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Organic Selenium Supplementation Increases Mercury Excretion and Decreases Oxidative Damage in Long-Term Mercury-Exposed Residents from Wanshan, China

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Abstract

Due to a long history of extensive mercury mining and smelting activities, local residents in Wanshan, China, are suffering from elevated mercury exposure. The objective of the present study was to study the effects of oral supplementation with selenium-enriched yeast in these long-term mercury-exposed populations. One hundred and three volunteers from Wanshan area were recruited and 53 of them were supplemented with 100 μg of organic selenium daily as selenium-enriched yeast while 50 of them were supplemented with the nonselenium-enriched yeast for 3 months. The effects of selenium supplementation on urinary mercury, selenium, and oxidative stress-related biomarkers including malondialdehyde and 8-hydroxy-2-deoxyguanosine were assessed. This 3-month selenium supplementation trial indicated that organic selenium supplementation could increase mercury excretion and decrease urinary malondialdehyde and 8-hydroxy-2-deoxyguanosine levels in local residents.

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... Several studies support the theory that Hg toxicity is related to a Se deficiency induced by the irreversible binding of Hg to selenocysteines, the active seleno-amino acid in selenoproteins ( Raymond and Ralston, 2020 ;Manceau et al., 2021 ;Spiller, 2018 ). For instance, Inuit with high blood Se/Hg ratio had the lowest prevalence of cardiovascular diseases ( Hu et al., 2017 ), and a Chinese community exposed to Hg from mining waste that were given a high-Se yeast supplement (as selenomethionine) excreted more Hg than the people given the placebo ( Li et al., 2012 ). Furthermore, their lipid peroxidation was reduced after 30 days of Se supplementation ( Li et al., 2012 ). ...
... For instance, Inuit with high blood Se/Hg ratio had the lowest prevalence of cardiovascular diseases ( Hu et al., 2017 ), and a Chinese community exposed to Hg from mining waste that were given a high-Se yeast supplement (as selenomethionine) excreted more Hg than the people given the placebo ( Li et al., 2012 ). Furthermore, their lipid peroxidation was reduced after 30 days of Se supplementation ( Li et al., 2012 ). At high Hg concentrations, the Se-Hg binding could lead to a reduction of the selenoproteins activity ( Watanabe et al., 1999 ;Penglase et al., 2014 ), which are important in many physiological functions such as the reduction of oxygen free radicals ( Rayman, 2000 ). ...
... At high Hg concentrations, the Se-Hg binding could lead to a reduction of the selenoproteins activity ( Watanabe et al., 1999 ;Penglase et al., 2014 ), which are important in many physiological functions such as the reduction of oxygen free radicals ( Rayman, 2000 ). As most of Se in fish tissue is present as selenomethionine ( Janz et al., 2014 ;Cabanero et al., 2004 ), human Se intake from fish may increase Hg excretion and reduce the deleterious effects of Hg ( Li et al., 2012 ;Ribeiro et al., 2022 ). However, after 50 years of studies about Hg-Se interactions, we still need to reach a consensus about the benefits of Se consumed from fish and other food products in the context of human Hg toxicity ( Eagles-Smith et al., 2018 ). ...
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Mercury (Hg) and arsenic (As) contamination of fish can be toxic and limit safe human consumption, whereas selenium (Se) can potentially protect fish and consumers from the adverse effects of Hg and As. We assembled datasets of the above-mentioned elements in Canadian freshwater fish and compare them with risk assessment thresholds. We further assessed linkages between the elemental concentrations and anthropogenic activities and ecozones. Mercury concentrations exceeded the retail fish Canadian threshold (0.5 µg/g wet weight) in 31% of all Walleye; this proportion rose to 64% in reservoirs. Reservoirs and lakes impacted by logging and urbanization had higher fish [Hg] than other types of impacted systems. Se and As concentrations exceeded Canadian guidelines in 5% (aquatic life) and 0.2% of all fish, respectively. In mining areas, fish [Hg] were low and negatively correlated with [Se], and fish [Se] were positively correlated with [As]. In all areas, we observed an important overall and previously unpublished negative relationship between mean fish [As] and [Hg], suggesting an inverse consumption risk for these two elements. The ratio Se/Hg was lower than the protective value of 1 for 14% of all fish and was negatively correlated with fish length. However, the benefit-risk value (BRV) threshold, which accounts for the Se intake from other food products, did not suggest any fish consumption limitations, except for few very contaminated top predators (> 2 µg/g ww). More studies need to assess the role of Se against Hg toxicity and adjust fish consumption guidelines accordingly.
... (Se) has been reported to antagonize the toxicity of several heavy metals, including mercury (Falnoga & Tusek-Znidaric, 2007). To counteract or minimize Hg-induced toxicity, selenium compounds can act by improving antioxidant defenses ( Branco et al., 2014;Farina et al., 2011;Freitas et al., 2009;Kalender et al., 2013) and/or by inducing changes in the distribution, deposition and excretion of Hg (Farina et al., 2011;Freitas et al., 2009;Li et al., 2012). Nevertheless, there is a dearth of information about the molecular mechanism(s) involved in the protection afforded by organic forms of selenium against the toxicity of MeHg ( Freitas et al., 2009;Li et al., 2012). ...
... To counteract or minimize Hg-induced toxicity, selenium compounds can act by improving antioxidant defenses ( Branco et al., 2014;Farina et al., 2011;Freitas et al., 2009;Kalender et al., 2013) and/or by inducing changes in the distribution, deposition and excretion of Hg (Farina et al., 2011;Freitas et al., 2009;Li et al., 2012). Nevertheless, there is a dearth of information about the molecular mechanism(s) involved in the protection afforded by organic forms of selenium against the toxicity of MeHg ( Freitas et al., 2009;Li et al., 2012). ...
... As a corollary, it has been previously hypothesized that antioxidants might be useful tools to mitigate MeHg toxicity ( Barcelos et al., 2011;Farina et al., 2011;Franco et al., 2007;Liu et al., 2014;Lu et al., 2011), as there is no effective treatment to counteract completely its toxic effects. Accordingly, selenium compounds with antioxidant properties might offer efficacious treatment against injury caused by MeHg, as demonstrated here and in other studies (Cordero-Herrera et al., 2013;Farina et al., 2011;Freitas et al., 2009;Li et al., 2012). The protective effect of the selenium compounds, when cotreated with MeHg, might be related to the potential effects of these compounds to scavenge hydroxyl, superoxide and peroxyl radicals ( Cuello et al., 2007;Li et al., 2012). ...
Article
Exposure to methylmercury (MeHg), an important environmental toxicant, may lead to serious health risks, damaging various organs and predominantly affecting the brain function. The toxicity of MeHg can be related to the inhibition of important selenoenzymes, such as glutathione peroxidase (GPx) and thioredoxin reductase (TrxR). Experimental studies have shown that selenocompounds play an important role as cellular detoxifiers and protective agents against the harmful effects of mercury. The present study investigated the mechanisms by which diphenyl diselenide [(PhSe)2 ] and ebselen interfered with the interaction of mercury (MeHg) and selenoenzymes (TrxR and GPx) in an in vitro experimental model of cultured human neuroblastoma cells (SH-SY5Y). Our results established that (PhSe)2 and ebselen increased the activity and expression of TrxR. In contrast, MeHg inhibited TrxR activity even at low doses (0.5 μm). Coexposure to selenocompounds and MeHg showed a protective effect of (PhSe)2 on both the activity and expression of TrxR. When selenoenzyme GPx was evaluated, selenocompounds did not alter its activity or expression significantly, whereas MeHg inhibited the activity of GPx (from 1 μm). Among the selenocompounds only (PhSe)2 significantly protected against the effects of MeHg on GPx activity. Taken together, these results indicate a potential use for ebselen and (PhSe)2 against MeHg toxicity. Furthermore, for the first time, we have demonstrated that (PhSe)2 caused a more pronounced upregulation of TrxR than ebselen in neuroblastoma cells, likely reflecting an important molecular mechanism involved in the antioxidant properties of this compound. Copyright © 2017 John Wiley & Sons, Ltd.
... For decades, researchers have studied compounds to assist in reducing the amount of Hg in the body. Selenium (Se) is an element ingested to bind and form a compound with available Hg to excrete the compound out of the body (Chen et al. 2006;Hui et al. 2016;Li et al. 2012;Spiller 2018). ...
... Li et al. discovered that Se intake of approximately 42.1 µg via selenium yeast resulted in a 1.5-2.5-fold increase of excretion of Hg compared to the control group over 30 days (Li et al. 2012). There are common foods high in selenium, such as Brazil nuts (Moreda-Piñeiro et al. 2011), accessible near many active ASGM operations in South American regions. ...
... Eight criteria were used to assess each alternative. SMAA was used to assess the uncertainty of criteria ranges sampled using a uniform distribution and linear utility curves values for incorporating vegetable juices and Brazil nuts in diets to reduce mercury levels in target organ systems (Jovel et al., 2018;Li et al. 2012). As in the case of other chelation studies, we assumed that the community would have to consume the selenium product every day that this is a low-cost option (< 1 USD), and the environmental and human health impacts criteria (EIA, HQs, forms present, pathway reduction) stay the same as BAU criteria measurements. ...
Article
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Over 15 million people are involved in artisanal small-scale gold mining (ASGM) globally. Often, ASGM includes smelters that use mercury to extract gold. If mishandled, these actions may cause adverse health effects for smelters and their surrounding communities. There are multiple tools to reduce health risks while maintaining a sustainable economic profit, but each method has trade-offs, such as cost, efficiency, and potential health impacts that are not widely understood. Multicriteria decision analysis (MCDA) is a powerful tool in assessing multiple perspectives and factors that affect stakeholder decisions and can be used to inform smelters and community members on reducing exposure to mercury. Here, MCDA was used to determine the ranks of alternatives to reduce exposure to mercury based on socio-economic, ecological, and human health criteria. Stochastic processes were used to evaluate 12 alternatives, including mitigation strategies (i.e., chelation therapy techniques, retorts, water filters) as well as mercury-free mining substitutes. In this model, the borax method ranked first 72% of the time, followed by the gravity method (19%), a multicapture system retort (7%), and low-cost retorts (≤ 1%). While MCDA is an excellent tool, results tend to be generalized across a heterogenous landscape. More localized factors such as incorrect soil chemistry could cause performance challenges for options like mercury-free mining substitutes. To aid more localized decision-making, a decision tree model was developed to aid stakeholders to explore which alternatives are suitable based on context-specific factors using “Take-the-best” decision heuristics. This work can assist researchers and stakeholders involved with ASGM to identify which options are scalable for their region as well as to mitigate adverse effects of exposure to mercury.
