Low micromolar zinc exerts cytotoxic action under H2O2-induced oxidative stress: Excessive increase in intracellular Zn2+ concentration

Matsui, Hiroko; Oyama, Tomohiro M.; Okano, Yoshiro; Hashimoto, Erika; Kawanai, Takuya; Oyama, Yasuo

doi:10.1016/j.tox.2010.06.011

Cited by 51 publications

(42 citation statements)

References 45 publications

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“…concentration by releasing Zn 2? from intracellular source(s) [15]; NOR-3, a donor of nitric oxide, also does so [49]. NEM is suggested to decrease the cellular thiol content and increase the intracellular Zn 2?…”

Section: Implicationmentioning

confidence: 99%

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

et al. 2011

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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 Zn(2+) in cells suffering from oxidative stress, the effects of N-ethylmaleimide (NEM) and ZnCl(2) on cellular thiol content and intracellular Zn(2+) 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 Zn(2+)-free conditions. Results suggest that NEM decreases cellular thiol content and induces intracellular Zn(2+) release. Micromolar ZnCl(2) dose-dependently augmented both FluoZin-3 and 5-CMF fluorescences, suggesting that the elevation of intracellular Zn(2+) concentration increases cellular thiol content. Taken together, it is hypothesized that intracellular Zn(2+) release during oxidative stress is a trigger to restore cellular thiol content that is decreased by oxidative stress.

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Section: Implicationmentioning

confidence: 99%

“…Furthermore, under oxidative stress induced by hydrogen peroxide, zinc exerts cytotoxic action by excessive increase in intracellular Zn 2? concentration [15]. Chelation of intracellular Zn 2?…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2011

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“…In our study (Morita et al, 2012), we found that nanomolar concentrations (100-500 nM) of triclocarban significantly increased the intracellular Zn 2+ concentration in rat thymocytes. Intracellular Zn 2+ release, which results in an increase in the intracellular Zn 2+ concentration, occurs when cells are under oxidative stress (Matsui et al, 2010;Kinazaki et al, 2011). Therefore, there is a possibility that nanomolar concentrations of triclocarban additively increase the vulnerability of cells to oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Nanomolar concentration of triclocarban increases the vulnerability of rat thymocytes to oxidative stress

et al. 2013

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-It was recently reported that triclocarban was absorbed significantly from soap used during showering in human subjects and that its C max in their whole blood ranged from 23 nM to 530 nM. We revealed that a nanomolar concentration (300 nM) of triclocarban potentiated the cytotoxicity of 300 μM H 2 O 2 in rat thymocytes by using cytometric techniques with appropriate fluorescent probes. Although 300 nM triclocarban did not itself increase the population of dead cells (cell lethality), it facilitated the process of cell death induced by H 2 O 2 , resulting in a further increase in the population of dead cells. Nanomolar concentrations (300 nM or higher) of triclocarban significantly decreased the cellular content of nonprotein thiol (glutathione), which has a protective role against oxidative stress. Triclocarban at 300 nM or higher increased the cell vulnerability to oxidative stress. The results may suggest that nanomolar concentration (300 nM or higher) of triclocarban affects some cellular functions although there is no evidence for adverse effects of triclocarban in humans at present.

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“…The cytotoxicity of H 2 O 2 is potentiated by micromolar concentrations of Zn 2+ (Matsui et al, 2010). Therefore, to investigate the role of Zn 2+ in the synergistic increase in cell lethality induced by the combination of DCOIT and H 2 O 2 , the effect of 10 lM TPEN, a membrane permeable Zn 2+ chelator, was tested on cytotoxicity produced by 1 lM DCOIT, 300 lM H 2 O 2 , and their combination ( Fig.…”

Section: Effect Of Tpen On the Synergistic Increase In Cell Lethalitymentioning

confidence: 99%

Zn2+-dependence of the synergistic increase in rat thymocyte cell lethality caused by simultaneous application of 4,5-dichloro-2-octyl-4-isothiazolin-3-one (DCOIT) and H2O2

et al. 2015

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Low micromolar zinc exerts cytotoxic action under H2O2-induced oxidative stress: Excessive increase in intracellular Zn2+ concentration

Cited by 51 publications

References 45 publications

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

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

Nanomolar concentration of triclocarban increases the vulnerability of rat thymocytes to oxidative stress

Zn2+-dependence of the synergistic increase in rat thymocyte cell lethality caused by simultaneous application of 4,5-dichloro-2-octyl-4-isothiazolin-3-one (DCOIT) and H2O2

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