• Journal of Preventive Medicine and Public Health
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• 제45권6호
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• pp.353-363
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• 2012

Methylmercury is a hazardous substance that is of interest with regard to environmental health, as inorganic mercury circulating in the general environment is dissolved into freshwater and seawater, condensed through the food chain, ingested by humans, and consequently affects human health. Recently, there has been much interest and discussion regarding the toxicity of methylmercury, the correlation with fish and shellfish intake, and methods of long-term management of the human health effects of methylmercury. What effects chronic exposure to a low concentration of methylmercury has on human health remains controversial. Although the possibility of methylmercury poisoning the heart and blood vessel system, the reproductive system, and the immune system is continuously raised and discussed, and the carcinogenicity of methylmercury is also under discussion, a clear conclusion regarding the human health effects according to exposure level has not yet been drawn. The Joint FAO/WHO Expert Committee on Food Additives proposed to prepare additional fish and shellfish intake recommendations for consumers based on the quantified evaluation of the hazardousness of methylmercury contained in fish and shellfish, methylmercury management in the Korea has not yet caught up with this international trend. Currently, the methylmercury exposure level of Koreans is known to be very high. The starting point of methylmercury exposure management is inorganic mercury in the general environment, but food intake through methylation is the main exposure source. Along with efforts to reduce mercury in the general environment, food intake management should be undertaken to reduce the human exposure to methylmercury in Korea.

• Applied Microscopy
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• 제23권1호
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• pp.15-24
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• 1993

버들붕어 뇌와 아가미의 미세구조에 미치는 메틸수은의 독성적 영향과 이에 대한 홍삼의 보상효능을 전자현미경적 방법에 의하여 연구하였다. 뇌 신경세포의 미세구조 변화에 있어서 대조군에 비하여 메틸수은만을 투여한 군에서는 수상돌기와 축색돌기가 상당히 확장되고 핵질과 세포질이 부분적으로 손실되었으며 ribosome의 수적감소와 mitochondria의 팽대가 관찰되었다. 그리고 파괴된 핵과 공포화된 mitochondria를 함유한 괴사세포의 출현은 특이한 관찰이었다. 반면 메틸수은과 홍삼을 병행 투여한 군에서는 메틸수은만을 투여한 군에서 보다 수상돌기와 축색돌기의 확장이 감소되고 ribosome의 수가 증가되었으며 mitochondria의 팽대정도가 상당히 감소되었다. 아가미 새판의 미세구조에 있어서는 Pillar cell과 arm의 붕괴, 표피세포의 확장 및 기저막의 비후가 메틸수은만을 투여한 군에서 관찰되었고 메틸수은과 홍삼을 병행 투여한 군에서는 메틸수은만을 투여한 군에서 보다 arm의 붕괴정도와 기저막의 비후정도가 감소되어 정상세포와 거의 같은 정도로 호전되었다.

• 한국환경보건학회:학술대회논문집
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• 한국환경보건학회 2006년도 Perspectives of Evironmental Health Issues in Asia-Pacific Region
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• pp.90-110
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• 2006

In the natural course of events, most human exposure to MeHg is through fish/shellfish consumption. The methylmercury exposure levels depends on the amount and species of fish/shellfish consumed daily. The developing brain in the late gestation period is known to be most vulnerable. Further, more methylmercury accumulates in the fetuses than in mothers. Therefore, efforts must be made to protect the fetuses from the risk of methylmercury, especially in populations which consume a lot of fish/shellfish.

• Toxicological Research
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• 제35권1호
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• pp.25-35
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• 2019

The extracts of Plathymenia reticulata and Connarus favosus are widely used in the folk medicine. The potential protective effects of these extracts have been evaluated against cadmium in the yeast Saccharomyces cerevisiae, and against mercurial contamination in zebrafish Danio rerio. In yeast, both extracts efficiently protected the ${\Delta}ycf1$ mutant strain exposed to cadmium chloride restoring the growth, the expression of stress-response genes and decreasing the level of oxidative stress. In zebrafish, the supplementation of methylmercury-contaminated diet with both plant extracts similarly protected fish through the suppression of the methylmercury-induced lipid peroxidation, decrease of acetylcholinesterase activity, and restoring the expression levels of stress-response genes. This study particularly demonstrates the protective potential of both aqueous extracts against methylmercury, and could represent an interesting alternative for the Amazonian fish-eating communities to cope with the impact of chronic exposure to contaminated diets.