... A recent study in humans suggested that supplementation with organic selenium may be protective against Hg intoxication because it enhances excretion of Hg [17]. Interestingly, this excretion does not occur until 15-30 days following exposure [17]. ...
... A recent study in humans suggested that supplementation with organic selenium may be protective against Hg intoxication because it enhances excretion of Hg [17]. Interestingly, this excretion does not occur until 15-30 days following exposure [17]. Little is known about how Se alters the disposition of inorganic forms of Hg within target organs during the initial period after exposure. ...
... Published studies have suggested that dietary supplementation with selenium may offer protection from mercury-induced intoxication [17,26]. One potential mechanism for this protection relates to the role of selenium as a component of glutathione peroxidase (GPx). ...
Article
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Mercury (Hg) is a common environmental toxicant to which humans are exposed regularly through occupational and dietary means. Although selenium supplementation has been reported to prevent the toxic effects of Hg in animals, the mechanisms for this prevention are not well understood. The purpose of the current study was to determine the effects of selenium on the disposition and toxicity of Hg. Wistar rats were injected intravenously with a non-nephrotoxic dose (0.5 μmol kg⁻¹) or a nephrotoxic dose (2.5 μmol kg⁻¹) of HgCl2 (containing radioactive Hg) with or without co-administration of sodium selenite (Na2SeO3). Twenty-four hours after exposure, rats were euthanized, and organs were harvested. Co-administration of SeO3²⁻ with HgCl2 reduced the renal burden of Hg and the urinary excretion of Hg while increasing the amount of Hg in blood and spleen. We propose that Hg reacts with reduced selenite in the blood to form large Hg–Se complexes that are unable to be filtered at the glomerulus. Consequently, these complexes remain in the blood and are able to accumulate in blood-rich organs. These complexes, which may have fewer toxic effects than other species of Hg, may be eliminated slowly over the course of weeks to months.
... Page 3/33 been studied for their ability to modulate metabolic pathways involved in detoxi cation processes. Several preliminary studies have demonstrated that food extracts and nutrients can regulate the transduction and eventual excretion of toxins [10][11][12][13][14][15]. Typically, detox diets are calorie-restricted diets consisting of a single fruits, vegetables, or beverages (tea, vinegar, lemon juice, salt water, or drinks mixed with micronutrients) [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25]. ...
... Several preliminary studies have demonstrated that food extracts and nutrients can regulate the transduction and eventual excretion of toxins [10][11][12][13][14][15]. Typically, detox diets are calorie-restricted diets consisting of a single fruits, vegetables, or beverages (tea, vinegar, lemon juice, salt water, or drinks mixed with micronutrients) [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25]. The diet detox program known as the lemon diet and hypocaloric Mediterranean diet [16,26] were a very low-calorie diet (LCD) that allows 500 to 1,000 kcal per day and is effective in reducing body weight and fat; however, this dietary intervention is di cult to maintain and can lead to shortages of minerals, vitamins, and dietary ber, as well as increased binge eating and stress [27,28]. ...
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Background: Detox diet are known as a popular dieting strategies that helps toxins elimination and weight manage but there is very little clinical evidence. The Wellnessup diet (WD) used in the present study designed as a healthy meals based on organic plant based diets including various vegetables, fruits, whole grains, nuts and phytonutrients. Methods: To evaluate the effects of 4 week intake of the WD on toxic trace element detoxification, body fat reduction, and safety parameters. Forty-five women with body mass index (BMI) of 23.5-30 kg/m 2 were recruited. Thirty of them were assigned 1:1 to the test group (WD, 15 subjects) and control group 1 (calorie-restricted diet, CRD, 15 subjects) in a single blind and randomized, and the remaining 15 subjects were assigned to control group 2 (maintaining regular diet, MRD). The primary outcome were toxic trace element levels in hair (29 types of heavy metals), and the secondary outcomes were changes in anthropometric and urinary organic acids. Results: The levels of four toxic trace elements in hair decreased in the WD group after the diet compared to before the diet. Ni, Rh, Sn, and Ga were significantly lower in the WD group than in the CRD or MRD group (p<0.05). At the end of the trial, both WD and CRD groups had lower BMI, Waist Circumference(WC), Hip Circumference(HC) and WHR compared to the baseline values (p<0.05). Compared to the WD group, the CRD group had a greater mean change (p<0.05) from the baseline for weight loss (-3.22±0.48kg vs -1.88±0.95kg vs) and fat free mass (-2.08 kg vs -1.09 kg). The weight, BMI, body fat mass, fat free mass, WC, and HC of the CRD group were significantly decreased compared to the MRD (p<0.05). No significant changes in any safety parameter were observed. Conclusions: Use of WD might have several beneficial effects and safety such as body fat reduction and improving some the element detoxification through caloric restriction but did not reducing body fat mass more than calorie-restricted diet.
... In analogy, hydrogen selenide (H 2 Se) can be considered a nonorganic equivalent of the selenol (−SeH) group For adult humans, the dietary recommended daily intake of selenium is about 1 μg/kg of body weight (Metanis et al. 1995;NAS 2000). The deficiency of dietary selenium has been considered an important factor in diseases such as the Keshan disease (endemic cardiomyopathy) and Kashin-Beck disease (degenerative osteoarthropathy) (Navarro-Alarcon and López-Martínez 2000;Chen 2012). In contrast, intentional, accidental, or chronic intake of selenium has been associated with problems in nail and hair structure, in the gastrointestinal function or neurological damage (Vinceti et al. 2001(Vinceti et al. , 2009Aldosary et al. 2012). ...
... Selenite is oxidized to selenide in the erythrocytes. In the plasma, selenide plus reduced glutathione (GSH) may interact with Hg 2+ -albumin complexes, forming HgSe-SG complex, which binds to SepP1, diverging Hg 2+ from the brain and kidneys Of particular therapeutic significance for remediating the toxicity of mercury, Li et al. (2012) demonstrated that inhabitants of extensive mercury mining areas in China supplemented with 100 μg of organic selenium (selenium-enriched yeast) daily presented an increase in the excretion of mercury in the urine and a decrease in markers of oxidative stress (urinary malondialdehyde and 8-hydroxy-2deoxyguanosine), when compared to the placebo group. The study was performed during 90 days, and the beneficial effects of organic selenium was detected from 30 to 90 days after starting the supplementation. ...
Chapter
Full-text available
Methylmercury (MeHg), an organomercurial, is one of the most prevalent and toxic environmental pollutants. The major route of human exposure occurs via consumption of MeHg-adulterated seafood. Historically, MeHg epidemics in Minamata Bay, Japan, and in Iraq provided evidence of its developmental toxicity and neurological damage. This chapter describes MeHg kinetics in the human body and focuses predominantly on mechanisms involved in neuropathological and reproductive effects. The chapter also discusses the differential susceptibility to MeHg in fetuses and adults, with a special emphasis on its aberrant effects in the developing central nervous system. Discussions on risk assessment, treatment, and future directions are also covered in this chapter.
... In analogy, hydrogen selenide (H 2 Se) can be considered a nonorganic equivalent of the selenol (−SeH) group For adult humans, the dietary recommended daily intake of selenium is about 1 μg/kg of body weight (Metanis et al. 1995;NAS 2000). The deficiency of dietary selenium has been considered an important factor in diseases such as the Keshan disease (endemic cardiomyopathy) and Kashin-Beck disease (degenerative osteoarthropathy) (Navarro-Alarcon and López-Martínez 2000;Chen 2012). In contrast, intentional, accidental, or chronic intake of selenium has been associated with problems in nail and hair structure, in the gastrointestinal function or neurological damage (Vinceti et al. 2001(Vinceti et al. , 2009Aldosary et al. 2012). ...
... Selenite is oxidized to selenide in the erythrocytes. In the plasma, selenide plus reduced glutathione (GSH) may interact with Hg 2+ -albumin complexes, forming HgSe-SG complex, which binds to SepP1, diverging Hg 2+ from the brain and kidneys Of particular therapeutic significance for remediating the toxicity of mercury, Li et al. (2012) demonstrated that inhabitants of extensive mercury mining areas in China supplemented with 100 μg of organic selenium (selenium-enriched yeast) daily presented an increase in the excretion of mercury in the urine and a decrease in markers of oxidative stress (urinary malondialdehyde and 8-hydroxy-2deoxyguanosine), when compared to the placebo group. The study was performed during 90 days, and the beneficial effects of organic selenium was detected from 30 to 90 days after starting the supplementation. ...
Chapter
The antagonism of mercury toxicity by selenium has been well documented. Mercury is a toxic metal, widespread in the environment. The main target organs (kidneys, lungs, or brain) of mercury vary depending on its chemical forms (inorganic or organic). Selenium is a semimetal essential to mammalian life as part of the amino acid selenocysteine, which is required to the synthesis of the selenoproteins. This chapter has the aim of disclosing the role of selenide or hydrogen selenide (Se⁻² or HSe⁻) as central metabolite of selenium and as an important antidote of the electrophilic mercury forms (particularly, Hg²⁺ and MeHg). Emphasis will be centered on the neurotoxicity of electrophile forms of mercury and selenium. The controversial participation of electrophile mercury and selenium forms in the development of some neurodegenerative disease will be briefly presented. The potential pharmacological use of organoseleno compounds (Ebselen and diphenyl diselenide) in the treatment of mercury poisoning will be considered. The central role of thiol (−SH) and selenol (−SeH) groups as the generic targets of electrophile mercury forms and the need of new in silico tools to guide the future biological researches will be commented.
... Moreover, Se is an essential trace element for plants, animals and human beings, although high levels of Se in soil could lead to potential environmental risk [22,23], e.g., > 10 mg/kg of Se amendment into soil resulted in a decreased dry matter yield of rice shoots [24]. Studies have indicated that Se can protect mammals, aquatic organisms and humans from Hg toxicity and bioaccumulation [16,[25][26][27], and Se intake/supplementation may be beneficial for mitigating the health risk of Hg exposure [27,28]. Thus, applying a certain amount of Se in Hg-contaminated paddy soil could be helpful for increasing Se levels in rice grain which may further reduce the health risk of dietary MeHg exposure from rice consumption. ...
