• The Journal of Korean Medicine
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• v.22 no.3
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• pp.63-73
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• 2001

Objectives : The objective of the current study is to determine the protective effect of Ukyium(Yougui-yin) on the apoptosis induced by zinc. Methods : Zinc is known to generate reactive oxygen species (ROS), including superoxide anion ($O_2$) and hydrogen peroxide ($H_2O_2$), which eventually contribute to cytotoxicity in a variety of cell types. We investigated the viablity of cells, $H_2O_2$ generation, chromatin condensation and nuclear fragmentation in Hoechst dye staining and $IkB-{\alpha}$ degradation in C6 glial cells of $ZnCl_2$ between pretreatment- and not pretreatment-group with Ukyium. The former methods were researched by Time- and Dose-dependent manners. Results : We demonstrated that pretreatment with Ukyium prevented zinc-induced cell death of C6 glial cells and apoptotic characteristics including chromatin condensation and nuclear fragmentation. Ukyium also prevented $H_2O_2-induced$ cell death. We further confirmed that Ukyium decreased zinc-induced generation of $H_2O_2$ and inhibited degradation of $IkB-{\alpha}$ by zinc in C6 glial ceHs. Conclusions : These data indicated that Ukyium (Yougui-yin) prevents zinc-induced apoptotic death of C6 glial cells via inhibition of ROS generation, such as $H_2O_2$ as well as inhibition of $IkB-{\alpha}$ degradation.

• Journal of the Korean Society of Food Science and Nutrition
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• v.44 no.5
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• pp.649-656
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• 2015

The protective effect of zinc against cortisol-induced cell injury was examined in rainbow trout gill epithelial cells. Cells exposed to cortisol for 24 h showed increased leakage of lactate dehydrogenase (LDH) as well as decreased cell viability in a dose-dependent manner. Treatment with zinc ($100{\mu}M$ $ZnSO_4$) reduced the severity of both LDH release and cell death as well as protected cells against cortisol-induced caspase-3 activation, indicating reduction of apoptosis. Cortisol-induced cell death, leakage of LDH, and caspase-3 activation were blocked by the glucocorticoid receptor antagonist Mifepristone (RU-486), suggesting that cell injury was cortisol-dependent. In addition, we studied the effect of zinc on the expression of antioxidant genes such as metallothionein A (MTA), metallothionein B (MTB), glutathione-S-transferase (GST), and glucose-6-phosphate dehydrogenase (G6PD) during cortisol-induced cell injury. MTA, MTB, GST, and G6PD mRNA levels increased after treatment with zinc or cortisol, separately or in combination. Higher mRNA levels of MTA, MTB, GST, and G6PD were detected when cells were treated with $100{\mu}M$ $ZnSO_4$ and $1{\mu}M$ cortisol in combination at the same time compared to treatment with zinc or cortisol separately. Cells treated with zinc showed increased intracellular free zinc concentrations, and this response was significantly enhanced in cells treated with cortisol and zinc. In conclusion, zinc treatment inhibited cortisol-induced cytotoxicity and apoptosis through indirect antioxidant action.

• Korean Journal of Materials Research
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• v.27 no.10
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• pp.530-533
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• 2017

ZnO micro/nanocrystals with different morphologies were synthesized by thermal evaporation of various zinc source materials in an air atmosphere. Zinc acetate, zinc carbonate and zinc iodide were used as the source materials. No catalysts or substrates were used in the synthesis of the ZnO crystals. The scanning electron microscope(SEM) image showed that the morphology of ZnO crystals was strongly dependent on the source materials, which suggests that source material is one of the key factors in controlling the morphology of the obtained ZnO crystals. Tetrapods, nanogranular shaped crystals, spherical particles and crayon-shaped crystals were obtained using different source materials. The X-ray diffraction(XRD) pattern revealed that the all the ZnO crystals had hexagonal wurtzite crystalline structures. An ultraviolet emission was observed in the cathodoluminescence spectrum of the ZnO crystals prepared via thermal evaporation of Zn powder. However, a strong green emission centered at around 500 nm was observed in the cathodoluminescence spectra of the ZnO crystals prepared using zinc salts as the source materials.

