• Biomedical Science Letters
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• v.12 no.4
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• pp.451-455
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• 2006

It is demonstrated that inorganic mercury has cytotoxic effect on glial cells. Recently, oxygen radicals is involved in methylmercuric chloride (MMC)-induced cytotoxicity. But, the toxic mechanism of MMC is left unknown. The purpose of this study was to examine the cytotoxicity of MMC on $C_6$ glioma cells. The cytotoxicy was measured by cell viability using XTT assay in $C_6$ glioma cells. Colorimetric assay is regarded as a very sensitive screening method for the determination of the cell viability on various agents. In this study, MMC decreased cell viability according to the dose- and time dependent manners after $C_6$ glioma cells were grown with various concentrations of MMC for 48 hours. In the protective effect of allopurinol on MMC-induced cytotoxicity, allopurinol was effective in the prevention of MMC-induced cytotoxicity in these cultures. These results suggest that MMC has highly cytotoxic effect on $C_6$ glioma cells by the decrease of cell viavility, and free radical scavenger such as allopurinol was effective on organic mercury-induced cytotoxicity in these cultures.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.3
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• pp.738-741
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• 2003

In order to evaluate the cytotoxicity of methylmercuric chloride(MMC) in cultured spinal motor neurons of neonatal mouse, cell viability was measured by MTT assay in spinal motor neurons treated with 1-30 μM MMC for 48 hours. And also, the protective effect of Radix Polygoni Multiflori(RPM) was examined by cell viability in these cultures. Cell viability was significantly decreased in dose-dependent manner after cultured cells were exposured to 20 μM MMC for 48 hours. Protective effect of RPM on MMC-mediated toxicity was very effective in these cultures. From above the results, it suggests that MMC has toxic effect in cultured mouse spinal motor neurons and herb extract such as RPM is very effective in blocking the neurotoxicity induced by MMC.

• Toxicological Research
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• v.7 no.1
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• pp.73-81
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• 1991

The present study was performed to explore the antioxidant effect of selenium on damaged brain induced by organic mercury. Male ICR mice were given consecutively 7 injections for 7 days of : (I) sodium selenite 1 mg/kg s.c. alone, (2) methylmercuric chloride 10mg/kg s.c. alone, (3) methylmercuric chloride simultaneously in combination with sodium selenite, and (4) saline alone as control respectively. Based on the above protocol, we monitored various oxyradical scavenging system as well as the finding of electron microscopy. The results from brain tissues were as follows` 1. Selenium inhibited the rate of generation of superoxide radical.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.5
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• pp.1231-1234
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• 2003

To clerify the toxic effect of methylmercuric chloride(MMC) in cultured mouse myocardial cells, cytotoxic effect was measured by MTT assay after cultured myocardial cells were incubated for 48 hours in the media containing 1～30 uM concentrations of MMC. And also, the protective effect of Benincasae Semen (BS) was assessed in these cultrures. Cell viability was significantly decreased in a dose-dependent manner after cultured myocardial cells were exposed to 30 uM MMC for 48 hours. In the neuroprotective effect of BS on MMC-induced cytotoxicity, BS blocked the MMC-induced myotoxicity in these cultures. From these results, it suggests that MMC is toxic on cultured mouse myocardial cells and BS is effective in blocking the neurotoxicity induced by MMC.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.4
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• pp.764-767
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• 2002

To evaluate the osteotoxic effect of methylmercuric chloride(MMC) on cultured mouse osteoblasts, cytotoxic effect was measured by MTT assay after cultured mouse osteoblasts were incubated with various concentrations of MMC for 20 hours. The protective effect of Flos Carthami(FC) against MMC-induced osteotoxicity was also examined in these cultures. MMC decreased cell viability of cultured mouse osteoblasts remarkably in a dose- and time-dependent manners. In protective effect of FC was remarkably effective in blocking the osteotoxicity induced by MMC. From aboved the results, it is suggested that MMC induce osteotoxicity, and the selective herba extract such as FC is very effective in blocking MMC-mediated neurotoxicity on cultured mouse osteoblasts.

• Journal of Environmental Health Sciences
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• v.27 no.2
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• pp.73-81
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• 2001

The purpose of this study was to determine the adverse effects of methylmercuric chloride(MMC) against the fetal growth and the ossification rate of fetal pectoral and pelvic girdle, stermebrae, ribs and tail in pregnant Fischer 344 rats administered orally on day 7 of gestation. The resulted obtained are as follows. The weight and size of fetus were highly reduced by MMC. The reduction of fetal weight and size were 16. 2%~24.5%(p<0.01), and 34.1%~48.8%(p<0.01), and that of the litter’s weight were 67.0%(p<0.01) and 89.2%(p<0.01) by 20 and 30mg/kg MMC, respectively. Ossification centers were never formed in pectoral and pelvic phalanges and sternebrae, and was reduced as much as 70% in tail by 30mg/kg MMC. And also those were 82.4%~ 91.2%(p<0.01) in ischium, and 52.4~66.7%(p<0.01) in the others(ilium, fenur, tibia, fibula, metatarsals)of pelvic girdle by 30 mg/kg MMC. Ossification of sternebrae was terrible. 5th bone of sternebrae was not ossificated by 20 and 30 mg/kg MMC(p<0.01), and 2nd was also not ossificated by 30 mg/kg MMC(p<0.01).And reduction of ossification rate was 84.8~97.8%(p<0.01) in the others of sternebrae by 30 mg/kg MMC. And then, the reduction of ossification rate was 26.65~49.8%(p<0.01) in fetal ribs by 30 mg/kg MMC, and they were trend to increased as following from center to each edge. In conclusion, it was observed that fetal weight, size, and ossification of each bone were highly significantly reduced by the increased dosage of MMC.