... Moreover, Se is an essential trace element for plants, animals and human beings, although high levels of Se in soil could lead to potential environmental risk [22,23], e.g., > 10 mg/kg of Se amendment into soil resulted in a decreased dry matter yield of rice shoots [24]. Studies have indicated that Se can protect mammals, aquatic organisms and humans from Hg toxicity and bioaccumulation [16,[25][26][27], and Se intake/supplementation may be beneficial for mitigating the health risk of Hg exposure [27,28]. Thus, applying a certain amount of Se in Hg-contaminated paddy soil could be helpful for increasing Se levels in rice grain which may further reduce the health risk of dietary MeHg exposure from rice consumption. ...
Article
Methylmercury (MeHg) accumulation in rice is an emerging food safety issue in China and other countries; however, mitigation methods are scarce. Here, the effects of selenium (Se) and multiple applications of Se and biochar on rice MeHg bioaccumulation were investigated using pot and microcosm experiments. We report that Se amendment was still effective in reducing MeHg levels in paddy soil and rice grain after three years of aging. Biochar amendment (0.5% w/w) further decreased grain (brown rice) MeHg levels by 82–87%. The grain MeHg level decrease following the combination of Se and biochar amendment could be partly attributed to inhibition of net MeHg production in soil by Se. In addition, biochar decreased not only net MeHg production but also MeHg bioavailability in the soil, which could be due to organosulfur compounds in the biochar. Our findings suggest that multiple applications of Se and biochar could be a novel remediation strategy to mitigate MeHg accumulation in rice.
... mcg/L) after initiation of oral Se and NAC and remained elevated for four months ( Figure 2). Li et al. [25,26] showed an increase in urinary Hg in humans after supplementation with organoselenium as selenomethionine. The increase in urinary Hg did not occur for 15-30 days post-selenium supplementation, suggesting a redistribution of total body mercury rather than any direct renal effect [25,26]. ...
... Li et al. [25,26] showed an increase in urinary Hg in humans after supplementation with organoselenium as selenomethionine. The increase in urinary Hg did not occur for 15-30 days post-selenium supplementation, suggesting a redistribution of total body mercury rather than any direct renal effect [25,26]. The urine mercury at five and eight months has fallen. ...
Article
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A healthy 15-year-old male spilled elemental mercury contaminating his garage and bedroom. The patient developed new onset hypertension, significant weight loss, pain (muscular, testicular, and abdominal), insomnia, delusions, hallucinations, tachycardia, palmar desquamation, diaphoresis, tremor, and ataxia leading to two consecutive hospitalizations. Blood and urine mercury were 23 and 330 µg/L, respectively. He received 21 days of chelation with 2,3-Dimercaptosuccinic acid during his second hospital stay. He continued to deteriorate. Three weeks post-chelation, he was transferred to our facility and his exam was unchanged. He could not stand or feed himself unassisted. He was started on selenium 500 mcg/day and N-acetylcysteine (NAC) 50 mg/kg/day. By day 3 of Se and NAC, he showed noticeable improvement, and by day 11, delusions, delirium, tachycardia, and abdominal pain resolved. Muscle strength, weight gain, speech, unassisted ambulation, and emotional liability improved. After five months with Se and NAC (1) he had regained 45 pounds, (2) restored to premorbid emotional, academic, and athletic performance, and (3) tachycardia, hypertension, rash, palmar skin changes, tremor, and insomnia had resolved. Features of this case include (1) improvement after selenium and NAC supplementation (2) contrasted with continued deterioration after DMSA chelation.
... In dietary MeHg þ exposure in cats and quail, groups with selenium supplementation in the diet showed reduced incidence of toxicity and none of the fatalities seen with the MeHg þ alone groups [43]. Similar "protective" effects have been reported in additional animal models and humans [57,[90][91][92][93]. In healthy marine mammals, marine fish, and humans, the selenium:mercury molar ratio approximates 1:1 [39,[94][95][96][97]. ...
... In long-term models more consistent with the human exposures, selenium supplementation decreases whole body retention of Hg [105,115]. Li et al. [92,93] showed an increase in urinary Hg in humans after supplementation with organoselenium as seleomethionine. The increase did not occur for 15-30 days post-selenium supplementation, suggesting a redistribution of total body mercury rather than any direct renal effect. ...
Article
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Introduction: There is increasing evidence that the pathophysiological target of mercury is in fact selenium, rather than the covalent binding of mercury to sulfur in the body’s ubiquitous sulfhydryl groups. The role of selenium in mercury poisoning is multifaceted, bidirectional, and central to understanding the target organ toxicity of mercury. Methods: An initial search was performed using Medline/PubMed, Toxline, Google Scholar, and Google for published work on mercury and selenium. These searches yielded 2018 citations. Publications that did not evaluate selenium status or evaluated environmental status (e.g., lake or ocean sediment) were excluded, leaving approximately 500 citations. This initial selection was scrutinized carefully and 117 of the most relevant and representative references were selected for use in this review. Binding of mercury to thiol/sulfhydryl groups: Mercury has a lower affinity for thiol groups and higher affinity for selenium containing groups by several orders of magnitude, allowing for binding in a multifaceted way. The established binding of mercury to thiol moieties appears to primarily involve the transport across membranes, tissue distribution, and enhanced excretion, but does not explain the oxidative stress, calcium dyshomeostasis, or specific organ injury seen with mercury. Effects of mercury on selenium and the role this plays in the pathophysiology of mercury toxicity: Mercury impairs control of intracellular redox homeostasis with subsequent increased intracellular oxidative stress. Recent work has provided convincing evidence that the primary cellular targets are the selenoproteins of the thioredoxin system (thioredoxin reductase 1 and thioredoxin reductase 2) and the glutathione-glutaredoxin system (glutathione peroxidase). Mercury binds to the selenium site on these proteins and permanently inhibits their function, disrupting the intracellular redox environment. A number of other important possible target selenoproteins have been identified, including selenoprotein P, K, and T. Impairment of the thioredoxin and glutaredoxin systems allows for proliferation intracellular reactive oxygen species which leads to glutamate excitosis, calcium dyshomeostasis, mitochondrial injury/loss, lipid peroxidation, impairment of protein repair, and apoptosis. Methylmercury is a more potent inhibitor of the thioredoxin system, partially explaining its increased neurotoxicity. A second important mechanism is due to the high affinity of mercury for selenium and the subsequent depletion of selenium stores needed for insertion into de novo generation of replacement selenoproteins. This mercury-induced selenium deficiency state inhibits regeneration of the selenoproteins to restore the cellular redox environment. The effects of selenium on mercury and the role this plays in biological response to mercury: Early research suggested selenium may provide a protective role in mercury poisoning, and with limitations this is true. The roles selenium plays in this reduction of mercury toxicity partially depends on the form of mercury and may be multifaceted including: 1) facilitating demethylation of organic mercury to inorganic mercury; 2) redistribution of mercury to less sensitive target organs; 3) binding to inorganic mercury and forming an insoluble, stable and inert Hg:Se complex; 4) reduction of mercury absorption from the GI tract; 5) repletion of selenium stores (reverse selenium deficiency); and 6) restoration of target selenoprotein activity and restoring the intracellular redox environment. There is conflicting evidence as to whether selenium increases or hinders mercury elimination, but increased mercury elimination does not appear to be a major role of selenium. Selenium supplementation has been shown to restore selenoprotein function and reduce the toxicity of mercury, with several significant limitations including: the form of mercury (methylmercury toxicity is less responsive to amelioration) and mercury dose. Conclusions: The interaction with selenium is a central feature in mercury toxicity. This interaction is complex depending on a number of features such as the form of mercury, the form of selenium, the organ and dose. The previously suggested “protective effect” of selenium against mercury toxicity may in fact be backwards. The effect of mercury is to produce a selenium deficiency state and a direct inhibition of selenium’s role in controlling the intracellular redox environment in organisms. Selenium supplementation, with limitations, may have a beneficial role in restoring adequate selenium status from the deficiency state and mitigating the toxicity of mercury.
... The sample introduction system consists of a classical Meinhard nebuliser with a Scott double-pass quartz spray chamber at room temperature. The collision cell technique (CCT) was employed for the elimination of the polyatomic interferences of 40 Ar and others in the detection of 80 Se. The ICP-MS and the HPLC operating conditions used in this work are summarized in Table 1. ...
... C3 and S3: the isotope ratio chromatograms for 202 Hg/ 199 Hg after mathematical corrections. a consequence of the increased excretion of Hg through urine, feces, or inhalation etc [40,41]. Noticeably, the reduced level of Hg in serum was closely associated with the elevated level of Se (the second column from left, Table 1). ...
Article
Selenium (Se) has been found to promote weight gain, decrease hepatic damage, but redistribute mercury (Hg) in brains and livers in methylmercury (MeHg)-poisoned rats. The aims of the present work were to examine the effects of Se on the levels of Hg in serum and the role of serum selenoproteins in binding with Hg in MeHg-poisoned rats. The concentration of Se, Hg and MeHg were studied using ICP-MS and CVAFS. The Hg- and Se-binding selenoproteins were separated and quantified using affinity chromatography with post-column isotope dilution analysis using both enriched 78Se and 199Hg. It was found that Se treatment reduced Hg levels in serum in MeHg-poisoned rats. Among the three separated selenoproteins, the amounts of SelP-bound Hg and Se increased to 73% and 93.6%, from 64.4% and 89.3% of the total Hg and Se, respectively after Se treatment, suggesting that SelP acts as a major transporter for Hg and pool for Se in serum. Over 90% of the total Hg was MeHg in serum, and the molar ratios of MeHg to Se as 1:4 and 1:9 in the formed MeHg-Se-SelP complex in the control and the Se treatment group, respectively. The elevated Se level binding with SelP facilitated the Hg extraction from tissues and organs, as well as its redistribution in brains and livers through blood circulation in the MeHg-poisoned rats. Together, our findings provide direct evidence that serum SelP is the major Hg transporter in MeHg-poisoned rats.
... Nevertheless, food-based nutrients have been studied for their ability to modulate metabolic pathways involved in detoxification processes. Several preliminary studies have demonstrated that food extracts and nutrients can regulate the transduction and eventual excretion of toxins [10][11][12][13][14][15]. Typically, detox diets are calorie-restricted diets consisting of a single fruits, vegetables, or beverages (tea, vinegar, lemon juice, salt water, or drinks mixed with micronutrients) [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25]. ...
