Abstract

Adult Japanese quail were fed isolated soybean protein diets to which methylmercuric chloride (CH3 HgCl) or mercuric chloride (HgCl2) were added with or without supplemental selenium for seven days. Samples of blood and liver were analyzed for total selenium via atomic absorption spectrophotometry and for glutathione peroxidase (GSH-Px) activity by spectrophotometry assay. The addition of 285 ppm mercury as HgCl2 caused a significant depression in weight gain and feed consumption. Selenium administration alleviated the depression in weight gain and feed consumption. Selenium administration alleviated the depression in most cases. No other overt signs of toxicity were observed.Selenium addition increased the selenium concentration of the liver and to a lesser extent of the blood. CH3 HgCl addition resulted in increased selenium concentration in the blood of the selenium-supplemented group. Liver selenium was unaffected by the mercury addition.Selenium administration increased blood GSH-Px activity, but not liver GSH-Px activity. HgCl2 decreased blood GSH-Px activity in the selenium-supplemented group; CH3 HgCl had no effect. Since CH3 HgCl increased blood selenium and there was no concurrent increase in blood GSH-Px activity, it appears that the redistributed selenium is not available to be incorporated into GSH-Px. Therefore, mercury may be decreasing selenium bioavailability by some as yet unknown mechanism.

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