• Journal of Environmental Health Sciences
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• v.27 no.2
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• pp.82-91
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• 2001

This study was carried out to elucidate the protective effect of zinc chloride(ZnCl$_2$) and its mechanism against the immuno-cytotoxicity of methylmercury chloide($CH_3$HgCl). This study was observed in the culture of EMT-6 cells which are originated from mammary adenocarcinoma of Balb/c mouse. Cytotoxicity of metals was measured by cell viability and NO$_2$$^{[-10]}$ , and mitochondrial function was evaluated by adenosine triphosohate (ATP) production. $CH_3$HgCl significantly decreased the sythesis of nitric oxide(NO), ATP and glutathione(GSH) in a dose-dependent manner. ZnCl$_2$ significantly increased the synthesis of GSH in a dose-dependent manner, but synthesis of NO and ATP were not changed. The immuno-cytotoxicity of $CH_3$HgCl was not fully protected when combined addition of ZnCl$_2$, whereas ZnCl$_2$ prior to addition of $CH_3$HgCl completly protected the Hg-induced immuno-cytotoxicity. Similarly, intracellular accumulation of mercury significantly decreased by ZnCl$_2$. Degree of diminution of intracellular mercury was larger in ZnCl$_2$ prior to addition of $CH_3$HgCl than in combined addition of ZnCl$_2$ and $CH_3$HgCl.. Dithiothreitol(DTT) or buthionine sulfoximine(BSO) addition at 50$\mu$M or less, which was not toxic to the cells, did not affect synthesis of NO and ATP. DTT increased intracellular GSH level and DTT pretreatment protected toxicity induced by $CH_3$HgCl as shown complete recover in the NO and ATP values. BSO decreased intracellular GSH level and BSO pretreatment exaggerated toxicity induced by $CH_3$HgCl as shown synergistic reduction in the NO and ATP values. These results indicated that the protective effects of zinc against immuno-cytotoxicity of methylmercury associated with increasing cellular level of GSH. Increased intracellular GSH transports methylmercury to out of cells. In accordance with intracellular level of mercury decreased, immuno-cytotoxicity of methylmercury decreased. These result also suggest that the protective mechanism of zinc against the mercury toxicity would be exerted in the immune system in vivo.

• Environmental Analysis Health and Toxicology
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• v.22 no.2 s.57
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• pp.171-175
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• 2007

Indigenous species means a species that is likely, due to historical presence, to occur at a specified site for some portion of its life span. Therefore, indigenous species can be useful as an indicator to assess environmental risk caused by hazardous chemicals in a specific site. So far a few toxicity studies using freshwater species which are indigenous to Korea have been carried out. In this study, a freshwater shrimp (Neocardina denticulata) indigenous to Korea was used for acute toxicity test of heavy metals. Neocardina denticulata were exposed to cadmium chloride $(CdCl_2)$, copper chloride $(CuCl_2)$ and zinc chloride $(ZnCl_2)$ using automatic flow-through system for 96 hours. The 96h LC50s were calculated as 0.043 $(0.042{\sim}0.045)mg\;CdCl_2/L,\;0.104(0.098{\sim}0.113)mg\; CuCl_2/L\;and\;2.021\;(1.633{\sim}2.594)mg\;ZnCl_2/L$. When compaired with some international standard species such as medaka(Oryzias latipes), Neocardina denticulata had high sensitivity. Therefore, this study suggested that Neocardina denticulata have possibilities for a sensitive test species to test heavy metal toxicity in aqua-system.

• Korean Journal of Environmental Biology
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• v.30 no.2
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• pp.128-135
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• 2012