... Several preliminary studies have demonstrated that food extracts and nutrients can regulate the transduction and eventual excretion of toxins [10][11][12][13][14][15]. Typically, detox diets are calorie-restricted diets consisting of a single fruits, vegetables, or beverages (tea, vinegar, lemon juice, salt water, or drinks mixed with micronutrients) [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25]. The diet detox program known as the lemon diet and hypocaloric Mediterranean diet [16,26] were a very low-calorie diet (LCD) that allows 500 to 1000 kcal per day and is effective in reducing body weight and fat; however, this dietary intervention is difficult to maintain and can lead to shortages of minerals, vitamins, and dietary fiber, as well as increased binge eating and stress [27,28]. ...
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Background: Detox diet are known as a popular dieting strategies that helps toxins elimination and weight manage but there is very little clinical evidence. The Wellnessup diet (WD) used in the present study designed as a healthy meals based on organic plant based diets including various vegetables, fruits, whole grains, nuts and phytonutrients. Methods: To evaluate the effects of 4 week intake of the WD on toxic trace element detoxification, body fat reduction, and safety parameters. Forty-five women with body mass index (BMI) of 23.5-30 kg/m2 were recruited. Thirty of them were assigned 1:1 to the test group (WD, 15 subjects) and control group 1 (calorie-restricted diet, CRD, 15 subjects) in a single blind and randomized, and the remaining 15 subjects were assigned to control group 2 (maintaining regular diet, MRD). The primary outcome were toxic trace element levels in hair (29 types of heavy metals), and the secondary outcomes were changes in anthropometric and urinary organic acids. Results: The levels of four toxic trace elements in hair decreased in the WD group after the diet compared to before the diet. Ni, Rh, Sn, and Ga were significantly lower in the WD group than in the CRD or MRD group (p < 0.05). At the end of the trial, both WD and CRD groups had lower BMI, Waist Circumference(WC), Hip Circumference(HC) and WHR compared to the baseline values (p < 0.05). Compared to the WD group, the CRD group had a greater mean change (p < 0.05) from the baseline for weight loss (- 3.22 ± 0.48 kg vs - 1.88 ± 0.95 kg vs) and fat free mass (- 2.08 kg vs - 1.09 kg). The weight, BMI, body fat mass, fat free mass, WC, and HC of the CRD group were significantly decreased compared to the MRD (p < 0.05). No significant changes in any safety parameter were observed. Conclusions: Use of WD might have several beneficial effects and safety such as body fat reduction and improving some the element detoxification through caloric restriction but did not reducing body fat mass more than calorie-restricted diet. Trial registration: This study was registered at Clinical Research Information Service (CRIS) of Republic of Korea (KCT0003002).
... A pilot Se supplementation trial in peoples exposed to MeHg through fish consumption found significantly reduced pubic hair Hg level, suggesting Se could reduce the body load of Hg in these exposed populations (Seppanen et al. 2000). Treatment with appropriate level of Se in rice planted in Hg contaminated farmland was found to reduce Hg accumulation in grains, thereafter to protect the health of the rice-consuming populations (Li et al. 2015b) Se supplementation was also found to decrease urinary malondialdehyde (MDA) and 8-hydroxy-2-deoxyguanosine levels in the Hg exposed residents due to Hg mining, thus promoted their health status (Li et al. 2012). Our recent animal study found decreased hepatic MDA levels and urinary Hg excretion in MeHg poisoned rats after Se treatment (Jing et al. 2014). ...
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Methylmercury is a toxic pollutant and is generated by microbial methylation of elemental or inorganic mercury in the environment. Previous study found decreased hepatic MDA levels and urinary mercury levels in methylmercury poisoned rats after sodium selenite treatment. This study further found increased mercury levels in serum samples from methylmercury poisoned rats after selenium treatment. By using size exclusion chromatography coupled to inductively coupled plasma mass spectrometry, three Hg- binding protein fractions and two Se-binding protein fractions were identified with the molecular weight of approximately 21, 40, and 75 kDa and of 40 and 75 kDa, respectively. Elevated mercury level in the 75 kDa protein fraction was found binding with both Hg and Se, which may explain the decreased urinary Hg excretion in MeHg poisoned rats after Se treatment. MALDI-TOF-MS analysis of the serum found that the 75 kDa protein fractions were albumin binding with both Hg and Se and the 21 kDa fraction was Hg- binding metallothionein.
... previous study showed that sodium selenite (Se 4+ ) promoted weight gain and reduced the oxidative damage to the liver in MeHg-poisoned rats (Jing et al., 2014). Moreover, oral supplementation of Se-enriched yeast in Hg-exposed people could promote urinary excretion of Hg and reduce oxidative damage (Li et al., 2012). Se and Vitamin E cosupplements in MeHg-poisoned rats altered the reproductive and developmental toxicity of MeHg (Beyrouty and Chan, 2006). ...
... For example, a large-scale study evaluating exposure by dentists to low levels of mercury confirmed the inhibition of mercury absorption by dietary ethanol [8]. Residents of a former mercury mining area in Wanshan, China, with mild mercury exposure as indicated by blood analysis, showed benefits of a selenium-enriched diet [9]. Subjects of this three-month controlled study took selenium yeast product and had a higher urinary mercury excretion than the placebo group. ...
... The holistic overview of Hg-Se relationships, where Se plays direct and/or indirect (through mainly selenoproteins) role is a well-known topic among many scientists. Data on the occurrence of correlation between metabolism of Hg and expression of selenoproteins in the occupationally (elemental Hg vapor) and environmentally (organic form of Hg) exposed people is still limited [33, [89][90][91]. Studies on humans concerning dysfunction of cellular redox system, disruption of the glutathione system and system-related enzymes glutathione-S-transferase (GST), TrxR and glutamate cysteine ligase (GCL) by exposure to Hg are inadequate. ...
Article
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Diverse forms of mercury (Hg) have various effects on animals and humans because of a variety of routes of administration. Inorganic mercury (iHg) binds to thiol groups of proteins and enzymes in one's body or is methylated by microorganisms. Organic form of Hg, contrary to the iHg, is more stable but may be demethylated to Hg2+ in the tissue of intestinal flora. Selenium (Se) also occurs in a variety of chemical forms in one's body but both of these elements behave very differently from one another. Mercury binding to selenide or Se-containing ligands is a primary molecular mechanism that reduces toxicity of Hg. Complexes formed in such a way are irreversible, and thus, biologically inactive. Se deficiency in a human body may impair normal synthesis of selenoproteins and its expression because expression of mRNA may be potentially regulated by the Se status. This paper provides a comprehensive review concerning Hg-Se reciprocal action as a potential mechanism of protective action of Se against Hg toxicity as well as a potential detoxification mechanism. Although interactions between Hg-Se have been presented in numerous studies concerning animals and humans, we have focused mainly on animal models so as to understand molecular mechanisms responsible for antagonism better. The review also investigates what conclusions have been drawn by researchers with respect to the chemical species of Se and Hg (and their relationship) in biological systems as well as genetic variations and expression and/or activity of selenoproteins related to the thioredoxin (thioredoxin Trx/TrxR) system and glutathione metabolism.
... Selenium's potential to moderate mercury toxicity has been the subject of studies suggesting the existence of buffering effects on mercury toxicity when the 366 ADAMS selenium : mercury molar ratio exceeds 1:1 (Ralston 2008;Peterson et al. 2009), but this has not been proven in humans (Gribble et al. 2016). Organic selenium in the human diet may increase elimination of mercury (Li et al. 2012). Perry et al. (2012) analyzed 31 Cobias from the northern Gulf and found that 23% contained more mercury than selenium, but the relationship to mercury toxicity is not known. ...
Article
In marine ecosystems, upper-trophic-level pelagic fish often contain high concentrations of mercury. Individuals of several frequently landed marine fish species bioaccumulate mercury at concentrations linked directly to effects on fish physiology and human health risks. Knowledge of mercury in Cobia Rachycentron canadum has been limited. With this study, I addressed that problem by providing a comprehensive assessment of mercury in muscle taken from Cobia specimens within a range of size and age classes representative of those targeted by the recreational and commercial fisheries operating in the southeastern United States (Atlantic Ocean and eastern Gulf of Mexico). Total mercury concentration (THg) in muscle ranged from 0.025 to 3.9 mg/kg (wet weight), with a mean of 0.743 mg/kg (± 0.609 SD). In approximately 95% of all legal-size Cobia (≥838.2 mm fork length) THg exceeded 0.3 mg/kg (U.S. Environmental Protection Agency human health screening value for mercury). Proposed and recent increases in size limits for Cobia in some waters of the southeastern United States would further increase this percentage. These results for Cobia from the western Atlantic and Gulf of Mexico further substantiate current fish consumption advisories and provide guidance for new or revised advisories in other regions.
... Selenium also affects mercury elimination by reducing its urinary and fecal excretion, the main pathway for the elimination of inorganic mercury from the body (Fang 1977;Magos and Webb 1976). Li et al. (2012) studied residents in Hg mine areas with inorganic Hg poisoning, and the results indicated that a moderate 3-month selenium supplementation could increase mercury elimination and decrease urinary malondialdehyde and 8-hydroxy-2-deoxyguanosine levels in local residents. Epidemiological studies indicated a possible benefit of Se intake to reduce Hg cardiovascular toxicity (Buettner 2003;Yoshizawa et al. 2002). ...
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The aim of the study was to evaluate Hg and Se concentrations and Se:Hg molar ratios in the placenta, umbilical cord and fetal membranes, and to examine the relationship between the concentrations of the elements and selected factors. The study material consisted of the placenta, umbilical cord and fetal membranes obtained from 91 healthy women from northwestern and central Poland. In our study mean Hg and Se concentrations in afterbirth were ~ 0.01 mg/kg dry weight (dw) and ≤ 0.5 mg/kg dw, respectively. Correlation analysis showed negative relationships between placenta weight and Se concentration in the placenta and umbilical cord, as well as between placenta length and Se levels in the umbilical cord. We found negative correlations between THg concentration in the placenta and birth weight and between Se concentration in the placenta and umbilical cord and the morphological parameters of the placenta. Furthermore, we noted new types of interactions in specific parts of the afterbirth. In our study, Se:THg molar ratios ranged from 5 to 626; these values indicate protection against Hg toxicity.
... Selenite and organic Se compounds (selenocysteine and selenomethionine) tend to be more protective than species such as selenate (Cuvin-Aralar and Furness 1991; Khan and Wang 2009;Dang and Wang 2011). Although a consensus is still lacking, the ameliorative effects of Se on Hg toxicity have been postulated to occur through a range of mechanisms, including reducing assimilation and (Bjerregaard et al. 2011;Bjerregaard and Christensen 2012;Li et al. 2012;Huang et al. 2013), rendering Hg biologically unavailable through covalent bonding between Hg and Se (Yang et al. 2008), demethylation of MeHg in the liver or other organs (Eagles-Smith et al. 2009;Khan and Wang 2009), or through supporting the glutathione antioxidant pathway (Sormo et al. 2011). Various degrees of empirical support exist for each of these mechanisms, highlighting both the complexity of the Hg-Se interaction as well as its ubiquity across physiological processes. ...
