Mercury, Selenium, and Cadmium in Human Autopsy Samples from Idrija Residents and Mercury Mine Workers
ABSTRACT Total Hg and Se concentrations were determined in autopsy samples of retired Idrija mercury mine workers, Idrija residents living in a Hg-contami-nated environment, and a control group with no known Hg exposure from the environment. In selected samples we also checked the presence of MeHg. The highest Hg concentrations were found in endocrine glands and kidney cortex, regardless of the group. MeHg contributed only to a negligible degree to the total mercury concentrations in all analyzed samples. In the Hg-exposed groups the coaccumulation and retention of mercury and selenium was confirmed. Selenium coaccumulation with a Hg/Se molar ratio near 1 or higher was notable only in those tissue samples (thyroid, pituitary, kidney cortex, nucleus dentatus) where the mercury concentrations were >1 μg/g. After tissue separation of such samples the majority of these elements were found in the cell pellet. Because the general population is continuously exposed to Cd and possibly also to Pb from water, food, and/or air, in some samples the levels of these elements were also followed. In all examined control tissue samples the average values of Cd (kidney cortex, thyroid, hippocampus, cortex cerebellum, nucleus dentatus) and Pb (thyroid, hippocampus) exceeded the average values of Hg. Cd concentrations were the highest, particularly in kidney cortex and thyroids (μg/g), but no relationship between Cd and Se concentration was evident at the tissue level. Regarding the results in the control group, it is debatable which element is the more hazardous for the general population as concerns neurotoxicity.
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ABSTRACT: Reports from human case studies indicate a half-life for inorganic mercury in the brain of years - contradicting older radioisotope studies that estimated half-lives in the order of weeks to months in duration. This study systematically reviews available evidence on the retention time of inorganic mercury in humans and primates to better understand this conflicting evidence. A broad search strategy was used to capture 16,539 abstracts on the Pubmed database. Abstracts were screened to include only study types containing relevant information. 131 studies of interest were identified. Only 1 primate study made a numeric estimate for the half-life of inorganic mercury (227 - 540 days). Eighteen human mercury poisoning cases were followed up long term including autopsy. Brain inorganic mercury concentrations at death were consistent with a half-life of several years or longer. 5 radionucleotide studies were found, one of which estimated head half-life (21 days). This estimate has sometimes been misinterpreted to be equivalent to brain half-life - which ignores several confounding factors including limited radioactive half-life and radioactive decay from surrounding tissues including circulating blood. No autopsy cohort study estimated a half-life for inorganic mercury, although some noted bioaccumulation of brain mercury with age. Modeling studies provided some extreme estimates (69 days vs 22 years). Estimates from modeling studies appear sensitive to model assumptions, however predications based on a long half-life (27.4 years) are consistent with autopsy findings. In summary, shorter estimates of half-life are not supported by evidence from animal studies, human case studies, or modeling studies based on appropriate assumptions. Evidence from such studies point to a half-life of inorganic mercury in human brains of several years to several decades. This finding carries important implications for pharmcokinetic modeling of mercury and potentially for the regulatory toxicology of mercury.Toxicology and Applied Pharmacology 12/2013; · 3.98 Impact Factor
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ABSTRACT: Selenium–mercury interactions were most extensively studied in relation to alleviation of Hg toxicity by added selenium. This presentation considers the influence of mercury on endogenous selenium, on its tissue and cellular “status” after lifelong or acute exposure to mercury vapor (Hgo). Discussed are data obtained from (1) humans living near or working in a mercury mine, and (2) rats experimentally exposed in the mine. Mercury vapor is unique—or similar to methylmercury—because of its ability to penetrate cell membranes and so invade all cells, where it is oxidized in the biologically active form (Hg++) by catalase. Such in situ-generated ions can react with endogenously generated highly reactive Se metabolites, like HSe−, and render a part of the selenium unavailable for selenoprotein synthesis. Data on human populations indicate that in moderate Hg exposure combined with an adequate selenium supply through diet, Se bioavailability can be preserved. On the other hand, the results of an acute exposure study emphasize the dual role of selenium in mercury detoxification. Besides the well-known Se coaccumulation through formation of nontoxic Hg–Se complexes, we observed noticeable Se (co)excretion, at least at the beginning of exposure. The higher Hg accumulation rate in the group of animals with lower basal selenium levels can also point to selenium involvement in mercury excretion. In such conditions there is a higher probability for decreased selenoprotein levels (synthesis) in some tissues or organs, depending on the synthesis hierarchy.Biological Trace Element Research 119(3):212-220. · 1.31 Impact Factor
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ABSTRACT: This paper reviews the growing literature dealing with the antagonistic effect of selenium (Se) compounds on the toxicity of mercury (Hg) compounds in higher animals and organisms present in the aquatic environment. It covers both laboratory and field studies and summarizes the possible mechanisms that explain the protective action of Se compounds on mercuric mercury (Hg2+) and methylmercury (CH3Hg+) toxicity. The review is subdivided according to the molecular form of Hg and the organisms in which the antagonism has been studied. Many authors suggest that the protective effect of selenite on the toxicity of Hg2+ in mammals is due mainly to the in vivo formation of mercuric selenide (HgSe), a stable and biologically inert complex. The detection of HgSe has been confirmed in several studies in support of this mechanism. Possible mechanisms that may be involved in the antagonism between Se compounds and CH3Hg+ in mammals and aquatic organisms are also presented. The possibility of adding Se compounds to contaminated lakes and reservoirs as a remediation technique to limit the bioaccumulation of Hg2+ and CH3Hg+ is critically discussed.Environmental Reviews 05/2008; 16:71-92. · 1.65 Impact Factor