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Abstract
This study was conducted to investigate the metallothionein induction by sodium selenite in mercuric Chloride intoxication. Mercuric chloride of 3.0 mg/kg of body weight was administered simultaneously with sodium selenite of either a high dosage of 2.5 mg/kg or low dosage of 1mg/kg via intraperitioneal injecion to rats. After the treatment, 6, 12, 24 and 72 hours later, mercury and selenium content in liver and kidney tissues, serum transaminase activities(SGOT, SGPT), metallothionein, glutathione, glutathione peroxidase sotivity and histological changes were determined.
The results were summarized as follows on:
1. The combined administration of mercury and selenium significantly more decreased mercury concentrations in liver and kidney compared to the administration of mercury only.
2. The combined administration of mercury and selenium significantly more increased renal metallothionein compared to administration of mercury only. This phenomenon was more remarkable when a large dose(2.5 mg/kg of selenium was administered with mercuric chloride.
3. Glutathione concentration, glutathione peroxidase activity in liver and kidney and serum transaininase activity(SGOT, SGPT) were less suppressed in the combined administration group than the mercury only group.
4. Histological damage in renal tissue was not revealed in rats treated with mercury and selenium.
From the above results, selenium administered simultaneously with mercury decreased mercury concentration in liver and kidney, increased renal metallothionein concentration and decreased the toxicity of mercury. The hypothetic mechanism suggested is that selenium induces the metallothionein combined with Hg and redistributes Hg in tissues.
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