Content of non-mercury-associated selenium in human tissues.
Recent studies have shown that at a higher mercury (Hg) burden, the molar ratio of selenium (Se) and Hg in tissues tends to approximate 1:1 by the formation of biologically largely inert adducts. From the toxicological standpoint, this trapping of free Hg is welcome. However, this binding of Se to Hg reduces the portion of Se in tissues, which is available for the formation of essential selenoenzymes like glutathione peroxidase, type I deiodase, and so forth and could result in a relative deficiency of Se. Therefore, we tried to determine the concentration of non-Hg-associated Se in several human tissues. As there is no proved trace method for the speciation of non-Hg-bound and Hg-bound Se in tissues, the total concentrations of Hg and Se were determined and the portion of non-Hg-associated Se was calculated by the difference of the molar concentrations of Se and Hg. For this investigation, the following tissues were obtained by autopsy from 133 adults: kidney cortex, thyroid gland, liver, spleen, cerebrum cortex, and pituitary gland. In no case was an occupational Hg burden known. The results confirm the assumption of a 1:1 association of Hg and Se in human tissues. The mean concentration of non-Hg-bound Se was calculated to 576 microg/kg in the kidney cortex, 363 microg/kg in the thyroid gland, 308 microg/kg in the liver, 205 microg/kg in the spleen, 111 microg/kg in the cerebrum cortex, and 545 microg/kg in the pituitary gland. In none of the cases under investigation in any tissue was the molar Se/Hg ratio below 1. This means that a total deficiency of non-Hg-bound Se could not be seen in this normal population, even at a higher Hg burden. Nevertheless, at a suboptimal Se supply like in Germany, any reduction of the part of Se, which is available for the formation of essential seleno-enzymes, should be avoided. Therefore, any additional Hg burden such as from dental amalgam should to be considered critically. The different distribution of Hg and Se in the body confirms that there is a controlled hierarchy in the Se supply of different organs, which tries to prevent a Se deficiency in organs with essential seleno-enzymes like the thyroid gland even under an suboptimal Se supply.
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Institut für Rechtsmedizin der Ludwig-Maximilians-Universität München, Germany.
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Schlosser
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D000293:Adolescent; D000328:Adult; D000367:Age Factors; D002540:Cerebral Cortex / Q000378:metabolism; D006801:Humans; D007672:Kidney Cortex / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008628:Mercury / Q000378:metabolism*; D008875:Middle Aged; D010902:Pituitary Gland / Q000378:metabolism; D012643:Selenium / Q000378:metabolism*; D013054:Spectrophotometry, Atomic; D013154:Spleen / Q000378:metabolism; D013961:Thyroid Gland / Q000378:metabolism
D008628:Mercury; D012643:Selenium