• Animal cells and systems
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• v.15 no.3
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• pp.181-187
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• 2011

Transient receptor potential vanilloid type 1 (TRPV1) receptor plays an important role as a molecular detector of noxious signals in primary sensory neurons. Activity of TRPV1 can be modulated by the change in the environment such as redox state and extracellular cations. In the present study, we investigated the effect of the mercury chloride ($HgCl_2$) on the activity of TRPV1 in rat dorsal root ganglia (DRG) neurons using whole-cell patch clamp technique. Extracellular $HgCl_2$ reversibly reduced the magnitudes of capsaicin-activated currents ($I_{cap}$) in DRG neurons in a dose-dependent manner. The blocking effect of $HgCl_2$ was prevented by pretreatment with the reducing agent dithiothreitol (DTT). Inhibition of $I_{cap}$ by $HgCl_2$ was abolished by point mutation of individual cysteine residues located on the extracellular surface of TRPV1. These results suggest that three extracellular cysteines of TRPV1, Cys616, Cys634 and Cys621, are responsible for the oxidative modulation of $I_{cap}$ by $HgCl_2$.

• Korean Journal of Veterinary Research
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• v.43 no.4
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• pp.641-648
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• 2003

Changes of plasma DNA contents and serum biochemical values were measured in rats administered with $HgCl_2$ to investigate the in vivo cytotoxic effects of mercury and examine the usefulness of these changes as indicators of mercury exposure and diagnosis of mercury poisoning. Rats were given once intraperitonealy $HgCl_2$(0.13. 0.32. 0.8 and 2 mg/kg b.w) and the changes of plasma DNA contents and serum biochemical values were measured at the time of 2, 4, 8, 24, 48 and 72 hours after the administration of $HgCl_2$. Plasma DNA contents began to increase from 2 hours after the administration of $HgCl_2$ in all the treatment groups significantly compared to control with dose-dependent pattern. The levels of plasma DNA reached to peak at 48 hours as 2.77, 7.60, 15.46 and 16.51 times higher than control in each treatment group of 0.13, 0.32, 0.8 and 2 mg/kgb.w, respectively and remained to be higher until 72 hours after the administration. The values of creatine kinase, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, blood urea nitrogen and glucose of serum were increased, however the values of alkaline phosphatase, total protein and triglyceride were decreased. These changes of increase and decrease showed dose-dependent pattern but the starting time, maintenance and magnitude of change were various and characteristic according to serum biochemical indices. Among the changes of serum biochemical values, those of aspartate aminotransferase, lactate dehydrogenase and blood urea nitrogen were apparently and significantly increased compared to control from 2 to 72 hours by the administration of 2 mg/kg $HgCl_2$. This study demonstrates that plasma DNA and serum biochemical values such as aspartate aminotransferase, lactate dehydrogenase, blood urea nitrogen and etc. are valuable as biomarkers for mercury exposure assessment and diagnosis of mercury poisoning.

• Journal of Plant Biology
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• v.36 no.3
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• pp.195-201
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• 1993

The room temperature fluorescence induction of chloroplasts was utilized as a probe to locate the site of inhibition by mercury, copper and zinc on PS II by mercury. Inhibitory effect of Hg2+ on electron transport activity was notable as compared with Cu2+ and Zn2+. At concentrations of HgCl2 over 50 $\mu$M, activities of PS II and whole-chain electron transport decreased more than 70%, while that of PS I decreased about 10~30%. This suggests that PS II is more susceptible to Hg2+ than PS I is. In the presence of diphenylcarbazide (DPC), 50 $\mu$M HgCl2 inhibited the reduction of dichlorophenolindophenol (DCPIP) about 50%. Addition of heavy metals induced marked decrease in maximal variable fluorescence/initial fluorescence [(Fv)m/Fo], but no changes in Fo. With various concentrations of heavy metals, changes of chlorophyll a fluorescence emitted by PS II showed gradual decrease in photochemical quenching (qQ), which indicates an increase in reduced state of electron acceptor, QA. Especially, the addition of HgCl2 caused a notable decrease of qQ. In the presence of 50 $\mu$M CuCl2, energy-depended quenching (qE) was completely reduced, whereas in the presence of 50 $\mu$M CuCl2 and ZnCl2 it was still remained. The above results are discussed on the effects of mercury in relation to water-splitting system and plastoquinone (PQ) shuttle system.