The individual toxicity of lead (Pb) and zinc (Zn) has been investigated by using the sea urchin (Hemicentrotus pulcherrimus) germ cell and pluteus-larvae. The gametotoxic and embryotoxic effects of Pb and Zn on H. pulcherrimus were each investigated at 31, 63, 125, 250, 500 ppb and 16, 31, 63, 125, 250 ppb, respectively. Spawning was induced by 0.5 M KCl solution and the fertilization and normal embryogenesis rates test were performed for 10 min and 64 h after fertilization, respectively. In exposure to Pb, the fertilization rate was not significantly changed compared with control but normal embryogenesis rate was significantly decreased with concentration dependent manner. Fertilization and normal embryogenesis rates showed a significant decreased with concentration dependent manner in exposed to Zn. The normal embryogenesis rates were significantly inhibited in exposed to Pb ($EC_{50}$=45.13 ppb, 95% Cl=40.12~50.05 ppb) and Zn ($EC_{50}$=19.82 ppb, 95% Cl=18.26~21.31 ppb). In exposure to Pb and Zn, the NOEC of normal embryogenesis rate was <31.25 and <15.63 ppb, respectively. The LOEC showed each 31.25 and 15.63 ppb in exposed to Pb and Zn. These results suggest that the early embryo development of H. pulcherrimus is highly sensitive to heavy metals such as Pb and Zn, H. pulcherrimus can be used as a test organism for risk assessment in marine ecosystems.

• Transactions of the Korean hydrogen and new energy society
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• v.28 no.4
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• pp.419-425
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• 2017

In this study, an efficient dye-sensitive solar cells (DSSC) was developed after post-treatment of ZnO on $TiO_2$ photoelectrode. The $TiO_2$ electrode with ZnO post treatment was prepared with Titanium isoporopoxide in Zinc Nitrate Hexahydrate aqueous solution by incineration for 30 min at $450^{\circ}C$. The ZnO-post treated $TiO_2$ electrode showed strong dispersion force between particles in relation to the control $TiO_2$, referring high specific surface area and dye-adsorption rate. Proper addition of ZnO enhanced electron mobility and reduced internal resistance and electron recombination. Light conversion efficiency of DSSCs containing the ZnO-posttreated $TiO_2$ electrode increased 35.4% when compared to the DSSCs using $TiO_2$ electrode. It is similar to the DSSCs with $TiCl_4$ post treatment $TiO_2$ electrode. Increasing of light conversion efficiency was due to high specific surface area and dispersion force, and low dye-adsorption rate and electron recombination. Taken together, ZnO may be used as posttreatment of photoelectrode and replaced $TiCl_4$ that has high toxicity and causticity.

• KOREAN JOURNAL OF CROP SCIENCE
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• v.44 no.2
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• pp.163-165
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• 1999

The study was conducted to find the critical concentrations of zinc toxicity and to determine the changes of the contents of free proline and organic acids with treatment of different zinc chloride concentrations during rice germination and seedlings grown for seven days. The concentration of zinc chloride, 140 ppm, inhibited root elongation as much as 46 times compared with the control, and the germination rate was also decreased in all treatments of zinc chloride, showing that the germination rate decreased more with increasing concentrations of zinc chloride. Its rate was only 13% with treatment of 140 ppm zinc chloride. The content of free proline with treatment of zinc chloride, 140 ppm, was highest about 4,873 $\mu$M at 3 days compared with the control. Malic acid concentration with treatment of zinc chloride, 140 ppm, increased to approximately 4 times compared to the control. Citric and succinic acid content were also slightly increased in all treatments of zinc chloride.

• Korean Journal of Soil Science and Fertilizer
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• v.48 no.5
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• pp.397-403
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• 2015

