• 한국환경독성학회:학술대회논문집
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• 한국환경독성학회 2004년도 춘계학술대회
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• pp.66-68
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• 2004

• 한국환경보건학회지
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• 제33권3호
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• pp.175-179
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• 2007

• 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)

• 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.294.2-295
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• 2002

Methylmercury (MeHg: CH3HgCl) is a ubiquitous environmental toxicant that readily bioaccumulates in aquatic foodchains. This toxicant is most highly exposed to humans through the ingestion of contaminated food. and thus is an ongoing health concern. Thus far. MeHg has been suggested to exert its toxicity through its high reactivity to thiols of bioactive proteins. elevation in intracellular Ca2＋ concentration. and generation of reactive oxygen species. but its mechanism remains poorly understood. (omitted)

• Toxicological Research
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• 제5권1호
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• pp.43-48
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• 1989

The average value of total mercury contents in scalp hair of Korean male was found to be 1.66+1.10 ppm (S.D.) and that of methylmercury was 1.02+0.72 ppm (61.0% of the total mercury). In case of total mercury contents of female was 1.06+0.46 ppm and that of methylmercury was 0.51+0.27 ppm (48.4% of total mercury level). When compared with data reported by Japanese, the levels were about half. The levels of mercury in scalp hair of male subjects were significantly different with their occupations, but in case of female, the variation was not so much.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-1
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• pp.74-74
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• 2003

Methylmercury (MeHg) is a ubiquitous environmental toxicant that can be exposed to humans by ingestion of contaminated food including fish and bread. MeHg has been suggested to exert its toxicity through its high reactivity to thiols, generation of arachidonic acid and reactive oxygen species (ROS), and elevation of intracellular $Ca^{2+}$ levels ([$Ca^{2+}$]i). However, the precise mechanism has not been fully defined. (omitted)

• 한국유전체학회:학술대회논문집
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• 한국유전체학회 2005년도 The 14th Korea Genome Conference
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• pp.69-69
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• 2005

• Molecular & Cellular Toxicology
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• 제4권2호
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• pp.164-169
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• 2008

Methylmercury (MeHg) is known to have devastating effects on the mammalian nervous system. In order to characterize the mechanism of MeHg-induced neurotoxicity, we investigated the analysis of transcriptional profiles on human 8k cDNA microarray by treatment of $1.4{\mu}M$ MeHg at 3, 12, 24 and 48h in human neuroblastoma SH-SY5Y cell line. Some of the identified genes by MeHg treatment were significant at early time points (3h), while that of others was at late time points (48h). The early response genes that may represent those involved directly in the MeHg response included pantothenate kinase 3, a kinase (PRKA) anchor protein (yotiao) 9, neurotrophic tyrosine kinase, receptor, type 2 gene, associated with NMDA receptor activity regulation or perturbations of central nervous system homeostasis. Also, when SH-SY5Y cells were subjected to a longer exposure (48h), a relative increase was noted in a gene, glutamine-fructose-6-phosphate transaminase 1, reported that overexpression of this gene may lead to the increased resistance to MeHg. To confirm the alteration of these genes in cultured neurons, we then applied real time-RT PCR with SYBR green. Thus, this result suggests that a neurotoxic effect of the MeHg might be ascribed that MeHg alters neuronal receptor regulation or homeostasis of neuronal cells in the early phase. However, in the late phase, it protects cells from neurotoxic effects of MeHg.

• 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.