• Journal of Environmental Health Sciences
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• v.23 no.4
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• pp.26-32
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• 1997

To evaluate the cytogenetic toxicity, of cadmium and the reducing effect of selenium or zinc on cadmium toxicity, the induction of SCEs in cultured human lymphocytes by the concentraion of 0.5 $\mu$M to 16.0 $\mu$M of cadmium chloride and those of cadmium chloride combined with sodium selenite or zinc chloride 1.2 $\mu$M, respectively was investigated. The induction of SCEs by cadmium chloride in the range of 0.5 $\mu$M to 16.0 $\mu$M increased in a dose-dependent manner. A notable increase in SCEs by sodium selenite as well as zinc chloride was also observed. However, the frequency of SCEs by cadmium chloride was inhibited by the simultaneous addition of sodium selenite and zinc chloride 1.2 $\mu$M, respectively. The mitotic index significantly decreased in higher concentration of cadmium chloride but not was significantly different in any concentration of cadmium chloride with the simultaneous addition of sodium selenite or zinc chloride. The results showed that the decreased additive SCE effect was observed when induced by the combined treatment which could suggest that sodium selenite and zinc chloride have a protective effect on cadmium chloride.

• Toxicological Research
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• v.23 no.1
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• pp.33-38
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• 2007

Zinc is an endogenous transition metal that can be synaptically released during neuronal activity. However, zinc may contribute to the neuropathology associated with a variety of conditions. Carnosine expressed in glial cells can modulate the effects of zinc on neuronal excitability as a zinc chelator. We hypothesize that carnosine may protect against neurotoxicity of zinc in cortical neuronal cells. The cortical neuronal cells from newborn rats were prepared and exposed to zinc chloride and/or carnosine at various concentrations. Zinc at the doses of 0 to $500{\mu}M$ decreased neuronal cell viability in a dose-dependent manner. Additionally, at the concentrations of 100 and $200{\mu}M$, it significantly decreased cell viability in an exposed time-dependent manner (p < 0.05). Treatment with carnosine at the concentrations of 20 and $200{\mu}M$ significantly increased neuronal cell proliferation by approximately 14% and 20%, respectively, compared to the control (p < 0.05). At the concentrations of 100 and $200{\mu}M$ zinc, $20{\mu}M$ carnosine significantly increased the viability of neuronal cells by 18.3% and 12.1 %, and $200{\mu}M$ carnosine also increased it by 33.5% and 28.6%, respectively, compared to the normal control group (p < 0.01). These results suggest that carnosine at a physiologically relevant level may protect against zinc-mediated toxicity in neuronal cells as an endogenous neuroprotective agent.

• Toxicological Research
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• v.35 no.1
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• pp.83-91
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• 2019

Nanoparticles (NPs) have been recognized as both useful tools and potentially toxic materials in various industrial and medicinal fields. Previously, we found that zinc oxide (ZnO) NPs that are neurotoxic to human dopaminergic neuroblastoma SH-SY5Y cells are mediated by lipoxygenase (LOX), not cyclooxygenase-2 (COX-2). Here, we examined whether human bone marrow-derived mesenchymal stem cells (MSCs), which are different from neuroblastoma cells, might exhibit COX-2- and/or LOX-dependent cytotoxicity of ZnO NPs. Additionally, changes in annexin V expression, caspase-3/7 activity, and mitochondrial membrane potential (MMP) induced by ZnO NPs and ZnO were compared at 12 hr and 24 hr after exposure using flow cytometry. Cytotoxicity was measured based on lactate dehydrogenase activity and confirmed by trypan blue staining. Rescue studies were executed using zinc or iron chelators. ZnO NPs and ZnO showed similar dose-dependent and significant cytotoxic effects at concentrations ${\geq}15{\mu}g/mL$, in accordance with annexin V expression, caspase-3/7 activity, and MMP results. Human MSCs exhibited both COX-2 and LOX-mediated cytotoxicity after exposure to ZnO NPs, which was different from human neuroblastoma cells. Zinc and iron chelators significantly attenuated ZnO NPs-induced toxicity. Conclusively, these results suggest that ZnO NPs exhibit both COX-2- and LOX-mediated apoptosis by the participation of mitochondrial dysfunction in human MSC cultures.

