Mercury Toxicity and the Mitigating Role of Selenium (original) (raw)
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Selenium as a potential protective factor against mercury developmental neurotoxicity
Environmental Research, 2008
Experimental studies suggest that selenium (Se) may decrease methylmercury (MeHg) toxicity under certain exposure regimens. In epidemiological studies, the exposure to MeHg occurs from fish and seafood, which are also a source of beneficial nutrients such as selenium. However, little is known about the potential protective effects of dietary Se against MeHg neurotoxicity in humans. The possible interaction was assessed in two birth cohorts in the Faroe Islands, consisting of singleton term births from 1986 to 1987 (N = 1,022), and 1994 to 1995 (N = 182), respectively. Dietary habits in this fishing population included frequent consumption of seafood, including whale meat high in mercury. Both Hg and Se were measured in cord whole blood. Neurodevelopmental outcomes were evaluated at age 7 years in both cohorts, and the smaller cohort also included neurological assessment on several prior occasions. Each outcome was modeled as a function of Hg and Se interactions (with adjustments for potential risk factors) by expressing the effects of log 10 (Hg) within the lowest 25%, the middle 50%, and the highest 25% of the Se distribution. Surplus Se was present in cord blood, the average being a 10-fold molar excess above MeHg. Regression analyses failed to show consistent effects of Se, or statistically significant interaction terms between Se and MeHg. Overall, no evidence was found that Se was an important protective factor against MeHg neurotoxicity. Prevention, therefore, needs to address MeHg exposures rather than Se intakes. Because of the benefits associated with fish intake during pregnancy, consumers should be advised to maintain a high fish and seafood intake that is low in Hg contamination. Additional research is needed to determine the identity of the nutrients responsible for the beneficial effects.
Selenium–Mercury Interactions in Man and Animals
Biological Trace Element Research, 2007
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 (Hg o ). 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.
New Insights into Traditional Health Risk Assessments of Mercury Exposure: Implications of Selenium
Environmental Science & Technology, 2014
There is increasing evidence that selenium (Se) has a significant effect on mercury (Hg) toxicology; however, Hg exposure risk assessments usually consider only the amount of Hg present in the environment or in food. Based on the present understanding of mechanisms of interaction between Se and Hg, the physiology/toxicology of Se, and the toxicology of Hg, we propose a new criterion for Se/Hg exposure assessment. This criterion, which is based on Se-Hg interactions, considers not only the toxicological consequences of Hg exposure but also the benefits and/or adverse effects of Se intake, especially the adverse effects related to a Se deficiency/excess. According to an illustrative assessment based on the new criterion and nine existing criteria, large knowledge gaps in the traditional assessments of exposure to Hg and/or Se were found, including those that assessed the interactions between Hg and Se. These results suggest that future assessments of Hg exposure (or Se intake) should include both Se and Hg.
Antagonistic interactions between mercury (Hg) and selenium (Se), were evaluated in mouse (Mus mus-culus), as a mammalian model, in a series of controlled exposure experiments. The beneficial effect of Se against Hg toxicity involves a variety of biochemical and toxicological processes that have not been clarified yet. For this purpose, a metallomic workflow based on the use of size-exclusion chromatography (SEC) with inductively coupled plasma mass spectrometry (ICP-MS) detection was complemented with the speciation of selenoproteins and low molecular mass selenium species in serum and liver cytosolic extracts using a multidimensional approach based on SEC-AF-HPLC-ICPMS, using species-unspecific isotope dilution (SUID)-ICP-MS for selenium quantification. The results showed potential interactions between Hg/Se in organs and serum related to accumulation and detoxification processes, in addition to the effects of mercury on selenoproteins in hepatic cytosolic extracts and bloodstream when both elements are administrated at the same time. These results provide information about elements distribution , interactions and homeostasis and reveal the potential of metallomic approaches in exposure experiments.
