ABSTRACT
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.
Subject(s)
Animals , Mice , Apoptosis , Cell Membrane , DNA Fragmentation , DNA Nucleotidylexotransferase , Flow Cytometry , SeleniumABSTRACT
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)
Subject(s)
Animals , Mice , Abelson murine leukemia virus , Acetylcysteine , Adenosine Triphosphate , Buthionine Sulfoximine , Glutathione , Macrophages , Nitric OxideABSTRACT
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)
Subject(s)
Animals , Mice , Abelson murine leukemia virus , Acetylcysteine , Adenosine Triphosphate , Buthionine Sulfoximine , Glutathione , Macrophages , Nitric OxideABSTRACT
During the 8 months from October 1985 to May 1986, the survey was performed on 211 leprosy patients over fifty years old, settled in the four villages of Iksan country, North of Chulla province. In that observation, we investigated the frequency and the degree of impairments according to sex, age, and anatomical location by the "guides to the evaluation of permanent impairment". The noticeable findings were made as follows: 1) Frequency of impairment by anatomical location was significantly higher in hand than eye and foot (p<0.01). 2) Frequency of impairment was significantly increased in eye according as age increase (p<0.01). 3) The degree of impairments of all patients was the highest in hand as 28.7%. 4) By the kinds of impairments, the flextion and the amputation were most common in hand and foot, and loss of central vision was common symptom in eye. 5) The degree of impairments of 211 leprosy patients was shown as 44.1% and increased according as age increase.