• BMB Reports
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• v.31 no.2
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• pp.189-195
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• 1998

Methylmercury (MeHg), which is widely distributed in the environment, is well known for both its acute and chronic poisoning effects on the human health; however, the precise biochemical mechanisms by which this compound elicits its toxicity in a cellular level are still poorly understood. To examine whether MeHg-induced liver injury involves activation of Phospholipase $A_2$ ($PLA_2$), the $PLA_2$ activity of control and MeHg-administrated livers was measured. MeHg stably enhanced a liver form of cytosolic $PLA_2$ activity, which exhibited several biochemical properties similar to those of the 100 kDa $cPLA_2$, except in its elution profile of a DEAE-5PW HPLC, and it migrated as a molecular weight of 80 kDa in Western blot analysis. This blotting analysis also indicated that the MeHg-induced enhancement of the activity could be due to the increase in the amount of the enzyme protein rather than a stable modification of the enzyme such as phosphorylation. Our data also showed the higher myeloperoxidase activity in MeHg-administrated liver than in the control, suggesting that this increase in the amounts of the 80 kDa $PLA_2$ and its activity may be resulted from infiltration of neutrophils into the liver during a hepatic injury process such as MeHg-induced inflammation. Taken together, these data suggest that MeHg-induced liver injury may be mediated by activation of the 80 kDa form of liver cytosolic $PLA_2$.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2002.10a
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• pp.167-167
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• 2002

Methylmercury (MeHg), one of the heavy metal compound, can cause severe damage to the central nervous system in humans. Many reports have contributed MeHg poisoning to contaminated foods and release into the environment. Despite many studies on the pathogenesis of MeHg-induced central neuropathy, no useful mechanism of toxicity has been established. To find genes differentially expressed by MeHg in neuronal cell, we peformed forward and reverse suppression subtractive hybridization (SSH) method on mRNA derived from neuroblastoma cell line, SH-SY5Y treated with solvent (DMSO) and 6.25 uM (IC$\sub$50/) MeHg. Differentially expressed CDNA clones were sequenced and the mRNAs were re-examined on Northern blots. These sequences were identified by BLAST homology search to known genes or expressed sequence tags (ESTs). Analysis of these sequences has provided 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 common environmental pollutants.

• Molecular & Cellular Toxicology
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• v.2 no.1
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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.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2003.10a
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• pp.13-13
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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. Here we show that phosphatidylcholine-specific phospholipase C (PC-PLC) is a critical pathway for MeHg-induced toxicity. MeHg activated the acidic form of sphingomyelinase (A-SMase) and group IV cytosolic phospholipase $A_2$ ($cPLA_2$) downstream of PC-PLC, but these enzymes as well as protein kinase C were not linked to MeHg's toxicity. Furthermore, MeHg produced ROS, which did not cause the toxicity. However, D6O9, an inhibitor of PC-PLC, significantly reversed the toxicity in a time- and dose-dependent manner in MDCK and SH-5YSY cells. Addition of EGTA to culture media resulted in partial decrease of [$Ca^{2+}$］$_{i}$ and partially blocked cell death. In contrast, D609 completely prevented cell death with parallel decreases in diacylglycerol and ［$Ca^{2+}$］$_{i}$. Together, our findings indicated that MeHg-induced toxicity was caused by elevation of ［$Ca^{2+}$]$_{i}$ through activation of PC-PLC. The toxicity was not attributable to the signaling pathways such as $cPLA_2$, A-SMase, and PKC, or to the generation of ROS.

• Journal of Environmental Health Sciences
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• v.31 no.3
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• pp.179-186
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• 2005

The purpose of this paper was to concisely review the practical changes in MeHg concentrations in fetus and offspring throughout gestation and suckling from our recent animal and human studies. In the animal study, adult female rats were given a diet containing 5ug/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 (RBC-Hg) in 16 pairs of maternal and umbilical cord blood samples were compared at birth and 3 months of age after parturition. RBC-Hg 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. RBC-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.