• Journal of the Korean Chemical Society
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• v.31 no.6
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• pp.534-541
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• 1987

The study of reaction mechanism for the substitution of ethylenediamine (en) for Cl and Hedta from $[CoCl(Hedta)]^-$ in the presence of $Hg^{2+}$ ion was carried out by uv and CD spectra. From the kinetic data, we proposed that the first ethylenediamine be substituted through the associative reaction path by means of interaction of $Hg^{2+}$ ion with Co(III), and that the second and the third ethylenediamine be substituted stepwise. From the optical purities of $[Co(en)_3]^{3+}$ which was formed after reaction, we suggested the critical stereochemical step and new substitution reaction paths.

• Korean Journal of Environmental Agriculture
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• v.24 no.2
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• pp.146-152
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• 2005

The objective of present study was to investigate the effect of onion extracts on mercuryinduced cytotoxicity, lipid peroxidation and antioxidant enzyme activities in primary monolayer cultures of rat hepatocytes. Primary cultures of rat hepatocytes were incubated for 6 hr in the presence of various concentrations (0, 1, 5, 10, 30 or 50 ppm) of $HgCl_2$. Cytotoxicity and cell viability were determined by measuring glutamic oxaloacetic transaminase (GOT) activity, lactate dehydrogenase (LDH) activity and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) value. Lipid peroxidation w as evaluated using thiobarbituric acid reactive substances (TBARS) assay. Effects of onion extract on antioxidant system were determined by measuring catalase, glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Rd) activities as well as DPPH free radical scavenging activity. $HgCl_2$ at the concentration of 10 ppm increased GOT activity and TBARS concentration but decreased %MTT reduction, whereas $HgCl_2$ at the concentration of 30 ppm increased LDH activity, representing that $HgCl_2$ caused cytotoxicity and lipid peroxidation in dose-dependent manner, $HgCl_2$ at the concentration of 30 ppm significantly decreased catalase, GSH-Px and GSH-Rd activities. When primary cultures of rat hepatocytes were incubated with various concentrations (0, 0.01, 0.05, 0.1 or 0.3 mg/ml) of onion extract for 6 hr in the presence of 30 ppm of $HgCl_2$, onion extracts at the concentration of 0.05 mg/ml decreased GOT activity, but increased %MTT reduction by 30 ppm of $HgCl_2$. $HgCl_2-induced$ LDH activity and TBARS concentration were decreased by onion extract at the concentration of 0.01 mg/ml. Taken together, onion extract prevented H$HgCl_2-induced$ hepatocyte injury and lipid peroxidation. Onion extracts at the concentration of 0.1 mg/ml almost or completely inhibited $HgCl_2-induced$ catalase and GSB-Px activities. GSH-Rd activity, however, was not affected by onion extract. Free radical scavengjing activity was increased as concentration of onion extract increased. Onion extract at the concentrion of 5 mg/ml possesed mote than 93% scavenging activity comparing to 100% radical scavenging activity by pyrogallol solution as a reference. These results demonstrate that onion extracts suppressed mercury-induced cytoctoxicity and lipid peroxidation by scavenging free radical and increasing catalase and GSH-Px activities.

• Journal of Preventive Medicine and Public Health
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• v.39 no.3
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• pp.199-204
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• 2006