Heavy metals reduce the photosynthetic efficiency and disrupt metabolic reactions in a concentration-dependent manner. Moreover, by replacing the metal ions in metalloproteins that use essential metal ions, such as Cu, Zn, Mn, and Fe, as co-factors, heavy metals ultimately lead to the formation of reactive oxygen species (ROS). These, in turn, cause destruction of the cell membrane through lipid peroxidation, and eventually cause the plant to necrosis. Given the aforementioned factors, this study was aimed to understand the physiological responses of rice to cadmium (Cd) and arsenic (As) toxicity and the effect of essential metal ions on homeostasis. In order to confirm the level of physiological inhibition caused by heavy metal toxicity, hydroponically grown rice (Oryza sativa L. cv. Dongjin) plants were exposed with $0-50{\mu}M$ cadmium (Cd, $CdCl_2$) and arsenic (As, $NaAsO_2$) at 3-leaf stage, and then investigated malondialdehyde (MDA) contents after 7 days of the treatment. With increasing concentrations of Cd and As, the MDA content in leaf blade and root increased with a consistent trend. At 14 days after treatment with $30{\mu}M$ Cd and As, plant height showed no significant difference between Cd and As, with an identical reduction. However, As caused a greater decline than Cd for shoot fresh weight, dry weight, and water content. The largest amounts of Cd and As were found in the roots and also observed a large amount of transport to the leaf sheath. Interestingly, in terms of Cd transfer to the shoot parts of the plant, it was only transported to upper leaf blades, and we did not detect any Cd in lower leaf blades. However, As was transferred to a greater level in lower leaf blades than in upper leaf blades. In the roots, Cd inhibited Zn absorption, while As inhibited Cu uptake. Furthermore, in the leaf sheath, while Cd and As treatments caused no change in Cu homeostasis, they had an antagonist effect on the absorption of Zn. Finally, in both upper and lower leaf blades, Cd and As toxicity was found to inhibit absorption of both Cu and Zn. Based on these results, it would be considered that heavy metal toxicity causes an increase in lipid peroxidation. This, in turn, leads to damage to the conductive tissue connecting the roots, leaf sheath, and leaf blades, which results in a reduction in water content and causes several physiological alterations. Furthermore, by disrupting homeostasis of the essential metal ions, Cu and Zn, this causes complete heavy metal toxicity.

• Environmental Analysis Health and Toxicology
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• v.19 no.2
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• pp.191-200
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• 2004

Zinc (Zn) is an essential element in biological process, however inadequate Zn status in general population have been recognized. To update the knowledge for Zn-cadmium (Cd) interaction, we studied the intestinal uptake and transport, and the expression of metal transporter proteins (divalent metal transporter 1, DMT1 ; metal transporter protein 1, MTP1 ; zinc transporter 1, ZnTl ; metallothionein 1 , MT1) in duodenum after Cd exposure using Zn deficient animal model. Rats were led Zn deficient (ZnD, 0.5-1.0 mgZn/kg) or Zn supplemented (ZnS, 50mg Zn/kg) diet for 4 weeks, and followed single administration of $^{109}$ CdCl$_2$orally. The body Zn flatus and tissue Cd concentration were determined at 24 hrs after Cd administration. Total body burden of Cd and Cd absorption index (AI, %) were estimated based on the tissue Cd analyzed. DMT1, MTP1, ZnTl and MT1 mRNA were analyzed by using RT-PCR method. Feeding of Zn deficient diet for 4 weeks produced a reduced body weight gain and a depletion of body Zn. Tissue Cd concentration, body burden of Cd and Cd absorption index were higher in the ZnD diet fed rats than the ZnS diet red rats. Especially, Cd concentration in the small intestine (duodenum, jejunum and ileum) and the colon of FeD diet fed rats were higher markedly than in the FeS diet group. The expression levels of DMT1, MTP1 and ZnT1 mRNA in FeD diet fed rats were similar to the FeS diet. The level of MT1 mRNA expression was significantly lower in the FeD than the FeS diet fed rats. Taken together, theses results indicate that Zn deficiency in diet induce an increased intestinal absorption and tissue retention of Cd, and down -regulate the MT1 expression in the intestine which might be play a part of role in Cd absorption and transport in mammalian. These findings suggest that deficiency of essential metal could be enhanced the toxicity of toxic, non-esstial metals through the metal-metal interaction.

• Korean Chemical Engineering Research
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• v.50 no.2
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• pp.217-222
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• 2012

