A method for extracting mercury from soil sequentially using H N 0 3 and a saturated solution of sodium sulphide (ss-Na2S) is described. Most chemical forms of mercury are soluble in HN03, with the exception of HgS. Because HgS is soluble in Na2S solution, a sequential extraction procedure was developed t o determine the distribution of HgS in soil. To determine the efficiency of this sequential extraction procedure, soil samples were spiked with either 203HgS o r 203HgCI2 and extracted sequentially with H N 0 3 and ss-Na2S. For samples spiked w i t h 203HgCI2, H N 0 3 extracted 95 and ss-Naps 1 % of the added 203HgCI2. In contrast, for soil spiked with 203HgS, H N 0 3 extracted 1 and ss-Na2S 98% of the added 203HgS. When this sequential extraction procedure was applied t o mercury-contaminated soil, the mercury concentrations in the combined H N 0 3 and ss-Na2S extracts accounted for 99% of the total mercury present. Further, of the total mercury present, 74-100% was HgS as determined b y the concentration of mercury in the ss-Na2S extract. These results suggest that the proposed sequential extraction procedure can selectively differentiate HgS from other species and compounds of mercury in soil.

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The relationship of dietary protein to cadmium absorption and tissue deposition was studied in male Sprague-Dawley rats exposed to different levels of cadmium in the drinking water. In animals fed a high-protein or low-protein diet and drinking water containing 25 or 50 ppm cadmium, liver and kidney cadmium and metallothionein were both significantly higher in rats fed the high-protein diet for 2 to 4 months. These differences may possibly be explained by the concentration of cysteine observed between these two diets. When cysteine was added to the low-protein diet to the level observed in the high-protein diet and fed to rats receiving 25 ppm cadmium in the drinking water, significant dietary differences in liver and kidney cadmium and metallothionein were not observed. The importance of dietary protein to cadmium-induced toxicity was also assessed in these studies. The activity of catechol-o-methyltransferase was used as a measure of cadmium-induced toxicity. The activity of this enzyme in the lung, liver and heart was significantly lower in rats fed a low-protein diet than those fed the high-protein diet and 50 ppm cadmium. Metallothionein concentration in the lung and liver from low-protein-fed rats was approximately half the level observed in rats fed the high-protein diet, which suggests a relationship between cadmium-induced toxicity and metallothionein concentrations. These results illustrate the importance of considering dietary protein (and possibly cysteine) when studying cadmium metabolism in experimental animals.

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.The relationship of dietary protein to cadmium absorption and tissue deposition was studied in male Sprague-Dawley rats exposed to different levels of cadmium in the drinking water. In animals fed a high-protein or low-protein diet and drinking water containing 25 or 50 ppm cadmium, liver and kidney cadmium and metallothionein were both significantly higher in rats fed the high-protein diet for 2 to 4 months. These differences may possibly be explained by the concentration of cysteine observed between these two diets. When cysteine was added to the low-protein diet to the level observed in the high-protein diet and fed to rats receiving 25 ppm cadmium in the drinking water, significant dietary differences in liver and kidney cadmium and metallothionein were not observed. The importance of dietary protein to cadmium-induced toxicity was also assessed in these studies. The activity of catechol-o-methyltransferase was used as a measure of cadmium-induced toxicity. The activity of this enzyme in the lung, liver and heart was significantly lower in rats fed a low-protein diet than those fed the high-protein diet and 50 ppm cadmium. Metallothionein concentration in the lung and liver from lowprotein-fed rats was approximately half the level observed in rats fed the high-protein diet, which suggests a relationship between cadmium-induced toxicity and metallothionein concentrations. These results illustrate the importance of considering dietary protein (and possibly cysteine) when studying cadmium metabolism in experimental animals.