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Environmental mercury (Hg) contamination is an urgent global health threat. The complexity of Hg in the environment can hinder accurate determination of ecological and human health risks, particularly within the context of the rapid global changes that are altering many ecological processes, socioeconomic patterns, and other factors like infectious disease incidence, which can affect Hg exposures and health outcomes. However, the success of global Hg-reduction efforts depends on accurate assessments of their effectiveness in reducing health risks. In this paper, we examine the role that key extrinsic and intrinsic drivers play on several aspects of Hg risk to humans and organisms in the environment. We do so within three key domains of ecological and human health risk. First, we examine how extrinsic global change drivers influence pathways of Hg bioaccumulation and biomagnification through food webs. Next, we describe how extrinsic socioeconomic drivers at a global scale, and intrinsic individual-level drivers, influence human Hg exposure. Finally, we address how the adverse health effects of Hg in humans and wildlife are modulated by a range of extrinsic and intrinsic drivers within the context of rapid global change. Incorporating components of these three domains into research and monitoring will facilitate a more holistic understanding of how ecological and societal drivers interact to influence Hg health risks.
... Sodium selenite has been shown to reduce the Hg content in rice [29]. Yeast Se increased Hg content in urine [30], but also reduced Hg deposition in the body [31]. In this experiment, Se was found to significantly affect toxic microelements. ...
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Se entering the mammalian body from diverse sources shows different liver accumulation patterns. However, the effects of Se from diverse sources on the body’s I on spectrum and the relationship between the changes in the ion spectrum and antioxidant function are not clear. In this study, 80 3-week-old female mice were randomly divided into four groups: a control group, sodium selenite group, yeast Se group, and seaweed Se group. The estimated Se contents were 0.03, 0.23, 0.23, and 0.23 mg/kg, respectively. The liver was collected from mice on day 60. The results showed that, compared with the control group, sodium selenite significantly reduced Na and Li contents and significantly increased Cr, Ni, Se, and Sb contents (P < 0.05); yeast Se significantly increased Mg, Ca, Si, Cr, Fe, Co, Cu, Se, Sb, and Al contents, and significantly reduced Tl, As, and Hg contents (P < 0.05); seaweed Se significantly increased B, Si, Cr, Fe, Se, As, and Hg contents, and significantly reduced Zn and Tl contents (P < 0.05). The results of antioxidant parameter analysis showed that Se from three sources increased total superoxide dismutase content and significantly reduced malondialdehyde content (P < 0.05), whereas no clear effect was observed on total antioxidant capacity (P > 0.05). Combined with the ion spectrum and antioxidant test results, yeast Se was found to most effectively promote the accumulation of beneficial elements, enhance antioxidant capacity, and reduce the concentration of toxic elements. The variety of ion spectrum antioxidants followed a similar trend, which indicated that the ion spectrum might be related to antioxidant activity.
... Selenium (Se) is an essential trace element for animals [18] and is involved in various biological processes [19,20]. Se can antagonize toxicity induced by heavy metals, such as mercury in K-562 cells [21] and in residents [22], cadmium (Cd) in chicken livers [23], and Pb in chicken bursa of Fabricius [24]. Se alleviated Pb-induced iNOS mRNA and protein expression in chicken neutrophils [25], Cd-induced ER stress in chicken kidneys [26] and neutrophils [27], and apoptosis in chicken livers [23] and neutrophils [27]. ...
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Lead (Pb) is a toxic heavy metal and can harm organisms by inducing apoptosis. Selenium (Se), an essential trace element for humans and animals, can alleviate heavy metal toxicity. The aim of our study is to investigate alleviative effect of Se on Pb-induced apoptosis via endoplasmic reticulum (ER) stress in chicken kidneys. One hundred and eighty male chickens were randomly divided into four groups at 7 days of age and were fed with commercial diet (containing 0.49 mg/kg Se) and drinking water, Na2SeO3-added commercial diet (containing 1 mg/kg Se) and drinking water, the commercial diet and (CH3OO)2Pb-added drinking water (containing 350 mg/L Pb), and Na2SeO3-added commercial diet (containing 1 mg/kg Se) and (CH3OO)2Pb-added drinking water (containing 350 mg/L Pb), respectively. On the 30th, 60th, and 90th days of the experiment period, 15 chickens in each group were euthanized and the kidneys were collected. Following contents were performed: kidney ultrastructure; nitric oxide (NO) content; inducible nitric oxide synthase (iNOS) activity; relative messenger RNA (mRNA) and protein expression of iNOS, ER-related genes (glucose-regulated protein (GRP)78, GRP94, activating transcription factor (ATF)4, ATF6, and iron-responsive element (IRE)), and apoptosis-related genes (caspase-3 and B cell lymphoma-2 (Bcl-2)); and caspase-12 protein expression. The results indicated that Pb changed kidney ultrastructural structure; decreased Bcl-2 mRNA and protein expression; and increased NO content, iNOS activity, relative mRNA and protein expression of iNOS, ER-related genes, and caspase-3 and caspase-12 protein expression. Se attenuated above changes caused by Pb. Pb had time-dependent manners on NO content, GRP78, GRP94, ATF4, IRE, and caspase-3 mRNA expression. Se attenuated Pb-induced apoptosis via ER stress in the chicken kidneys.
... Despite the benefits which these fatty acids provide, fish consumption may come with the potential for harm from contaminants such as mercury (Hg) [16]. However, fish is also a dietary source of selenium (Se) that can increase Hg elimination and ameliorate its toxic effects [17,18]. Thus, it is important to consider both the benefits and risks of consuming fish as routes of exposure to LCω3PUFA, Se, and Hg [9]. ...
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Purpose The prevalence of chronic kidney disease (CKD) is increasing rapidly in many countries and has become a major public health concern. Although intakes of long-chain omega-3 polyunsaturated fatty acids (LCω3PUFA) and its food source—fish—may have renal protective effects, little is known about the longitudinal association between these dietary factors and CKD incidence. Methods A total of 4133 healthy individuals of black and white race aged 18–30 at baseline (1985–1986) from the Coronary Artery Risk Development in Young Adults study were enrolled and followed up over 25 years. LCω3PUFA and fish intake were assessed by an interview-based dietary history questionnaire at baseline, year 7 (1992–1993) and 20 (2005–2006). Results Four hundred and eighty-nine incident cases of CKD were identified. After adjustment for potential confounders, LCω3PUFA intake was inversely associated with CKD incidence [HR = 0.73 (95% CI 0.60–0.89), P = 0.002, with one standard division (0.19 g/day) increment in LCω3PUFA]. This inverse association was persisted among females [0.64 (95% CI 0.48, 0.84; P = 0.002], but not males (Pinteraction = 0.070). A marginal significant inverse association was also found between non-fried fish consumption and CKD incidence (HR = 0.86, 95% CI 0.73, 1.01; P = 0.073). Conclusions Dietary LCω3PUFA intake was inversely associated with incidence of CKD among American young adults over 25 years of follow-up. The suggestive evidence of the inverse association between non-fried fish consumption with CKD incidence needs further confirmation.
... Se negatively associates with Hg (Lemire et al., 2012) and can alleviate its toxicity (Li et al., 2012). It was reported that individuals with poor dietary Se status are more susceptible to the clinically adverse effects of Hg (Ralston et al., 2016). ...
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Selenium (Se) is an essential element for human health and can also alleviate the toxicity of elements such as mercury (Hg), which is considered deleterious to health. The study area is an important coal mineral region in Brazil, generating 40% of all Brazilian coal. During the coal mining process, Se and Hg are released, which can induce potential human health risks via the food chain. The purpose of the present study is to determine total Se and its species and total Hg in drinking water and food locally produced from a coal mining area, to assess the impact of coal mining. The samples were collected in two cities, with and without coal mining influence. Total Se levels in drinking water and food were assessed by inductively coupled plasma mass spectrometry (ICP-MS) and its species by high-performance liquid-ICP-MS, while total Hg was determined by cold vapor atomic fluorescence spectrometry. Drinking water (1.1 ± 0.2 mg L−1 dry weight) (p = 0.02) and tomatoes (1.5 ± 0.1 mg kg−1 dry weight) (p = 0.01) from the coal mining area had higher total Se concentration than the control area. The highest Se concentrations were found in animal-based food (6.4 ± 0.8 mg kg−1 dry weight) with an important contribution of Se IV (65%). The analyzed sample did not accumulate a significant amount of Hg. Future studies on the estimates of daily intake of these elements and dietary pattern of the population are needed to make appropriate dietary recommendations and support public health action.
... The demand for Hg in PVC Table 2 The urinary Hg levels in occupationally exposed people in China from 1970s to 2010s. (Liu, 1987(Liu, ) 1990 Anhui Medical workers of a dental hospital in Hefei 23 4.4 - (Xu et al., 1990(Xu et al., ) 1990 Guizhou Workers of a distillation workshop in a Hg smelter 20 1.1 × 10 3 - (Xu et al., 1990(Xu et al., ) 1990 Guizhou Villagers who smelting Hg near the Danzhai Hg mine 41 167 18.0-362 (You, Zhang, 1990 Heilongjiang Medical staff of stomatology departments in 5 hospitals in Harbin 300 3.5 - (Xu et al., 1990) Shanghai Workers in a dental clinic 20 5. (Zhu et al., 2011(Zhu et al., ) 2012 Guizhou Workers in the Wanshan Hg-related enterprises 177 10.6 (GM) 0.7-181 (Li et al., 2012(Li et al., ) 2014 Jiangsu Workers of a thermometer factory in Jiangyan 263 194 9.9-3.7 × 10 3 Zhong (2014)) 2014 Liaoning Coal miners in Tieling 50 12.1 1.8-221 (Tang et al., 2014) Note: ND, not detected; SD, standard deviation; GM, geometric mean. production using this method accounted for about 85.0% of domestic Hg demand in China (Zhao et al., 2009). ...