• 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 Korean Society of Occupational and Environmental Hygiene
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• v.4 no.1
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• pp.43-70
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• 1994

The effects of potassium chromate (500ppm/500ppm), potassium dichromate (500ppm/500ppm), cobalt chloride (100ppm/10ppm), methylmercuric chloride (100ppm/10ppm) on the biosynthesis of phospholipid and their composition of fatty acids in E.coli and B.subtilis were analyzed. The contents of phosphatidylethanolamine, phosphatidylcholine, phosphatidylinositol, phosphatidylglycerol, cardiolipin and total lipids in treatment with metal compounds were lower to compare with the control. The major fatty acid utilized for biosynthesis of phospholipid was palmitic acid in control of E.coli and B.subtilis. However, in treatment with metal compounds, changes of fatty acid composition utilized for phospholipid formation were as follows. In E.coli major fatty acids were palimitic acid (ave. 26.26%) and cis-vaccenic acid (ave. 10.94%) in treatment with potassium chromate, palmitic acid (ave. 31.41%/31.42%) and stearic acid (ave. 17.92%/19.41%) in treatment with potassium dichromate and cobalt chloride. And in treatment with raethylmercuric chloride, palmitic acid (ave. 26.66%), stearic acid (ave. 15.50%) and cis-vaccenic acid (ave. 20.59%) were used in phospholipid formation. In B.subtilis, the major fatty acid was palmitoleic acid (ave. 15.29% /10.22%) in treatment with potassium chromate and cobalt chloride, and stearic acid (ave. 16.01%) in treatment with potassium dichromate. On the other hand, cis-vaccenic acid (ave. 9.09%), palmitic acid (ave. 17.23%), stearic acid (ave. 6.66%), myristic acid (ave. 6.34%) and lauric acid (ave. 4.75%) were analyzed into major fatty acids in treatment with methylmercuric chloride. As shown in results, specific fatty acid pattern was came out in treatment with metal compounds according to bacteria and treatments.

• Biomedical Science Letters
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• v.13 no.4
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• pp.355-360
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• 2007

In order to evaluate on the cytotoxicity of methyl mercury (MM) and antioxidant effect of phenolic compound, poncirin against MM-induced cytotoxicity, XTT assay was performed to determine the cell viability after human skin fibroblasts (Detroit 51) were grown in the media containing various concentrations of methylmercuric chloride (MMC). And also, the antioxidant effect of poncirin on the cytotoxicity induced by MMC was examined by cell viability and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity in these cultures. MMC decreased cell viability in dose-dependent manner in these cultures and the midcytotoxicity value was determined at concentration of 30 ${\mu}M$ MMC after human skin fibroblasts were treated with $10\sim50{\mu}M$ MMC for 72 hours, respectively. MMC was highly toxic on cultured human skin fibroblasts by toxic criteria. MMC-mediated cytotoxicity was related with oxidative stress by the diminution of toxic effect according to the treatment of vitamin E. In the antioxidant effect of poncirin, it showed vitamin E-like DPPH radical scavenging activity at 90 ${\mu}g/ml$ poncirin and also, remarkably increased cell viability compared with MMC-treated group. From these results, it is suggested that MMC-mediated cytoxicity was highly toxic and was related with oxidative stress in cultured human skin fibroblasts, and also phenolic compound such as poncirin showed the protection on MMC-induced cytotoxicity by antioxidant effect in these cultures.

• Journal of Environmental Health Sciences
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• v.23 no.2
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• pp.12-23
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• 1997

The biosynthesis of galactolipid, galactose and the fatty acid composition in E. cdi and B. subtills treated with potassium dichromate(PD, 500 ppm, 500 ppm), potassium chromate(PC, 500 ppm, 500 ppm), cobalt chloride(CC, 100 ppm, 10 ppm) and methylmercuric chloride(MC, 100 ppm, 10 ppm) during the culture were analyzed to compare with the control. The growth rate of cells, the contents of monogalactosyldiglyceride(MGDG), digalactosyldiglyceride(DGDG) and total lipid in the metal compound treatments were lower as compared with the control. And too, the contents of galactose utilized for the biosynthesis of galactolipids in these strains in the various metal compounds treatments were inhibited. The fatty acids used for the MGDG and DGDG formation in E. coli and B. subtills treated with each metal compounds during the culture were showed to the variant compositional change.