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Korean Journal of Preventive Medicine 1992;25(1): 13-25.
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
1Department of Neurology, Yonsei University College of Medicine, Korea.
2The Institute of Environmental Research, Yonsei University College of Medicine, Korea.
3Department of Preventive Medicine & Puvlic Health, Yonsei University College of Medicine, Korea.
ABSTRACT
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.
Key words: Sodium selenite; Methylmercuric chloride; Neurotoxicity; Synaptosome
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