Article
Mercury (Hg) is one of the most toxic heavy metals. It can migrate around the globe and magnify through the food chain, ultimately harming human health. Urinary Hg reflects recent exposure of Hg, which reflects the status of environmental contamination by Hg. This review summarized the levels and presented temporal trends of urinary Hg in Chinese people (both the general public and the occupationally exposed people) reported from 1970s to 2010s. It was found that urinary Hg levels in 92.3% of the reported population were less than the reference value (10.0 µg/L) recommended by Chinese health authority, while 76.9% were less than the reference value (4.0 µg/L) recommended by World Health Organization (WHO) in the general public in China. For the temporal trend from 1970s to 2010s, the urinary Hg levels in the general public in China were found to decrease gradually. In the occupationally exposed people, the urinary Hg levels generally exceeded the reference value (10.0 µg/L) for the general public, and about half of them were higher than the occupational exposure limit (35.0 µg/g creatinine) set by Chinese Occupational Health Standard (WS/T 265-2006). From 1970s to 2010s, the urinary Hg levels in occupationally exposed population increased first and then decreased slowly. Hg miners in Guizhou were found to have the highest urinary Hg levels, while workers in Anhui, Chongqing, Qinghai and Shanxi also had high levels of urinary Hg. In all, the urinary Hg levels in both the general public and the occupationally exposed people decreased from 1970s to 2010s, especially in recent decades. Attention should be paid to occupationally exposed people since high levels of urinary Hg were found in them. The message provided in this review can help better understand the situation of Hg burden in Chinese people and lay a basis for the coming effectiveness evaluation on the implementation of Minamata Convention on Mercury. Capsule abstract: The urinary Hg levels in both the general public and the occupationally exposed people in China are decreasing.
... previous study showed that sodium selenite (Se 4+ ) promoted weight gain and reduced the oxidative damage to the liver in MeHg-poisoned rats (Jing et al., 2014). Moreover, oral supplementation of Se-enriched yeast in Hg-exposed people could promote urinary excretion of Hg and reduce oxidative damage (Li et al., 2012). Se and Vitamin E cosupplements in MeHg-poisoned rats altered the reproductive and developmental toxicity of MeHg (Beyrouty and Chan, 2006). ...
Article
Selenite (Se 4+) has been found to counteract the neurotoxicity of methylmercury (MeHg) in MeHg-poisoned rats. However, Se 4+ has narrow range between its toxic and beneficial effects. Nanoelemental selenium (SeNPs) was found to be less toxic than other forms of Se such as Se 4+. In this study, the effects of SeNPs on the load of mercury (Hg) in rats were investigated. Hyphenated technique based on size-exclusion chromatography coupled with UV and inductively coupled plasma mass spectrometry (SEC-ICP-MS) detection and synchrotron radiation X-ray fluorescence spectroscopy (SR-XRF) were used to analyze the Hg-Se-containing proteins in the serum from MeHg-poisoned rats. The Hg-Se-containing fractions monitored by UV and ICP-MS were further characterized by MALDI-TOF-MS. Elevated serum Hg and Se levels were found in MeHg-poisoned rats after SeNPs treatment. Three main Hg-containing bands with molecular weights (MWs) of 25, 62 and 140 kDa were detected in the control samples. Treatment with SeNPs increased the Hg content in proteins at 62 and 170 kDa and decreased the Hg content at 25 kDa. The fraction with 25 kDa was assigned to metallothioneins (MTs), and fractions with 40 and 75 kDa were assigned to albumin. This study showed that the low-toxicity SeNPs could reduce the Hg load in the tissues and promote the formation of high molecular weight Hg-and Se-containing proteins in MeHg-poisoned rats.
... Alternatively, these Hg-Se complexes may precipitate in blood leaving insoluble complexes that are biologically inert, which consequently reduces the potential for Hginduced toxicity (Bjorklund, 2015). These findings are in contrast with those from studies using organic forms of Se wherein exposure to Se enhances urinary excretion of Hg (de Freitas et al., 2009;Li et al., 2012). Interestingly, pretreatment with Se reduced the cortical accumulation of Hg more in aged rats than in young rats. ...
Article
Mercury (Hg) is a prevalent environmental toxicant to which older individuals are particularly susceptible. Selenium (Se) has been used as an antidote following exposure to Hg. However, little is known about the effect of prophylactic supplementation with Se on the handling of Hg. The current study was designed to test the hypothesis that oral pre-treatment with Se alters the corporal disposition of Hg and reduces the risk of Hg-induced toxicity. Young and aged rats were gavaged for 10 days with sodium selenite or saline. On day 11, rats were injected intravenously with 0.5 μmol HgCl2·kg⁻¹·2 mL⁻¹ normal saline. After 24 h, rats were euthanized and organs and tissues were harvested for determination of Hg content. Accumulation of Hg in the kidney was reduced significantly by pre-treatment with Se in both young and aged rats. In the renal cortex, the magnitude of the reduction was greater in aged rats than in young rats but in the outer stripe of the outer medulla, the magnitude of the reduction was similar between groups of rats. Urinary excretion of Hg was also reduced in rats pre-treated with Se. In contrast, the hepatic and hematologic burden of Hg increased in rats pre-treated with Se. Fecal excretion of Hg was decreased significantly by pre-treatment with Se in young rats but not in aged rats. These data suggest that prophylactic supplementation with Se alters the corporal disposition of Hg in a way that may reduce Hg-induced toxicity in target organs.
... A Se supplementation trial in residents exposed to MeHg through fish consumption found reduced Hg level in pubic hair, suggesting Se could promote the excretion of Hg through urine, feces or redistribution to other organs (Seppanen et al., 2000). Our previous study found that Se-enriched yeast could increase the urinary excretion of Hg in residents living near Hg-mining area (Li et al., 2012). Recent animal study found that selenite could promote weight gain, and decrease hepatic damage in MeHg-poisoned rats (Jing et al., 2014). ...
Article
Introduction: Selenium plays important roles in antagonizing the toxicity of methylmercury. The underlying mechanism for the antagonism between Se and MeHg is still not fully understood. Objective: The role of gut flora against the toxicity of environmental contaminants is receiving more and more attention. The objective of this study was to investigate the role of Se against MeHg-poisoning in the modulation of gut flora and the decomposition of MeHg. Methods: MeHg-poisoned rats were treated with sodium selenite every other day for 90 days. Fecal samples were collected on Day 8, 30, 60 and 90. Gut flora in feces was determined using 16S rRNA gene profiling, and the concentrations of Se and total mercury (THg) were measured by ICP-MS, and the concentration of MeHg was measured by CVAFS. Results: Gut flora at both the ranks of phylum and genus in the MeHg-poisoned rats after Se treatment was modulated towards that in the control group, suggesting the restoration of the profile of gut flora. Increased THg was found in fecal samples after Se treatment on day 30. The percentage of MeHg (of total mercury) in the MeHg-poisoned group was in the range of 81-105% while it was 65-84% in the Se treatment group on different days, suggesting the increased decomposition of MeHg in MeHg-poisoned rats after Se treatment. Conclusions: This study suggests that MeHg poisoning damaged the abundance of gut flora and decreased their capacity for the decomposition of MeHg. After Se treatment, the abundance of gut flora was partially restored and the decomposition and excretion of MeHg was enhanced. These findings suggest that the modulation of gut flora may be one way to promote the health status in MeHg-poisoned rats and possibly in human beings.
... Therefore, the fish that have the least amount of Se tend to bioaccumulate the most CH 3 Hg. Likewise, increases in amounts of bioavailable Se have been shown to increase CH 3 Hg efflux from fish [36][37][38][39][40][41][42][43][44] and rapidly diminish their CH 3 Hg body burdens. This mechanism of depuration is augmented by production of insoluble HgSe in tissues of prey animals at each level of the food web. ...
Article
Selenium (Se)-dependent enzymes (selenoenzymes) protect brain tissues against oxidative damage and perform other vital functions, but their synthesis requires a steady supply of Se. High methylmercury (CH3Hg) exposures can severely diminish Se transport across the placenta and irreversibly inhibit fetal brain selenoenzymes. However, supplemental dietary Se preserves their activities and thus prevents pathological consequences. The modified Se health benefit value (HBVSe) is a risk assessment criterion based on the molar concentrations of CH3Hg and Se present in a fish or seafood. It was developed to reflect the contrasting effects of maternal CH3Hg and Se intakes on fetal brain selenoenzyme activities. However, the original equation was prone to divide-by-zero-type errors whereby the calculated values increased exponentially in samples with low CH3Hg contents. The equation was refined to provide an improved index to better reflect the risks of CH3Hg exposures and the benefits provided by dietary Se. The HBVSe provides a biochemically based perspective that confirms and supports the FDA/EPA advice for pregnant and breast-feeding women regarding seafoods that should be avoided vs. those that are beneficial to consume. Since Se can be highly variable between watersheds, further evaluation of freshwater fish is needed to identify locations where fish with negative HBVSe may arise and be consumed by vulnerable subpopulation groups.
... Selenium treatment has been investigated among patients with breast cancer and healthy BRCA carriers with a decent sample size demonstrated no effect of selenium treatment on 8-oxodG analyzed by GC-MS [220]. This is in contrast to other studies investigating selenium treatment, where one study showed a within group reduction in 8-oxodG, but did not report differences between groups [221] and another study demonstrated a between-group reduction in the urinary excretion of 8-oxodG, but did not correct the concentration for urinary flow [222]. Supplementation with other antioxidants such as α-lipoic acid, glutathione, and coenzyme Q10 has not shown any effect on 8-oxodG [45,165,182,217]. ...
Article
Oxidative stress is associated with the development and progression of numerous diseases. However, targeting oxidative stress has not been established in the clinical management of any disease. Several methods and markers are available to measure oxidative stress, including direct measurement of free radicals, antioxidants, redox balance, and oxidative modifications of cellular macromolecules. Oxidatively generated nucleic acid modifications have attracted much interest due to the pre-mutagenic oxidative modification of DNA into 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), associated with cancer development. During the last decade, the perception of RNA has changed from that of a 'silent messenger' to an 'active contributor', and, parallelly oxidatively generated RNA modifications measured as 8-oxo-7,8-dihydro-guanosine (8-oxoGuo), has been demonstrated as a prognostic factor for all-caused and cardiovascular related mortality in patients with type 2 diabetes. Several attempts have been made to modify the amount of oxidative modified nucleic acids. Thus, this review aims to introduce researchers to the measurement of oxidatively generated nucleic acid modifications as well as critically review previous attempts and provide future directions for targeting oxidative nucleic acid modifications.
... Therefore, the fish that have the least amount of Se tend to bioaccumulate the most CH 3 Hg. Likewise, increases in amounts of bioavailable Se have been shown to increase CH 3 Hg efflux from fish [36][37][38][39][40][41][42][43][44] and rapidly diminish their CH 3 Hg body burdens. This mechanism of depuration is augmented by production of insoluble HgSe in tissues of prey animals at each level of the food web. ...
