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Original Article
- Effects of Selenium on Apoptosis Induced by Methyl Mercury Chloride in RAW 264.7 Cells
- Keun Snag Kwon, Dai Ha Koh, Jung Ho Youm, Wook Hee Yoon
- Korean Journal of Occupational and Environmental Medicine 2003;15(3):237-251. Published online September 30, 2003
- DOI: https://doi.org/10.35371/kjoem.2003.15.3.237
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Abstract
PDF - OBJECTIVE: This study was performed to evaluate the protective effects of selenium against the methyl mercury chloride (MeHgCl) induced cell apoptosis.
METHODS
The effect of selenium on the MeHgCl induced cell apoptosis was observed in mouse macrophage-derived RAW 264.7 cells, in vitro. The cells were cultured in Dulbecco's modified Eagle's medium (DMEM).
RESULTS
MeHgCl exerted a dose dependent cytotoxicity, as demonstrated by the MTT assay, an assay dependent, in part, on mitochondrial function. Concurrent exposure to selenium provided complete protective effects against the cytotoxicity induced by MeHgCl. Pretreatment with selenium increased the protective effects of subsquent administrations of selenium in conjunction with MeHgCl, but pretreatment of selenium alone did not provide protection against MeHgCl when given alone. Selenium administered after exposure to MeHgCl did not repair the existing MeHgCl induced cytotoxicity.Furthermore, the apoptosis induced by MeHgCl was revealed by the DNA fragmentation, using the terminal deoxynucleotidyl transferase Biotin-dUTP nick end labeling (TUNEL) assay, alterations to the nuclear morphology, by nuclei staining, and the plasma membrane lipid organization, as shown by cell flow cytometry. The apoptosis induced by MeHgCl was prevented by the concurrent exposure to selenium, or pretreatment with selenium, prior to the administration of selenium in conjunction with MeHgCl. However, no inhibittion of the MeHgCl induced apoptosis was observed with selenium pretreatment prior to exposure to MeHgCl alone, or with the administration of selenium after exposure to MeHgCl.
CONCLUSIONS
These results suggest that the coexistence of selenium and MeHgCl are essential for the protective effects of selenium against the MeHgCl-induced apoptosis, and the cytotoxicity, in RAW 264.7 cells, and may involve selenium-MeHgCl binding.
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Original Article
- Induction of Apoptosis by Heavy Metals in HL-60 Cells
- Nam Song Kim, Tae Ho Seong, Kwang Ho Cho, Jung Ho Youm, Dai Ha Koh
- Korean Journal of Occupational and Environmental Medicine 1999;11(4):557-568. Published online December 31, 1999
- DOI: https://doi.org/10.35371/kjoem.1999.11.4.557
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Abstract
PDF
- OBJECTIVES
Apotosis induced by metals and metal-related deleterious conditions has only recently been studied. Although the toxic effects of heavy metal are well described, little is known about the mechanism of apoptosis by heavy metal toxicity. This study is designed to define the induction of apoptosis by which heavy metals exert the cytotoxic effect on human promyelocytic leukemic HL-60 cells.
Methods
After the incubation with CdC12, Na2SeO3 and HgC12, viability of the cells were measured by MTT assay. DNA fragmentation was analyzed by electrophoresis. For measurement of caspase 1 and 3-like proteases activity, the whole lysates were subjected to the proteolytic cleavage and then measured by using fluorospectrometry. c-JUN N-terminal kinase (JNK) activity was detected by an in vitro kinase assay. Transcriptional activities of activating protein-1 (AP-1) and nuclear factor-kB (NF-kB) were measured by elec trophoresis mobility shift assay (EMSA).
RESULTS
Cadmium (l2OuiN/I) and selenium (30,iM) induce the apoptosis of HL-60 cells which is characterized by the ladder pattern of DNA fragmentation. Cadmium and selenium induce the activation of caspase-3 in a time dependent manner. They also increase the phosphotransferase activities of c-JUN N-terminal kinase (JNK) in cadmium and selenium treated HL-60 cells. Furthermore, cadmium and selenium increase the activation of transcriptional factors including AP-i and NF-kB.