Objectives: Mercury is a hazardous organ-specific environmental contaminant. It exists in a wide variety of physical and chemical states, each of which has unique characteristics for the target organ specificity. Exposure to mercury vapor and to organic mercury compounds specifically affects the CNS, while the kidney is the target organ for inorganic Hg compounds. Methods: In this study, mercury chloride $(HgCl_2)$ was studied in a renal derived cell system, i.e., the tubular epithelial Madin-Darby canine kidney (MDCK) cell line, which has specific sensitivity to the toxic effect of mercury. MDCK cells were cultured for 6-24 hr in vitro in various concentrations (0.1-100 M) of $HgCl_2$, and the markers of apoptosis or cell death were assayed, including DNA fragmentation, caspase-3 activity andwestern blotting of cytochrome c. The influence of the metal on cell proliferation and viability were evaluated by the conventional MTT test. Results: The cell viability was decreased in a time and concentration dependent fashion: decreases were noted at 6, 12 and 24 hr after $HgCl_2$, exposure. The increases of DNA fragmentation were also observed in the concentrations from 0.1 to 10 M of $HgCl_2$ at 6 hr after exposure. However, we could not observe DNA fragmentation in the concentrations more than 25 M because the cells rapidly proceeded to necrotic cell death. The activation of caspase-3 was also observed at 6 hr exposure in the $HgCl_2$ concentrations from 0.1 to 10 M. The release of cytochrome c from the mitochondria into the cytosol, which is an initiator of the activation of the caspase cascade, was also observed in the $HgCl_2-treated$ MDCK cells. Conclusions: These results suggest that the activation of caspase-3 was involved in $HgCl_2-induced$ apoptosis. The release of cytochrome c from the mitochondria into the cytosol was also observed in the $HgCl_2-treated$ MDCK cells. These findings indicate that in MDCK cells, $HgCl_2$ is a potent inducer of apoptosis via cytochrome c release from the mitochondria.

• Journal of the Korean Chemical Society
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• v.55 no.1
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• pp.38-45
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• 2011

The complexation behavior of the $\alpha$-ketostabilized phosphorus ylides $Ph_3P$=CHC(O) $C_6H_4-X$ (X=Br, Ph) towards the transition metal ions mercury (II) and Silver (I) was investigated. The mercury(II) complex {$HgX_2$ [Y]} 2 ($Y_1$=4-bromo benzoyl methylene triphenyl phosphorane; X=Cl(1), Br(2), I(3), $Y_2$=4-phenyl benzoyl methylene triphenyl phosphorane; X=Cl(4), Br(5), I(6)) have been prepared from the reaction of $Y_1$ and $Y_2$ with $HgX_2$ (X=Cl, Br, I) respectively. Silver complexes [$Ag(Y_2)_2]$ X(X=$BF_4$(7), OTf(8)) of the $\alpha$-keto-stabilized phosphorus ylides ($Y_2$) were obtained by reacting this ylide with AgX (X=$BF_4$, OTf) in $Me_2CO$. The crystal structure of complexes (1) and (4) was discussed. These reactions led to binuclear complexes C-coordination of ylide and trans-like structure of complexes $[Y_1HgCl_2]_2$. $CHCl_3$ (1) and $[Y_2HgCl_2]_2$ (4) is demonstrated by single crystal X-ray analyses. Not only all of complexes have been studied by IR, $^1H$ and $^{31}P$ NMR spectroscopy, but also complexes 1-3 have been characterized by $^{13}$CNMR.

• Journal of the Korean Chemical Society
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• v.63 no.3
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• pp.160-165
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• 2019

A series of reactions between an amino alcoholic ligand, cis-2-((2-((2-hydroxyethyl)amino)ethyl)amino)cyclohexan-1-ol (HEAC), with the mixtures of group 12 metals including, $HgCl_2/CdCl_2$, $HgCl_2/CdI_2$, $ZnCl_2/CdCl_2$ and $ZnCl_2/CdCl_2/HgCl_2$ was experimentally and theoretically studied to determine the most stable product of these reactions. Furthermore, the Cambridge Structural Database (CSD) studies were done to evaluate the theoretical results. The products were characterized by elemental analysis, FT-IR, Raman, $^1H$ NMR spectroscopy and single-crystal X-ray diffraction. Based on these investigations a binuclear structure of cadmium, [$Cd_2(HEAC)_2({\mu}-Cl)_2Cl_2$] (1), is the most stable product that was formed in all studied reactions between HEAC and metals mixtures. In this structure, the cadmium atom has a $CdN_2O({\mu}-Cl)_2Cl$ environment and distorted octahedral geometry.