Article
Selenium (Se)-dependent enzymes (selenoenzymes) protect brain tissues against oxidative damage and perform other vital functions, but their synthesis requires a steady supply of Se. High methylmercury (CH3Hg) exposures can severely diminish Se transport across the placenta and irreversibly inhibit fetal brain selenoenzymes. However, supplemental dietary Se preserves their activities and thus prevents pathological consequences. The modified Se health benefit value (HBVSe) is a risk assessment criterion based on the molar concentrations of CH3Hg and Se present in a fish or seafood. It was developed to reflect the contrasting effects of maternal CH3Hg and Se intakes on fetal brain selenoenzyme activities. However, the original equation was prone to divide-by-zero-type errors whereby the calculated values increased exponentially in samples with low CH3Hg contents. The equation was refined to provide an improved index to better reflect the risks of CH3Hg exposures and the benefits provided by dietary Se. The HBVSe provides a biochemically based perspective that confirms and supports the FDA/EPA advice for pregnant and breast-feeding women regarding seafoods that should be avoided vs. those that are beneficial to consume. Since Se can be highly variable between watersheds, further evaluation of freshwater fish is needed to identify locations where fish with negative HBVSe may arise and be consumed by vulnerable subpopulation groups.
... 53 Exogenous Se addition may also be considered for augmenting biological treatment of various heavy-metal-containing waste streams or for bioremediation/ amendment of contaminated soil. 54 It has been demonstrated in previous studies that exogenous selenite can be used to efficiently amend Cd-contaminated soil by altering the soil Cd bioavailability and significantly reducing its accumulation in rice grains 15 and many other plants. 11,53 ■ ASSOCIATED CONTENT * sı Supporting Information ...
... The demand for Hg in PVC Table 2 The urinary Hg levels in occupationally exposed people in China from 1970s to 2010s. (Liu, 1987(Liu, ) 1990 Anhui Medical workers of a dental hospital in Hefei 23 4.4 - (Xu et al., 1990(Xu et al., ) 1990 Guizhou Workers of a distillation workshop in a Hg smelter 20 1.1 × 10 3 - (Xu et al., 1990(Xu et al., ) 1990 Guizhou Villagers who smelting Hg near the Danzhai Hg mine 41 167 18.0-362 (You, Zhang, 1990 Heilongjiang Medical staff of stomatology departments in 5 hospitals in Harbin 300 3.5 - (Xu et al., 1990) Shanghai Workers in a dental clinic 20 5. (Zhu et al., 2011(Zhu et al., ) 2012 Guizhou Workers in the Wanshan Hg-related enterprises 177 10.6 (GM) 0.7-181 (Li et al., 2012(Li et al., ) 2014 Jiangsu Workers of a thermometer factory in Jiangyan 263 194 9.9-3.7 × 10 3 Zhong (2014)) 2014 Liaoning Coal miners in Tieling 50 12.1 1.8-221 (Tang et al., 2014) Note: ND, not detected; SD, standard deviation; GM, geometric mean. production using this method accounted for about 85.0% of domestic Hg demand in China (Zhao et al., 2009). ...
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Mercury (Hg) is one of the most toxic heavy metals. It can migrate around the globe and magnify through the food chain, ultimately harming human health. Urinary Hg reflects recent exposure of Hg, which reflects the status of environmental contamination by Hg. This review summarized the levels and presented temporal trends of urinary Hg in Chinese people (both the general public and the occupationally exposed people) reported from 1970s to 2010s. It was found that urinary Hg levels in 92.3% of the reported population were less than the reference value (10.0 µg/L) recommended by Chinese health authority, while 76.9% were less than the reference value (4.0 µg/L) recommended by World Health Organization (WHO) in the general public in China. For the temporal trend from 1970s to 2010s, the urinary Hg levels in the general public in China were found to decrease gradually. In the occupationally exposed people, the urinary Hg levels generally exceeded the reference value (10.0 µg/L) for the general public, and about half of them were higher than the occupational exposure limit (35.0 µg/g creatinine) set by Chinese Occupational Health Standard (WS/T 265 - 2006). From 1970s to 2010s, the urinary Hg levels in occupationally exposed population increased first and then decreased slowly. Hg miners in Guizhou were found to have the highest urinary Hg levels, while workers in Anhui, Chongqing, Qinghai and Shanxi also had high levels of urinary Hg. In all, the urinary Hg levels in both the general public and the occupationally exposed people decreased from 1970s to 2010s, especially in recent decades. Attention should be paid to occupationally exposed people since high levels of urinary Hg were found in them. The message provided in this review can help better understand the situation of Hg burden in Chinese people and lay a basis for the coming effectiveness evaluation on the implementation of Minamata Convention on Mercury. Capsule abstract: The urinary Hg levels in both the general public and the occupationally exposed people in China are decreasing.
Article
The occurrence of mercury (Hg) in the environment globally has been linked largely to its use for gold processing. In this research, ore samples, agricultural soil and mine wastes were taken within the vicinity of an artisanal gold mine and processing sites in Niger state, a north-central part of Nigeria to determine Hg contamination in the environment and estimate the potential hazard to health. The values of Hg measured in ore, agricultural soil and mine wastes ranged between 0.03 and 5.9, 0.002 and 5.57 and 0.19 and 20.99 mg/kg, respectively, with the majority of samples observed above the crustal average values of 0.003 mg/kg. All of the samples were 100 times greater than the USEPA residential soil screening level of 0.0023 mg/kg, but were lower than comparable mine sites within the same region. Contamination indices were used to demonstrate the potential exposure to Hg contamination in the study area which ranged from a medium to high level of contamination. Average daily dose and hazard quotient (HQ) were calculated for adults and children in the study area and decreased in the following order: ADDvapour [ ADDingestion [ ADDdermal [ ADDinhalation. The non-carcinogenic health risk index (HI) of Hg calculated for children and adults in the study area was children: 7.42, 2.19, 1.49 and adults: 4.45, 1.26, 1.19, for mine wastes, agricultural soil and ore, respectively. All of these values were higher than a considered safe level (= 1) and therefore showed that Hg posed a serious non-carcinogenic HI for both adults and children exposed to the soil in the study area. The bioaccessible fraction as a measure of ingestion for Hg was generally \ 13% across all sample matrices, suggesting a low bioaccessibility. An HQ incorporating bioaccessible data (BHQ) ranged between 0.000005 and 4.06 with a mean value of 0.62. Values for the BHQ were still [ 1, threshold limit in some samples and showed that Hg could present a risk to health via ingestion, although further research is required to assess dermal and inhalation bioaccessi-bility to assess fully the risk to residents. However, the values were lower than the non-carcinogenic health risk index, which is assumed to be overestimated.
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Mercury (Hg) is highly toxic while selenium (Se) has been found to antagonize Hg. Both Hg and Se have been found to induce metallothioneins (MTs). In this study, the complexes formed by metallothionein-1 (MT-1) with HgCl2 and/or Na2SeO3 was studied using matrix-assisted laser desorption/ionization-time of flight-mass spectrometry (MALDI–TOF-MS) and X-ray absorption spectrometry (XAS). MALDI–TOF-MS and XAS indicated the formation of Hg–S bond or Se–S bond when MT-1 reacted with HgCl2 or Na2SeO3, respectively. The bond lengths of Hg–S and coordination number in MT–Hg are 2.41 ± 0.02 Å and 3.10 and in MT–Se are 2.50 ± 0.03 Å and 2.69. A MT–Se–Hg complex was formed when MT-1 reacted with both HgCl2 and Na2SeO3, in which the neighboring atom of Hg is Se, while the neighboring atoms of Se are S and Hg. Our study is an important step towards a better understanding of the interaction of HgCl2 and/or Na2SeO3 with proteins like MT-1.
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Long-term use of glucocorticoids (GC), especially dexamethasone (Dex), could result in osteoporosis through induction of oxidative stress-mediated apoptosis of osteoblasts and increased differentiation of osteoclasts, finally leading to bone loss. Therefore, searching for new agents that could block Dex-induced cytotoxicity would be a good way to treat osteoporosis. In this study, we show that, synthetic benzo[1,2,5]selenadiazole derivatives (SeDs) could be used as effective inhibitors of Dex-induced osteoblasts apoptosis. This protective effect was correlated with their lipophilicity, cellular uptake and antioxidant activities. Furthermore, mechanistic studies reveal that, treatment of osteoblast cells with Dex resulted in overproduction of intracellular reactive oxygen species (ROS), DNA fragmentation, activation of caspase-3/-9, mitochondria fragmentation, phosphorylation of p53, and activation of MAPKs and AKT pathways. However, pre-treatment of the cells with the synthetic SeDs effectively blocked these intracellular events, which suggest that SeDs could protect osteoblast cells against Dex-induced cell apoptosis via attenuating oxidative stress and downstream signalling pathways. Therefore, this study demonstrates a new therapeutic application of SeDs to antagonize GC-induced osteoporosis.
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During the fetal development stage, the Central Nervous System (CNS) is particularly sensitive to methylmercury (MeHg). However, the mechanism underlying the antagonistic effect of selenium (Se) on MeHg toxicity is still not fully understood. In this study, female rat models with MeHg and Se co-exposure were developed. Pathological changes in the cerebellum and differential mRNA expression profiles in offspring rats were studied. In the MeHg-exposed group, a large number of Purkinje cells showed pathological changes and mitochondria were significantly swollen; co-exposure with Se significantly improved the structure and organization of the cerebellum. In total, 378 differentially expressed genes (DEGs) (including 284 up-regulated genes and 94 down-regulated genes) in the cerebellum of the MeHg-exposed group and 210 DEGs (including 84 up-regulated genes and 126 down-regulated genes) in the cerebellum of the MeHg+Se co-exposed group were identified. The genes involved in neurotransmitter synthesis and release and calcium ion balance in the cerebellum were significantly up-regulated in the MeHg-exposed group. These genes in the MeHg+Se co-exposed group were not changed or down-regulated. These findings demonstrate that the neurotoxicity caused by MeHg exposure is related to the up-regulation of multiple genes in the nerve signal transduction and calcium ion signal pathways, which are closely related to impairments in cell apoptosis and learning and memory. Supplementation with Se can mitigate the changes to related genes and protect neurons in the mammalian brain (especially the developing cerebellum) from MeHg toxicity. Se provides a potential intervention strategy for MeHg toxicity.