• 한국환경보건학회:학술대회논문집
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• 한국환경보건학회 2005년도 국제학술대회
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• pp.73-83
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• 2005

Higher methylmercury (MeHg) accumulation and susceptibility to toxicity in the fetus than in the mother at parturition is well known. However, the difference in MeHg exposure to fetus and offspring throughout gestation and suckling is not well established. In the human, the effects of MeHg exposure on pregnant and breast-feeding women remain an important issue for elucidation, especially those of continuous uptake in high-fish-consumption populations. The purpose of this paper was to evaluate the difference in MeHg exposure to fetus and offspring throughout gestation and lactation using our recent animal and human studies data. In the animal study, adult female rats were given a diet containing 5 ${\mu}$g/g Hg (as MeHg) for 8 weeks. Then they were mated and subsequently given the same diet throughout gestation and suckling. On embryonic days 18, 20, 22 and at parturition, the concentrations of Hg in the brains of fetus were approximately 1.5-2.0 times higher than those in the mothers. However, during the suckling period Hg concentrations in the brain rapidly declined to about 1/10 of that during late pregnancy. Hg concentrations in blood also decreased rapidly after birth. In human study, Hg concentrations in red blood cells (RBCs-Hg) in 16 pairs of maternal and umbilical cord blood samples were compared at birth and 3 months of age after parturition. RBCs-Hg concentration in the umbilical cords was about 1.6 times higher than those in the mothers at parturition. However, all the infants showed declines in Hg concentrations throughout the breast-feeding period. The Hg concentration in RBCs-Hg at 3 months of age was about half that at birth. Both the animal and human studies indicated that MeHg exposure to the fetus might be especially high but it dramatically decreases during the suckling period. Therefore, close attention should be paid to the gestation rather than the breast-feeding period to avoid the risk of MeHg to human infants.

• 한국환경과학회:학술대회논문집
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• 한국환경과학회 2019년도 정기학술대회 발표논문집
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• pp.46-46
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• 2019

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.228.2-229
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• 2002

Methylmercury (MeHg). a potent neurotoxicant. produces neuronal death that may be partially mediated by glutamate. Glutamine synthetase (GS), a glial-specific enzyme. catalyzes the synthesis of glutamine from glutamate and ammonia and is associated with ischemic injury and neurological diseases. Objectives of this experiment are to investigate whether in vivo and in vitro MeHg exposure have adverse effects on GS and whether duration of exposure to MeHg and glutamate co-treatment playa role in MeHg-induced toxicity. (omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.206-208
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• 2002

Methylmercury (MeHg; $CH_{3}HgCl$) is, second only to cadmium as being, the most toxic on the earth. Inorganic mercury from various waste sources can be easily methylated by bacteria in water and subsequently ingested by fishes and then highly accumulated in human. Although toxicity from mercury exposure occurs with both organic and inorganic forms, organic mercury is more potently toxic to central nervous system. Minamata disease is an example of organic mercury toxicity. (omitted)

• Journal of Preventive Medicine and Public Health
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• 제45권6호
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• pp.335-343
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• 2012

Mercury is emitted to the atmosphere from various natural and anthropogenic sources, and degrades with difficulty in the environment. Mercury exists as various species, mainly elemental ($Hg^0$) and divalent ($Hg^{2+}$) mercury depending on its oxidation states in air and water. Mercury emitted to the atmosphere can be deposited into aqueous environments by wet and dry depositions, and some can be re-emitted into the atmosphere. The deposited mercury species, mainly $Hg^{2+}$, can react with various organic compounds in water and sediment by biotic reactions mediated by sulfur-reducing bacteria, and abiotic reactions mediated by sunlight photolysis, resulting in conversion into organic mercury such as methylmercury (MeHg). MeHg can be bioaccumulated through the food web in the ecosystem, finally exposing humans who consume fish. For a better understanding of how humans are exposed to mercury in the environment, this review paper summarizes the mechanisms of emission, fate and transport, speciation chemistry, bioaccumulation, levels of contamination in environmental media, and finally exposure assessment of humans.

• Molecular & Cellular Toxicology
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• 제2권1호
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• pp.60-66
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• 2006

Methylmercury (MeHg), one of the heavy metal compounds, can cause severe damage to the central nervous system in humans. Many reports have shown that MeHg is poisonous to human body through contaminated foods and has released into the environment. Despite many studies on the pathogenesis of MeHg-induced central neuropathy, no useful mechanism of toxicity has been established so far. This study, using of suppression subtractive hybridization (SSH) method, was peformed to identify differentially expressed genes by MeHg in SH-SY5Y human neuroblastoma cell line. We prepared to total RNA from SH-SY5Y cells treated with solvent (DMSO) and $6.25\;{\mu}M\;(IC_{50})$ MeHg and performed forward and reverse SSH. Differentially expressed cDNA clones were screened by dot blot, sequenced and confirmed that individual clones indeed represent differentially expressed genes with real time RT-PCR. These sequences were identified by BLAST homology search to known genes or expressed sequence tags (ESTs). Analysis of these sequences may provide an insight into the biological effects of MeHg in the pathogenesis of neurodegenerative disease and a possibility to develop more efficient and exact monitoring system of heavy metals as ubiquitous environmental pollutants.