• Journal of Preventive Medicine and Public Health
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• v.25 no.1 s.37
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• pp.13-25
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• 1992

This study was conducted to investigate the mechanism of protective effect by sodium selenite in methylmercuric chloride neurotoxicity, increasing intracellular $Ca^{2+}$concentration of the neuron. Methylmercuric chloride of 3mg/kg of body weight was administered simultaneously with sodium selenite of 5mg/kg and pretreatment of sodium selenite via intraperitoneal injection to rats. Also, effect of methylmercuric chloride($25{\mu}M,\;50{\mu}M,\;100{\mu}M$) and sodium selenite($200{\mu}M$) on free intrasynaptosomal $Ca^{2+}$ concentration were studied using the fluorescent $Ca^{2+}$ indicator fura -2 in vitro. After the treatment, at 6, 24, and 48 hours later, mercury in the cerebral cortex, liver and kidney tissues, succlnic dehydrogenase activities, adenosin-5'-triphosphate concentration, acetylcholinesterase activities, and intracellular $Ca^{2+}$ concentration in the cerebral cortex were determined in vivo. Cerebral synaptosomes of rats were incubated with methylmercuric chloride and sodium selenite in Hepes buffer for 10 minutes and free intrasynaptosomal $Ca^{2+}$ concentration were measured with fura-2 in vitro. The results were summarized as follows ; 1. The combined administration of $CH_3HgCl$ and $Na_2SeO_3$ and pretreatment of $Na_2SeO_3$ according to time significantly more increased in the cerebral cortex and decreased in the liver, kidney mercury concentrations compared to the administration of $CH_3HgCl$ only. 2. The combined administration of $CH_3HgCl$ and $Na_2SeO_3$ and pretreatment of $Na_2SeO_3$ increased more succinic dehydrogenase and acetylcholinesterase activities compared to the administration of $CH_3HgCl$ only. Particularly pretreatment of $Na_2SeO_3$ significantly more compared to the administration of $CH_3HgCl$ only. The concentration of adenosine-5'-triphosphate in $Na_2SeO_3$ treatment groups revealed a favourable effect compared to the administration of $CH_3HgCl$ only. 3. Intracellular $Ca^{2+}$ concentration in administration of $CH_3HgCl$ only was increased significantly more than control group in all test hours but was increased significantly more at 48 hours only after treatment in combined administration of $CH_3HgCl$ and $Na_2SeO_3$ and pretreatment of $Na_2SeO_3$ according to time interval more decreased significantly intracellular $Ca^{2+}$ concentration compared to the administration of $CH_3HgCl$ only. 4. Free intrasynaptosomal $Ca^{2+}$ concentration in the combined administration of $CH_3HgCl$ and $Na_2SeO_3$ was decreased ($24%{\sim}40%$) significantly more than the administration of $CH_3HgCl$ only. From the above results, the specific dosage of $Na_2SeO_3$ decreased increment of intracellular $Ca^{2+}$ concentration induced by administration of $CH_3HgCl$. These findings suggest the protective mechanism of $Na_2SeO_3$ on the neurotoxicity of $CH_3HgCl$.

• Journal of the Korean Chemical Society
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• v.37 no.11
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• pp.951-960
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• 1993

$Hg^{2+}$-induced aquation trans-[Co(3,2,3-tet)$X_2]^+$(3,2,3-tet = 4,7-diazadecane-1,10-diamine, $X_2\;=\;Cl_2,\;(NO_2)Cl,\;Br_2,\;(NO_2)Br,\;(NO_3)_2)$ complexes was investigated in aqueous solution. The products and the reaction mechanism were confirmed by chromatography, UV/Vis. spectrum, and circular dichroism (CD) spectrum. From the results, $Hg^{2+}$-induced aquation of 3,2,3-tet system has been produced cis-${\beta}$ complex via trans complex. The kinetic studies on $Hg^{2+}$-induced aquation of trans-[Co(3,2,3-tet)$Cl_2]^+$ complex and trans-[Co(3,2,3-tet)$(NO_2)Cl]^+$ complex were also carried out to study the reaction mechanism. The results show that trans-[Co(3,2,3-tet)$Cl_2]^+$ complex undergoes the D(dissociative)-mechanism and trans-[Co(3,2,3-tet)$(NO_2)Cl]^+$ complex $I_d$(interchange dissociavite)-mechanism. In order to confirm steric course for the reaction mechanism, $Hg^{2+}$-induced aquation on trans-[Co(R,R-3,2,3-tet)$Cl_2]^+$ complex to which chiral R,R-3,2,3-tet was coordinated instead of the racemic(R,R:S,S) 3,2,3-tet was used has been examined by CD spectrum. From the results, the final complex was confirmed to be ${\Delta}-cis-{\beta}$-[Co(R,R-3,2,3-tet)$(OH_2)_2]^{3+}$ complex indicating the chirality was retained through whole process.