• Journal of the Korean Society of Radiology
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• v.14 no.1
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• pp.1-6
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• 2020

In this study, it was intended to replace the existing plane parallel ionization chamber, which requires cross-calibration in electron beam treatment. The semiconductor compounds HgI₂ was fabricated as detector, and the characteristics of HgI₂ detector for the 6, 9 and 12 MeV electron beam was analyzed in the linear accelerator. It was also intended to evaluate the possibility of substitution with existing detectors and their applicability as electron beam dosimetry and to use them as a basic study of the development of electronic beam dosimeter. As a result of reproducibility, RSD was 0.4246%, 0.5054%, and 0.8640% at 6, 9, and 12 MeV energy, respectively, indicating that the output signal was stable. As a result of the linearity, the R² was 0.9999 at 6 MeV, 0.9996 at 9 MeV, and 0.9997 at 12 MeV showed that the output signal is proportional to HgI₂ as the dose is increased. The HgI₂ detector of this study is highly applicable to electron beam measurement, and it may be used as a basic research on electron beam detection.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2003.10a
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• pp.177-177
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• 2003

Methylmercury (MeHg) is a well-known neurotoxicant that causes 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. In this study, suppressive subtractive hybridization (SSH) was performed to identify differentially expressed genes on human neuroblastoma cell line, SH-SY5Y treated with DMSO and MeHg (6.25 uM) for 6 hr. Differentially expressed cDNA clones were sequenced and were screened by dot blot to eliminate false positive clones. 13 of 35 screened genes were confirmed using real time RT-PCR. These genes include EB1,90-kDa heat-shock protein, chromosome condensation-related SMC-associated protein and brain peptide Al, etc. Analysis of these genes may provide an insight into the neurotoxic effects of MeHg in human neuronal cells and a possibility to develop more efficient and exact monitoring system of heavy metals as ubiquitous environmental pollutants.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.189.2-190
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• 2003

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. (omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.153-153
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• 2002

Methylmercury (MeHg), one of the heavy metal compound, can cause severe damage to the central nervous system in humans. Many reports have contributed MeHg poisoning to contaminated foods and release into the environment. Despite many studies on the pathogenesis of MeHg-induced central neuropathy, no useful mechanism of toxicity has been established.(omitted)

• Advances in environmental research
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• v.1 no.1
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• pp.15-35
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• 2012

Mercury (Hg) is a global environmental pollutant that has been the cause of many public concerns. One particular concern about Hg in aquatic systems is its trophic transfer and biomagnification in food chains. For example, the Hg concentration increases with the increase of food chain level. Fish at the top of food chain can accumulate high concentrations of Hg (especially the toxic form, methylmercury, MeHg), which is then transferred to humans through seafood consumption. Various biological and physiochemical conditions can significantly affect the bioaccumulation of Hg-including both its inorganic (Hg(II)) and organic (MeHg) forms-in fish. There have been numerous measurements of Hg concentrations in marine and freshwater fish worldwide. Many of these studies have attempted to identify the processes leading to variations of Hg concentrations in fish species from different habitats. The development of a biokinetic model over the past decade has helped improve our understanding of the mechanisms underlying the bioaccumulation processes of Hg in aquatic animals. In this review, I will discuss how the biokinetic modeling approach can be used to reveal the interesting biodynamics of Hg in fish, such as the trophic transfer and exposure route of Hg(II) and MeHg, as well as growth enrichment (the increases in Hg concentration with fish size) and biomass dilution (the decreases in Hg concentration with increasing phytoplankton biomass). I will also discuss the relevance of studying the subcellular fates of Hg to predict the Hg bioaccessibility and detoxification in fish. Future challenges will be to understand the inter- and intra-species differences in Hg accumulation and the management/mitigation of Hg pollution in both marine and freshwater fish based on our knowledge of Hg biodynamics.