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5 "Nitric oxide"
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Original Articles
Effect of Glutathione on Lead Induced Modulation of NO Synthesis in RAW 264.7 Cell.
Sae Ron Shin, Gyung Jae Oh, Keun Sang Kwon, Wook Hee Yoon
Korean J Prev Med. 2002;35(4):269-274.
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OBJECTIVES
To evaluate the effect of glutathione(GSH) on lead induced modulation of nitric oxide(NO) synthesis, and to examine how lead modulates NO production in macrophages. METHODS: This study was observed in a culture of RAW 264.7 cells, which originated from a tumor in a Balb/c mouse that was induced by the Abelson murine leukemia virus. The compounds investigated were lead chloride, N-acetyl-cystein(NAC), and Buthionine Sulfoximine(BSO). RESUJLTS: ATP synthesis in RAW 264.7 cells was unchanged by each lead concentration exposure in a dose dependent manner. The NO synthesis was decreased when exposed to lead(PbCl2) concentration 0.5 micro M. The presence of 300 micro M NAC, used as a pretreatment in the culture medium, caused the recovery of the lead induced decrease in NO synthesis, but in the presence of 300 micro M BSO as a pretreatment, there was no recoverey. Pretreatment with NAC and BSO had no affect on ATP synthesis at any of the lead concentrations used. CONCLUSIONS: These results indicated that GSH has a protective effect toward lead toxicity, and suggested that the inhibition of NO production in macrophage due to lead toxicity may be related to cofactors of iNOS (inducible nitric oxide synthase)
Summary
Nitric Oxide-Mediated Cytotoxicity of Manganese in Basal Ganglia Neuronal Cells.
Dong Hoon Shin, Yong Wook Jung, Jae Hoon Bae, Dae Kyu Song, Won Kyun Park, Bok Hyun Ko, Doo Hie Kim
Korean J Prev Med. 1999;32(4):459-466.
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OBJECTIVES
We have investigated to manifest whether manganese-induced neurotoxicity is mediated by nitric oxide(NO) in the rat primary neuronal cultures and assess the effect of Mn2+ on the N-methyl-D aspartate(NMDA) receptors. METHODS: We have used 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)assay to examine the effect of cytotoxicity of MnCl2 in neuronal cells . NO production was determined by measuring nirites, a stable oxidation product of NO. The neurons in the rat that contains neuronal nitric oxide synthase(nNOS) were examined by immunofluorescence and confocal microscopy. The effects of Mn2+ on the NMDA receptors was assesed by the whole cell voltage clamp technique. RESULTS: We showed that the NO release and NOS expression were increased with 500uM MnCl2 treatment and an NOS inhibitors, NG-nitro-L-arginine , prevented neurotoxicity elicited by manganese. In the electrophysiological study, Mn2+ does not block or activate the NMDA receptors and not pass through the NMDA receptors in a neurons of basal ganglia. CONCLUSIONS: It is concluded that manganese neurotoxicity in basal ganglia was partially mediated by nitric oxide in the cell culture model.
Summary
A Study on the Protective Effects of Glutathione on Cytotoxicity of Mercury and Cadmium.
Jae Ho Jeong, Jun Youn Kim, Dai Ha Koh
Korean J Prev Med. 1999;32(2):170-176.
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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.
Summary
The Influence of Smoking and Alcohol Intake on Copper, Zinc, and Nitric Oxide Concentration in Serum.
Yeon Pyo Hong, Byung Sun Choi, Jung Duci Park, Im Won Chang
Korean J Prev Med. 1998;31(2):265-274.
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To investigate the change of nitric oxide(No), copper, and zinc in serum on smoking and alcohol ingestion in young adults, this study was performed in a cross-sectional study in 127 healthy, men in Korea who had HBsAg(-), HCVAb(-), and no symptomatic liver, heart, gastrointestinal, chronic diseases, and inflammatory sign(lower than 10,000 white blood cell count in CBC). At the men's entry into the study, blood samples were drawn from each subject and immediately centrifuged for analysis of NO, copper, and zinc. Each man completed a questionnaire that provided information on smoking, alcohol intake and present and past medical history. NO was analyzed by HPLC(Green et al., 1982), copper and zinc by atomic absorption spectrophotometer with air-acetylene flame and total cholesterol(TC) by Spectrum EPX. smoking(number of cigarettes per day and pack-year) and alcohol intake was grouped tertile. Copper was adjusted for age and zinc and for age and TC. NO, copper, and zinc on smoking and alcohol ingestion were analyzed in general linear models, respectively. NO, copper and zinc in serum did not show statistical differences between non-smoking and high-smoking group and no-alcohol intake and high-alcohol intake group. This study, suggested that copper, zinc, and NO was not good biological marker for early effect by smoking and alcohol intake in young adults. However, selection bias should be Considered in evaluation of this result. A large prospective study, will be needed in advance on usefulness of copper, zinc, and NO as a marker for risk fictors and early change of atherosclerosis.
Summary
NO2- and ATP synthesis in the EMT-6 cell stimulated by mercury chloride.
Gyung Jae Oh, Dai Ha Koh, Jung Ho Youm
Korean J Prev Med. 1996;29(3):495-506.
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AbstractAbstract PDF
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.
Summary

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