The synthesis of dimethyl carbonate(DMC) is a promising reaction for the use of naturally abundant carbon dioxide. DMC has gained considerable interest owing to its versatile chemical reactivity and unique properties such as high oxygen content, low toxicity, and excellent biodegradability. In this study, the synthesis of DMC through the transesterification of ethylene carbonate(EC) with methanol was investigated by using ionic liquid and metal oxide catalysts. The screening test of different catalysts revealed that choline hydroxide ([Choline][OH]) and 1-n-butyl-3-methyl imidazolium hydroxide([BMIm][OH]) had better catalytic performance than metal salts catalysts such as MgO, ZnO and CaO. The effects of reaction parameters such as reaction temperature, MeOH/EC mole ratio, and carbon dioxide pressure on the reactivity of [Choline][OH] catalyst were discussed. High temperature and high MeOH/EC mole ratio were favorable for high conversion of EC. However, the yield of DMC showed a maximum when carbon dioxide pressure was 1.34 MPa, and then it decreased for higher carbon dioxide pressure. Zinc chloride($ZnCl_2$) was used as co-catalyst with the ionic liquid catalyst. The mixed catalyst showed a synergy effect on the EC conversion and DMC yield probably due to the acid-base properties of the catalysts.

• Journal of Preventive Medicine and Public Health
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• v.24 no.3 s.35
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• pp.287-304
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• 1991

Tolerance to several toxic effects of cadmium, including lethality has been shown following pretreatment with cadmium and zinc. This study was designed to determine if tolerance also develops to Cd-induced hepatotoxicityandrenaltoxicity. Three groups of rats (A, B, C), each consisting of 16 rats, were studied and each group was divided into four subgroups (1, 2, 3, 4), 4 rats for each subgroup. Rats were subcutaneously pretreated with saline (A), $CdCl_2$ (0.5 mg/kg, B), and $ZnCl_2$ (13.0 mg/kg, C) during time periods of $1{\sim}6$ weeks. At the end of the period, rats were challenged with $CdCl_2$ (3.0, 6.0 and 9.0 mg/kg, ip). After giving the challenge dose, cadmium and metallothionein (MT) concentrations were determined and also observed the histologic change in liver and kidney. The concentration of cadmium in liver and kidney increased dose-dependently to the challenge dosage. These da indicate the kidney is a major target organ of chronic cadmium poisoning, and suggest that cadmium induced hepatic injury, via release of Cd-MT, may play an important role in the nephrotoxicity observed in response to long-term exposure to cadmium. In addition, histologic examination of group $A_2,\;A_3\;and\;A_4$ revealed moderate to severe cadmium toxicity, evidenced by infiltration of inflammatory cells, cell swelling, pyknosis, enlarged sinusoids and necrosis in liver, and tubule cell necrosis and degeneration in kidney. However, MT concentrations in liver and kidney were increased by the pretreatment of $CdCl_2$ and $ZnCl_2$, and their morphological findings were not significantly changed, comparing with control group. Higher MT concentration in liver and kidney observed in the pretreated groups constitutes a plausible explanation of the protective effects of pretreatment against the cadmium toxicity after challenge dosing.

• Journal of Environmental Health Sciences
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• v.21 no.3
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• pp.1-15
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• 1995

Tolerance to toxic effects of cadmium(Cd), including lethality has been shown following pretreatment with cadmium and zinc. This study was designed to determine if tolerance also develops to Cd-induced hepatotoxicity and renal toxicity. Three groups of rats(A, B, C), each consisting of 52 rats, were studied and each group was divided into three subgroups(1,2,3), 28 rats for each subgroup. Rats were subcutaneously pretreated with saline(A), $CdCl_2$(0.5 mg/kg, B), and $ZnCl_2$(13.0 mg/kg, C) during time periods of 5 days. At the end of the period, rats were challenged with $CdCl_2$(3.0 and 6.0 mg/kg) by intraperitoneal injection. As for the cadmium levels in rat tissues after 1,3,5,6 days of pretreatments, it was highest in the liver. Then kidney, heart, blood and muscle followed it in that order. After 24, 48 and 96 hours of intraperitoneal injection by challenge doses the concentration of cadmium in liver and kidney increased proportionally to the increase of challenge dosage. However metallothioneins in liver and kidney were increased by the pretreatment of cadmium and zinc. These data indicate the liver is a major target-organ of acute Cd poisoning, and suggest that cadmium induced hepatic injury, via release of Cd-MT, may play an important role in the nephrotoxicity observed in response to short-term exposure to cadmium. This result suggest that increasing cadmium concentrations, gradually accumulating in liver and kidney as the result of the pretreatment, served to induce the synthesis of metallothionein, thus making them resistant to the challenge from cadmium.