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- Mercuric Chloride Induces Apoptosis in MDCK Cells.
- Ju Hyoung Lee, Jung Ho Youm, Keun Sang Kwon
- J Prev Med Public Health. 2006;39(3):199-204.
- 2,863 View
- 68 Download
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Abstract
PDF - OBJECTIVES
Mercury is a hazardous organ-specific environmental contaminant. It exists in a wide variety of physical and chemical states, each of which has unique characteristics for the target organ specificity. Exposure to mercury vapor and to organic mercury compounds specifically affects the CNS, while the kidney is the target organ for inorganic Hg compounds. METHODS: In this study, mercury chloride (HgCl2) was studied in a renal derived cell system, i.e., the tubular epithelial Madin-Darby canine kidney (MDCK) cell line, which has specific sensitivity to the toxic effect of mercury. MDCK cells were cultured for 6-24 hr in vitro in various concentrations (0.1-100 M) of HgCl2, and the markers of apoptosis or cell death were assayed, including DNA fragmentation, caspase-3 activity andwestern blotting of cytochrome c. The influence of the metal on cell proliferation and viability were evaluated by the conventional MTT test. RESULTS: The cell viability was decreased in a time and concentration dependent fashion: decreases were noted at 6, 12 and 24 hr after HgCl2 exposure. The increases of DNA fragmentation were also observed in the concentrations from 0.1 to 10 M of HgCl2 at 6 hr after exposure. However, we could not observe DNA fragmentation in the concentrations more than 25 M because the cells rapidly proceeded to necrotic cell death. The activation of caspase-3 was also observed at 6 hr exposure in the HgCl2 concentrations from 0.1 to 10 M. The release of cytochrome c from the mitocho-ndria into the cytosol, which is an initiator of the activation of the caspase cascade, was also observed in the HgCl2-treated MDCK cells. CONCLUSIONS: These results suggest that the activation of caspase-3 was involved in HgCl2-induced apoptosis. The release of cytochrome c from the mitochondria into the cytosol was also observed in the HgCl2-treated MDCK cells. These findings indicate that in MDCK cells, HgCl2 is a potent inducer of apoptosis via cytochrome c release from the mitochondria. -
SummaryOriginal Article
- Interaction of Sodium Selenite on Neurotoxicity Induced by Methylmercuric Chloride.
- J S Park, H M Lee, Y Chung, D C Shin, J H Roh, Y H Moon
- Korean J Prev Med. 1992;25(1):13-25.
- 2,811 View
- 22 Download
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Abstract
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- This study was conducted to investigate the mechanism of protective effect by sodium selenite in Methylmercuric chloride neurotoxicity, increasing intracellular Ca2+ concentration of the neuron. Methylmercuric chloride of 3 mg/kg of body weight was administered simultaneously with sodium selenite of 5 mg/kg and pretreatment of sodium selenite via intraperitoneal injection to rats. Also, effect of methylmercuric chloride(25 micrometer, 50 micrometer, 100 micrometer) and sodirum selenite(200 micrometer) on free intrasynaptosomal Ca2+ concentration were studied using the fluorescent Ca2+ indicator fura2 in vitro. After the treatment, at 6, 24, and 48 hours later, mercury in the cerebral cortex, liver and kidney tissues, succinic dehydrogenase activities, adenosin-5'-triphosphate concentration, acetylcholinesterase activities, and intracellular Ca2+ concentration in the cerebral cortex were determined in vivo. Cerebral synaptosomes of rats were incubated with methylmercuric chloride and sodium selenite in Hepes buffer for 10 minutes and free intrasynaptosomal Ca2+ concentration were measured with fura2 in vitro.The results were summarized as follows; 1. The combined administration of CH3HgCl and Na2SeO3 and pretreatment of Na2SeO3 according to time significantly more increased in the cerebral cortex and decreased in the liver, kidney mercury concentrations compared to the administration of CH3HgCl only. 2. The combined administration of CH3HgCl and Na2SeO3 and pretreatment of Na2SeO3 increased more succinic dehydrogense and acetylcholinesterase activities compared to the administration of CH3HgCl only. Particularly pretreatment of Na2SeO3 significantly more compared to the administration of CH3HgCl only. The concentration of adenosine-5'-triphosphate in Na2SeO3 treatment groups revealed a favourable effect compared to the administration of CH3HgCl only. 3. Intracellular Ca2+ concentration in administration of CH3HgCl only was increased significantly more than control group in all test hours but was increased significantly more at 48 hous only after treatment in combined administration of CH3HgCl and Na2SeO3 and pretreatment of Na2SeO3 according to time interval more decreased significantly intracellular Ca2+ concentration compared to the administration of CH3HgCl only. 4. Free intrasynaptosomal Ca2+ concentration in the combined administration of CH3HgCl and Na2SeO3 was decreased (24%-40%) significantly more than the administration of CH3HgCl only. From the above results, the specific dosage of Na2SeO3 decreased increment of intracellular Ca2+ concentration induced by administration of CH3HgCl. These findings suggest the protective mechanism of Na2SeO3 on the neurotoxicity of CH3HgCl.
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