• The Transactions of the Korean Institute of Electrical Engineers C
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• v.51 no.3
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• pp.111-114
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• 2002

Using the plasma that we developed to generate a low-temperature plasma at atmospheric pressure, we have investigated the etching possibility of an air-exposed zinc oxide(ZnO) thin films. Hydrogen and methane radicals generated from the plasma were observed and their intensity was found to be dependent on the isomer of butyl acetate by an analysis with optical emission spectrosxopy. The etching ability of this plasma was evaluated by an emission intensity, etching time, rf power.

• YAKHAK HOEJI
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• v.46 no.4
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• pp.258-264
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• 2002

Zinc plays an important role in immunobiological responses, while excessive zinc attenuates immune functions in a dose-dependent manner. Zinc excess has been reported to increase levels of plasma prostaglandin E$_2$ (PGE$_2$), which is known to inhibit production of Th (helper T) 1-associated cytokines and to induce inflammatory responses. Thus, this study was investigated the effects of indomethacin, a potent inhibitor of PGE$_2$ synthesis, on the proinflammatory cytokine and lymphokine production in ICR mice exposed to excessive zinc. Indomethacin at doses of 5 mg/kg was administered i.p. 30 minutes before zinc chloride (Zn) 30 mg/kg orally daily for 10 days. Excessive Zn remarkedly increased tumor necrosis factor (TNF)-$\alpha$ and interleukin (IL)-1$\beta$ levels in both serum and splenic supernatants compared with those in controls, while indomethacin significantly reduced the excessive Zn-induced levels of IL-1$\beta$. In serum, excessive Zn significantly decreased the levels of IL-2 and interferon (IFN)-${\gamma}$ compared with those in controls, whereas indomethacin significantly enhanced the excessive Zn-decreased levels of IFN-${\gamma}$ but did not affect the Zn-decreased levels of serum IL-2. In splenic supernatants, All of excessive Zn, indomethacin, and combination of Zn and indomethacin significantly enhanced IL-2 levels compared with those in controls, but indomethacin didn't affect the Zn-induced production of IL-2. These data, therefore, suggest that indomethacin significantly attenuated the in vivo and ex vivo IL-1$\beta$ production increased by excessive zinc and remarkedly enhanced the in vivo excessive zinc-suppressed production of IFN-${\gamma}$ but not IL-2.

• Applied Science and Convergence Technology
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• v.24 no.5
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• pp.151-155
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• 2015

The interfacial electronic structure between zinc phthalocyanine (ZnPc) and aluminumdoped zinc oxide (AZO) substrates has been evaluated by ultraviolet photoemission spectroscopy and angle-dependent x-ray absorption spectroscopy to understanding the molecular orientation of a ZnPc layer on the performance of small molecule organic photovoltaics (OPVs). We find that the ZnPc tilt angle improves the ${\pi}-{\pi}$ interaction on the AZO substrate, thus leading to an improved short-circuit current in OPVs based on phthalocyanine. Furthermore, the molecular orientation-dependent energy level alignment has been analyzed in detail using ultraviolet photoemission spectroscopy. We also obtained complete energy level diagrams of ZnPc/AZO and ZnPc/indium thin oxide.

• Bulletin of the Korean Chemical Society
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• v.30 no.6
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• pp.1401-1404
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• 2009