CONCLUSIONS
These results suggest that cadmium and selenium induce the apoptotic death of HL-60 cells via activation of DEVD-specific caspase, JNK and transcriptional factors such as AP-1 and NF-kB.
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Original Article
- A Study of Protective Effect of Selenium Against Cytotoxicity of Methylmercury Chloride
- Dai Ha Koh, Jung Ho Youm, Young Sang Koh, Sun Hwan Joh, Tak Soon Oh
- Korean Journal of Occupational and Environmental Medicine 1998;10(3):310-319. Published online August 31, 1998
- DOI: https://doi.org/10.35371/kjoem.1998.10.3.310
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Abstract
PDF
- The purpose of the present study was to elucidate the cytotoxical influence of mercurial compounds and the protective effect of selenium against mercurial compounds. The effects of mercury compounds and selenium on the syntheses of nitrite(NO2-) and ATP were observed in the cell cultures of EMT-6 cells and peritoneal macrophages from Balb/c mouse. The viabilities of EMT-6 cells and peritoneal macrophages at the end of culture were significantly decreased in dose-dependent manner by methylmercury chloride (CH3HgCl) added into the media. NO2- and ATP syntheses of the cells were dose-dependently inhibited by CH3HgCl. Simultaneous addition of the equimolar dose of selenium completely prevented mercury-induced inhibitions of NO2- and ATP syntheses, which were observed in both of EMT-6 cells and peritoneal macrophages. But these effects of selenium were not appeared in the new medium containing mercurials only which were removed the selenium after the pretreatment of selenium for 6 hours. These results suggest that protective effect of selenium against mercurial compounds was archived by the formation of a complex consisting of Se-Hg or Se-Hg-protein. Though its mechanism was not clear, the protective role of selemium against the mercury toxicity would be exhibited in the immunological system.
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Original Article
- A Study on Factors Related to NO Synthesis by Mercurial Compounds in the EMT-6 cell
- Jung Ho Youm
- Korean Journal of Occupational and Environmental Medicine 1997;9(1):122-130. Published online February 28, 1997
- DOI: https://doi.org/10.35371/kjoem.1997.9.1.122
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Abstract
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- The effects of several factors on the nitrite synthesis were observed in the culture of EMT-6 cells which are originated from mammary adenocarcinoma of Balb/c mouse. The cells were cultured in Dulbecco's Modified Eagle's Medium containing 10% fetal calf serum. Amounts of nitrite in the culture media after 24 and 36 hours of culture were about 2 fold, and 3-fold of those measured after 12 hours respectively. There were very close associations between the amounts of nitrite measured in the culture media. A significant nitrite synthesis by EMT-6 cells occurred when IL-1 was added to the culture medium with other cytokines as IFN gamma or TNF alpha . One of each cytokines were less effective as an inducer of nitrite than the combinations of cytokines. When mercury chloride or cinnamate was added in the culture medium, the nitrite synthesis was dose-dependently decreased by the concentration of these materials. The viability of EMT-6 cells were kept on 95% or above in 36 hours after beginning of culture without any specific additives except cytokines. While after 48 hours it went down to 85% or less. These viability were decreased by the prolongation of culture time (48 hours or more), the addition of TNF alpha to cytokine mixture, and the higher concentrations of mercury chloride or cinnamate to culture medium. Simultaneous addition of the equimolar dose of selenium completely prevented mercurial compounds-induced inhibitions of nitrite syntheses. But the single addition of selenium neither influenced the viability of cells nor the productions of nitrite. These results suggests that the disorder of cell mediated immunity by mercurial compounds could be related to the inhibition of nitric oxide synthesis and selenium decreased the cytotoxicity of mercurial compounds.
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