No abstract available.
Selenium*

Effect of Mercury chloride on the synthesis of NO2- and ATP were observed in EMT-6 cells which were culture with cytokines(IL-1alpha and IFN-gamma) and various concentrations of mercury chloride from 0.05 to 0.08 M. Viability of EMT-6 cells were observed above 90% in almost groups. There were not significant differences in the viability between mercury supplemented groups and control group. It suggests viability of EMT-6 cells were not influenced by these concentrations of mercury chloride. Results of the synthesis of nitrite showed significant time and group effect. There is a significant interaction effect between concentration of mercury chloride and culture time. The effect of various concentration of mercury chloride is not the same for all levels of culture time. There were significant differences in the synthesis of nitrite between mercury chloride supplemented groups and control group, and the synthesis of nitrite in EMT-6 cell by the supplement of mercury chloride was significantly decreased in a dose-dependent manner. Results of the synthesis of ATP showed a significant group effect, and the time main effect and the Group x Time interaction were also significant. There were significant differences in the synthesis of ATP between mercury chloride supplemented groups and control group, and the synthesis of ATP in EMT-6 cell by the supplement of mercury chloride was significantly decreased in a dose-dependent manner. These results suggest that the disorder of cell mediated immunity by mercury chloride could be related to the inhibition of nitric oxide synthesis which will be caused by the decreased synthesis of ATP.
Adenosine Triphosphate* ; Immunity, Cellular ; Nitric Oxide

The effects of treatment with mercury chloride on the nitrite and nitrate syntheses were observed in peritoneal macrophages from Balb/c mice and EMT-6 cells in vitro. The cells were cultured in Dulbecco's modified Eagle's medium(DMEM) with cytokines. Amounts of nitrite and nitrate 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 and nitrate measured in the culture media according to culture time. The survival rate of peritoneal macrophages was significantly decreased by mercury chloride added into the media in dose-dependent manner, however the survivals of EMT-6 cells were not influenced by mercury chloride concentration in media. Nitrite and nitrate syntheses were dose-dependently decreased by mercury chloride added in culture media. ATP synthesis also decreased in EMT-6 cells by mercury chloride. These results reported here suggest that the disorder of cell mediated immunity by mercurials could be related to the inhibition of nitric oxide synthesis which seems to be caused by the inhibition of ATP synthesis.
Adenosine Triphosphate ; Animals ; Culture Media ; Cytokines ; Immunity, Cellular ; Macrophages ; Macrophages, Peritoneal* ; Mice* ; Nitric Oxide* ; Survival Rate

Reciprocal exchanges of DNA in sister chromatids (SCEs) are induced by various carcinogens and mutagens, although the quantitative relationship between the number of mutations and SCEs induced varies among chemicals. Nevertheless, the analysis of SCEs production by various agents often proposed as a sensitive and quantitative assay for mutagenicity and cytotoxicity. Mercury, even if which has no evidences for mutagenicity and carcinogenicity, is reported to exert women cytotoxic effects, such as chromosomal aberrations or bad influences to ovulation and reproduction in experimental animals, etc. In this study, tests for sister chromatid exchanges have been carried out on normal human lymphocytes in whole blood culture to add mercury chloride (HgCl2) or methylmercury chloride(CH3 HgCl) for 72 hr. The results indicate the dose-dependent relationship between the frequencies of SCEs and the concentrations of HgCl2, CH3HgCl and 5-bromo-2-deoxyuridine (BrdU). Lymphocyte proliferation has depressed in the higher concentration of mercury.
Animals ; Carcinogens ; Chromatids ; Chromosome Aberrations ; DNA ; Female ; Humans ; Humans* ; Lymphocytes* ; Mercuric Chloride ; Mutagens ; Ovulation ; Reproduction ; Siblings* ; Sister Chromatid Exchange*

The protective effect of sodium selenite (Na2SeO3) against the cytogenetic toxicity of heavy metals was investigated on human whole-blood cultures in relation to induction of sister chromatid exchange(SCE) in secondary metaphase chromosome. Methlmercury chloride (CH3HgCl), cadmium chloride (CdCl2), Potassium dichromate (K2Cr2O7), and sodium selenite caused to the typically dose-dependent increase in sister chromatid exchanges (SCEs) by the concentrations ranging from 0.3 micro M to 10 micro M. However, the inductions of sister chromatid exchanges by methymercury chloride or cadmium chloride were inhibited by the simultaneous addition of sodium selenite 1.2 micro M. The frequencies of SCE were decreased to the level of control in the molar ratios as 2 : 1, 1 : 1, 1 : 2, and 1 : 4 of selenium selenite vs. methylmercury chloride, and as 1 : 1 and 1 : 2 of selenium selenite vs. cadmium chloride, while the frequencies of SCE induced by potassium dichromate were not changed by the addition of sodium selenite in culture condition. Mitotic indices were decreased in the higher concentrations of chemicals and not significantly changed by the simultaneous addition of sodium selenite to the culture condition containing each chemicals.
Cadmium Chloride ; Chromatids ; Cytogenetics ; Humans* ; Lymphocytes* ; Metals, Heavy* ; Metaphase ; Mitotic Index ; Molar ; Potassium Dichromate ; Selenious Acid ; Selenium* ; Siblings ; Sister Chromatid Exchange ; Sodium Selenite

