide and annexin V-FITC in order to see if clioquinol augments the toxicity caused by oxidative stress. Clioquinol (100 nM) alone did not change the process of spontaneous cell death. However, the agent accelerated the process of cell death induced by 300 μM H2O2. Result indicates that clioquinol augments the cytotoxicity induced by H2O2. Therefore, the use of clioquinol may be inadequate for the treatment of some diseases related to oxidative stress.

Published
2015

25. Zinc is a determinant of the cytotoxicity of Ziram, a dithiocarbamate fungicide, in rat thymic lymphocytes : possible environmental risks

Author

Kanemoto-Kataoka, Yumiko, Oyama, Tomohiro M., Ishibashi, Hitoshi, Oyama, Yasuo, Kanemoto-Kataoka, Yumiko, Oyama, Tomohiro M., Ishibashi, Hitoshi, and Oyama, Yasuo

Abstract

Ziram, one of dithiocarbamate fungicides, is widely applied to agriculture because the agent protects various crops from fungal infections. Risks of dithiocarbamate biocide use are concerned. It was previously reported that Ziram increased the intracellular concentration of Zn2+. Therefore, we cytometrically studied the mechanism of Zn2+-dependent lethal actions of Ziram on rat lymphocytes under environmentally relevant Zn2+ levels. Membrane and cellular parameters of rat lymphocytes were estimated by flow-cytometric techniques with appropriate fluorescent probes. The Ziram-induced increase in cell lethality was completely attenuated by Zn2+ chelators. A significant raise of cell lethality was found on the simultaneous application of Ziram at a sublethal concentration and ZnCl2. The combination of Ziram and ZnCl2 increased the cellular superoxide anion content and decreased the cellular GSH content, which possibly caused the increase in cell lethality. The zinc concentrations under present experimental conditions were comparable to the environmentally relevant concentrations found in rivers. Therefore, the environmental level of zinc may be critical in estimating the toxicity of Ziram to wild animals.

Published
2017

26. Ziram, a dithiocarbamate fungicide, exhibits pseudo-cytoprotective actions against oxidative stress in rat thymocytes : Possible environmental risks

Author

Kanemoto-Kataoka, Yumiko, Oyama, Keisuke, Oyama, Tomohiro M., Ishibashi, Hitoshi, Oyama, Yasuo, Kanemoto-Kataoka, Yumiko, Oyama, Keisuke, Oyama, Tomohiro M., Ishibashi, Hitoshi, and Oyama, Yasuo

Abstract

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.

Published
2017

33. Micromolar Zn2+ potentiates the cytotoxic action of submicromolar econazole in rat thymocytes: Possible disturbance of intracellular Ca2+ and Zn2+ homeostasis

Author

Kinazaki, Akio, primary, Sakanashi, Yoko, additional, Oyama, Tomohiro M., additional, Shibagaki, Haruka, additional, Yamashita, Kohei, additional, Hashimoto, Erika, additional, Nishimura, Yumiko, additional, Ishida, Shiro, additional, Okano, Yoshiro, additional, and Oyama, Yasuo, additional

Published
2009
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38. Putative role of intracellular Zn2+release during oxidative stress: a trigger to restore cellular thiol content that is decreased by oxidative stress

Author

Kinazaki, Akio, Chen, Hongqin, Koizumi, Kazuki, Kawanai, Takuya, Oyama, Tomohiro M., Satoh, Masaya, Ishida, Shiro, Okano, Yoshiro, and Oyama, Yasuo

Abstract

Although the ability of zinc to retard the oxidative process has been recognized for many years, zinc itself has been reported to induce oxidative stress. In order to give some insights into elucidating the role of intracellular Zn2+in cells suffering from oxidative stress, the effects of N-ethylmaleimide (NEM) and ZnCl2on cellular thiol content and intracellular Zn2+concentration were studied by use of 5-chloromethylfluorescein diacetate (5-CMF-DA) and FluoZin-3 pentaacetoxymethyl ester (FluoZin-3-AM) in rat thymocytes. The treatment of cells with NEM attenuated 5-CMF fluorescence and augmented FluoZin-3 fluorescence in a dose-dependent manner. These NEM-induced phenomena were observed under external Zn2+-free conditions. Results suggest that NEM decreases cellular thiol content and induces intracellular Zn2+release. Micromolar ZnCl2dose-dependently augmented both FluoZin-3 and 5-CMF fluorescences, suggesting that the elevation of intracellular Zn2+concentration increases cellular thiol content. Taken together, it is hypothesized that intracellular Zn2+release during oxidative stress is a trigger to restore cellular thiol content that is decreased by oxidative stress.

Published
2011
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