Role of Selenium in Mercury Intoxication in Mice
Industrial Health, 2007
Studies were conducted to examine the effect of pre and post-treatment of selenium in mercury intoxication (20 µ µ µ µ µmole/ kg b.w. each given intraperitoneally) in mice in terms of lipid peroxidation (LPO), glutathione (GSH) content, activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and mercury concentration in liver, kidney and brain. No significant alteration was observed in all the organs examined after mercury or selenium treatment in LPO and GSH but administration of selenium (pre and post) resulted in an increase in the level of LPO and GSH. The activity of SOD was depleted in liver and kidney while that of GPx was lowered in liver of mercury exposed animals. Selenium administration resulted in restoration of the depletion of these enzymatic activities. The activity of CAT in liver and brain was enhanced both in mercury and selenium treated animals. Administration of selenium significantly arrested enhanced CAT activity. Kidney showed the highest mercury concentration among the organs examined. Administration of selenium resulted in further enhancement of mercury concentration in the tissues. An increase in selenium level in liver was observed after mercury treatment, which was also restored by mercury selenium co-administration. Our results indicate that the prooxidant effect of selenium was greater by its pretreatment.
Mercury-binding capacity of organic and inorganic selenium in rat blood and liver
Biological trace element research, 1998
The mercury-binding capacity of seleno-DL-methionine and selenium dioxide was assessed in male Wistar rats. Mercury was supplied as fish loaves made of northern pike or rainbow trout. We used a selenium concentration of 3.4 mg/kg fish, about sixfold compared to the equivalent quantity of mercury. Seleno-DL-methionine had a tendency to increase both methyl mercury and total mercury in blood, although it also seemed to reduce the proportion of methyl mercury of total mercury. Selenium dioxide lowered mercury levels by 24-29% both in the blood and in the liver of rats that were fed with northern pike.
Selenium and Redox Enzyme Activity in Pregnant Women Exposed to Methylmercury
Antioxidants
Selenium (Se) is a micronutrient with essential physiological functions achieved through the production of selenoproteins. Adequate Se intake has health benefits and reduces mercury (Hg) toxicity, which is important due to its neurotoxicity. This study determined the Se status and redox enzyme, including selenoproteins’, activity in pregnant women highly exposed to Hg (between 1 to 54 µg Hg/L blood) via fish consumption. A cross-sectional study enrolling 513 women between the first and third trimester of pregnancy from Madeira, Portugal was conducted, encompassing collection of blood and plasma samples. Samples were analyzed for total Se and Hg levels in whole blood and plasma, and plasma activity of redox-active proteins, such as glutathione peroxidase (GPx), thioredoxin reductase (TrxR) and thioredoxin (Trx). Enzyme activities were related to Se and Hg levels in blood. Se levels in whole blood (65.0 ± 13.1 µg/L) indicated this population had a sub-optimal Se status, which translat...
Influence of selenium dose on mercury distribution and retention in suckling rats
Journal of Applied Toxicology, 2009
It is well known that metal–metal interactions in the body are age-dependent. We studied the influence of increasing selenium (Se) doses on mercury (Hg) distribution and retention in the postnatal period in Hg-exposed suckling rats. Seven-day-old Wistar pups were pretreated with three different oral doses of Se as sodium selenite (6.45, 12.9 and 19.4 µmol Se kg−1 b.w.) over 3 days. This was followed by simultaneous Se (as sodium selenite) and Hg (as mercury chloride) oral administration over 4 days. The molar ratio between Se and Hg given to pups was 1:1, 2:1 and 3:1, respectively. Mercury and Se were measured in brain, kidneys, liver, plasma, erythrocytes and urine of pups on the day after the last administration by atomic absorption spectrometry. Results showed that in all samples Se concentrations rose almost proportionally to the dose of Se given to pups. Mercury concentration in organs, plasma and urine decreased with higher oral doses of Se. However, Hg concentration in erythrocytes increased with increasing Se dose. There was evidently a redistribution of Hg from plasma to erythrocytes at higher ratio of Se:Hg. Approximately equimolar doses of Se and Hg are necessary to produce maximum uptake of Hg by plasma and liver and minimum retention of Hg in the kidney and erythrocytes. Copyright © 2009 John Wiley & Sons, Ltd.