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.
Adenosine Triphosphate ; Animals ; Cell Culture Techniques ; Macrophages, Peritoneal ; Mercury Compounds ; Mice ; Nitric Oxide ; Selenium*

BACKGROUND: This study is designed to indicate the role of 3D-surface rendering of the MRI in defining and resect-ing the epileptogenic zone. METHODS: 25 healthy volunteers and 55 patients were studied. Conventional MRI and 3D-surface rendering were performed. Sulcal and gyral patterns were assesed by a neuroradiologist and a neurologist with-out the clinical informations. Chronic video-EEG monitoring with surface and subdural grid electrodes, and PET were done. Resection was performed based on data of the EEG recordings and 3D-surface rendering. RESULTS: Conventional MRI identified structural abnormality ("MRI-identifiable lesion") in 20 patients. 20 of 35 patients without structural abnormality in conventional MRI revealed abnormal sulcal and gyral patterns in 3D-surface rendering of MRI ("3D-identifiable lesion"). Subdural grid EEGs recorded focal or diffuse ictal EEG onset from the region of "3D-identifiable lesion". Histopathologic findings revealed cortical dysplasia in 48 and neocortical gliosis in seven. Overall surgical out-come, at the average follow up period of 32.5 months, showed class I in 63.6%, class II in 25.5%, and class III in 10.9%. Among 20 patients with "MRI-identifiable lesion", 80% were in class I and 20% were in class II. Among 35 patients without "MRI-identifiable lesion", 54.3% were in class I, 28.6% were class II, and 17.1% were in class III. 80% of 20 patients with "3D-identifiable lesion" showed class I and 20% of 15 patients without "3D-identifiable lesion" showed class I. CONCLUSIONS: Identification of "MRI-identifiable lesion" or "3D-identifiable lesion" was of value in defining the epileptogenic zone. Resection of "MRI-identifiable lesion" or "3D-identifiable lesion", which were epilep-togenic in EEGs, promised a good surgical outcome.
Electrodes ; Electroencephalography ; Epilepsy* ; Equidae ; Follow-Up Studies ; Gliosis ; Healthy Volunteers ; Humans ; Magnetic Resonance Imaging* ; Malformations of Cortical Development

OBJECTIVES: To evaluate the protective effects of glutathione (GSH) on the cytotoxicity of mercurial compounds(CH3HgCl, HgCl2) or cadmium chloride(CdCl2) in EMT-6 cells. METHODS: The compounds investigated were CH3HgCl, HgCl2, CdCl2, GSH, buthionine sulfoximine(BSO), L-2-oxothiazolidine-4-carboxylic acid(OTC). Cytotoxicity analysis consist of nitric oxide(NO) production, ATP production and cell viability. RESULTS: Mercurial compounds and cadmium chloride significantly decreased cell viability and the synthesis of NO and cellular ATP in EMT-6 cells. GSH was not toxic at concentrations of 0 - 1.6 mM. In the presence of GSH, mercurial compounds and cadmium did not decrease the production of ATP and nitrite in EMT-6 cells. The protective effects of GSH against the cytotoxicity of mercurial compounds and cadmium depended on the concentration of added GSH to the culture medium for EMT-6 cells. We evaluated the effects of intracellular GSH level on mercury- or cadmium-induced cytotoxicity by the pretreatment experiments. Pretreatment of GSH was not changed NO2- and ATP production, and pretreatment of BSO was decreased in dose- and time-dependent manner. Pretreatment of OTC was increased NO2- and ATP production in dose- and time-dependent manner. Because intracellular GSH level was increased by OTC pretreatment, the protective effect on mercury- and cadmium-induced cytotoxicity was increased. CONCLUSIONS: These results indicated that sulfhydryl compounds had the protective effects against mercury-induced cytotoxicity by the intracellular GSH levels.
Adenosine Triphosphate ; Cadmium Chloride ; Cadmium* ; Cell Survival ; Glutathione* ; Mercuric Chloride ; Nitric Oxide ; Sulfhydryl Compounds

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.
Apoptosis* ; Cadmium ; Caspase 1 ; Caspase 3 ; DNA Fragmentation ; Electrophoresis ; Electrophoretic Mobility Shift Assay ; HL-60 Cells* ; Humans ; JNK Mitogen-Activated Protein Kinases ; Metals ; Metals, Heavy* ; NF-kappa B ; Peptide Hydrolases ; Phosphotransferases ; Selenium ; Transcription Factor AP-1

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.
Animals ; Apoptosis* ; Cell Membrane ; DNA Fragmentation ; DNA Nucleotidylexotransferase ; Flow Cytometry ; Mice ; Selenium*