Chapter
Selenium is a metalloid and exerts its biological functions mainly through selenoproteins. The incorporation of selenium into the selenoproteins is in the form of selenocysteine and mediated cotranslationally. Selenoproteins include three enzyme families (glutathione peroxidases, thioredoxin reductases, and iodothyronine deiodinases), thioredoxin-like, endoplasmic reticulum proteins, and others with functions related to selenium transport and storage. Gene knockout and overexpression mouse models have helped reveal physiological functions of selenoproteins and their paradoxical roles in metabolism such as the promotion of type 2 diabetes by glutathione peroxidase-1. Both selenium deficiency and excess affect expression of selenoproteins, and the regulation does not always lead to parallel changes in mRNA and protein for given selenoproteins. Incidences of animal and human selenium deficiency and toxicity often correlate well with available selenium contents in soil associated with their living environment. Chemical forms of selenium affect its absorption, retention, and utilization from diets. Interactions of selenium with vitamin E and metals such as mercury and lead can exert positive or negative health impacts. Current imaging and analytical tools, systems biology approaches, and animal models will continue to help advance our knowledge of selenium biology, enhancing basic, physiological, and applied understandings into the functions of the micronutrient.
Chapter
Selenium (Se) has been shown to act as a functional antagonist to mercury (Hg) and arsenic (As). Se may influence Hg and As toxicity by modulating redox homeostasis and inflammation. At the same time, the clinical significance of such interactions is questionable. Despite extensive experimental data, human studies on the interaction between these trace elements, as well as on the influence of such interaction on human health are limited. Current data are reviewed on how Hg and Se interplay impacts on cardiovascular diseases, neurotoxicity, neurodegeneration, diabetes and obesity. Studies also demonstrate that the interaction between Se and As significantly affects the development of certain cardiovascular diseases and cancer. This notion is further supported by the results of our analysis of 63,118 adults and 13,734 children from different regions of Russia indicating that the hair Se/Hg ratio is characterized by a tighter association with demographical indices (birth rate, mortality, life span, total morbidity) and morbidity than Hg or Se individually. It is proposed that modulation of the Se/As and Se/Hg ratios in humans may help to improve population health and demography.
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Human blood mercury (Hg), selenium (Se) and other trace element levels were investigated in the Wanshan mercury mining area. Residents living near the mine waste heaps had significantly elevated blood Hg, Se and arsenic (As) levels, which indicates the impact from Hg mining and smelting activities. Rice samples showed high Se levels, as 72.6% of total Se intake comes from rice consumption. The means of the Se:total Hg (THg) and Se:methyl Hg (MeHg) molar ratios were 60.7±27.1 and 110±53.6 respectively. Blood Se:Hg molar ratios were negatively correlated with blood Hg levels. 80.2% of the study population had blood THg levels that exceeded the 5.8μg/L regulation level set by the USEPA, which indicated the risk of Hg exposure. On the other hand, the blood Se levels were within a safe-level range, and dietary Se intake protected local residents who suffered from Hg exposure.
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The occurrence of mercury (Hg) in the environment globally has been linked largely to its use for gold processing. In this research, ore samples, agricultural soil and mine wastes were taken within the vicinity of an artisanal gold mine and processing sites in Niger state, a north-central part of Nigeria to determine Hg contamination in the environment and estimate the potential hazard to health. The values of Hg measured in ore, agricultural soil and mine wastes ranged between 0.03 and 5.9, 0.002 and 5.57 and 0.19 and 20.99 mg/kg, respectively, with the majority of samples observed above the crustal average values of 0.003 mg/kg. All of the samples were 100 times greater than the USEPA residential soil screening level of 0.0023 mg/kg, but were lower than comparable mine sites within the same region. Contamination indices were used to demonstrate the potential exposure to Hg contamination in the study area which ranged from a medium to high level of contamination. Average daily dose and hazard quotient (HQ) were calculated for adults and children in the study area and decreased in the following order: ADDvapour > ADDingestion > ADDdermal > ADDinhalation. The non-carcinogenic health risk index (HI) of Hg calculated for children and adults in the study area was children: 7.42, 2.19, 1.49 and adults: 4.45, 1.26, 1.19, for mine wastes, agricultural soil and ore, respectively. All of these values were higher than a considered safe level (= 1) and therefore showed that Hg posed a serious non-carcinogenic HI for both adults and children exposed to the soil in the study area. The bioaccessible fraction as a measure of ingestion for Hg was generally < 13% across all sample matrices, suggesting a low bioaccessibility. An HQ incorporating bioaccessible data (BHQ) ranged between 0.000005 and 4.06 with a mean value of 0.62. Values for the BHQ were still > 1, threshold limit in some samples and showed that Hg could present a risk to health via ingestion, although further research is required to assess dermal and inhalation bioaccessibility to assess fully the risk to residents. However, the values were lower than the non-carcinogenic health risk index, which is assumed to be overestimated.
Article
The Hg−C bond of MeHgCl, a ubiquitous environmental toxicant, is notoriously inert and exceedingly difficult to cleave. The cleavage of Hg−C bond of MeHgCl at low temperature, therefore, is of significant importance for human health. Among various bis(imidazole)‐2‐selones LnSe (n = 1‐4, or 6), the three‐spacer L3Se shows extraordinarily high reactivity on the degradation of various mercury alkyls including MeHgCl due to its unique ability to coordinate via k2‐fashion, in which both the Se atoms simultaneously attack to the Hg center of mercury alkyls for facile Hg−C bond cleavage. It has the highest softness (σ) parameter and the lowest HOMO(LnSe)‐LUMO(MeHgX) energy gap and, thus, L3Se is the most reactive among LnSe towards MeHgX (X = Cl or I). L3Se is highly efficient, than L1Se, in restoring the activity of antioxidant enzyme glutathione reductase (GR) which is completely inhibited by MeHgCl––80% GR activity is recovered by L3Se compared to 50% by L1Se. It shows excellent cytoprotective effect in liver cells against MeHgCl‐induced oxidative stress by protecting the inhibition of vital antioxidant enzymes caused by MeHgCl and, thus, does not allow to increase the intracellular ROS levels and protects the mitochondrial membrane potential (ΔΨm) perturbed by MeHgCl. Major Hg‐responsive genes analyses demonstrate that L3Se plays a significant role in MeHg+ detoxification in liver cells.
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Mercury (Hg) is widely distributed in the environment and is known to produce several adverse effects in organisms. The aim of the present study was to examine the in vitro antioxidant activity and Hg chelating ability of the hydroalcoholic extract of Psidium guajava leaves (HEPG). In addition, the potential protective effects of HEPG against Hg(II) were evaluated using a yeast model (Saccharomyces cerevisiae). HEPG was found to exert significant antioxidant activity in 2,2-diphenyl-1-picrylhydrazyl scavenger and inhibition of lipid peroxidation induced by Fe(II) assays in a concentration-dependent manner. The extract also exhibited significant Hg(II) chelating activity. In yeast, Hg(II) induced a significant decrease in cell viability. In contrast, HEPG partially prevented the fall in cell viability induced by Hg(II). In conclusion, HEPG exhibited protective effects against Hg(II)-mediated toxicity, which may be related to both antioxidant and Hg(II)-chelating activities.
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We reevaluate the treatment of mercury poisoning, incorporating recent advances in understanding of mercury toxicity and the mercury:selenium interaction. This review focuses on: 1) the role, limitations and benefits of chelation (Unithiol, succimer and N-Acetylcysteine); 2) the role of selenium supplementation; and 3) how the different forms of mercury are impacted by use of chelation and selenium. Unithiol and succimer produce increases in urinary excretion of mercury and to a lesser degree blood and total body mercury. The primary role of N-acetylcysteine is increasing renal mercury excretion, similar to the thiol-chelators. Additional unique features of acetylcysteine include increased efflux of methylmercury from the brain, and reduced oxidative stress via increased glutathione production. The role of selenium includes: 1) restoration of selenoprotein activity, 2) protection against mitochondrial injury and DNA damage, 3) demethylation of methylmercury, 4) sequestering of mercury via Hg:Se complexes, and 5) redistribution of Hg inside organisms. Selenium may increase blood Hg, via a “sink” effect, causing a redistribution of mercury away from the brain. A combined approach for mercury poisoning treatment was developed focusing on restoration of selenoprotein function, reduction of oxidative stress and increased mercury elimination.
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Mercury-binding protein profiles in rat plasma at different levels of mercury exposure in vitro and in vivo were systematically investigated using column gel electrophoresis coupled with inductively coupled plasma-mass spectrometry....
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Mercury (Hg) bioaccumulation in rice poses a health issue for rice consumers. In rice paddies, selenium (Se) can decrease the bioavailability of Hg through forming the less bioavailable Hg selenides (HgSe) in soil. Rice leaves can directly uptake a substantial amount of elemental Hg from the atmosphere, however, whether the bioaccumulation of Hg in rice leaves can affect the bioaccumulation of Se in rice plants is not known. Here, we conducted field and controlled studies to investigate the bioaccumulation of Hg and Se in the rice-soil system. In the field study, we observed a significantly positive correlation between Hg concentrations and BAFs of Se in rice leaves (r2 = 0.60, p < 0.01) collected from the Wanshan Mercury Mine, SW China, suggesting that the bioaccumulation of atmospheric Hg in rice leaves can facilitate the uptake of soil Se, perhaps through the formation of Hg-Se complex in rice leaves. This conclusion was supported by the controlled study, which observed significantly higher concentrations and BAFs of Se in rice leaf at a high atmospheric Hg site at WMM, compared to a low atmospheric Hg site in Guiyang, SW China.
Chapter
Selenium is both a toxic and an essential trace element. Both deficiency and overload are reported in humans due to geographical variability in soil concentrations. Selenium metabolically interacts with numerous nutrients and toxic substances. These interrelationships may be synergistic or antagonistic, and involve different biological pathways with opposite effects and a complex interplay of interactions involving numerous substances, lifestyle, and health status. The complexity of these interactions may contribute to inter-individual variability in the susceptibility to various chronic diseases. This review is focused on the interactions of selenium with heavy metals in the top ten chemicals of major public health concern (arsenic, cadmium, fluoride, mercury, and lead) and with the most common and widespread deficiencies in the world (iodine, iron, zinc, and vitamin A) according to the World Health Organization. The principal mechanisms of action and a summary of different studies in humans are briefly presented. More information is available in the reference listed.
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Background: Methylmercury (MeHg) is a ubiquitous environmental pollutant, with the nervous system as its main target; however, the neurotoxic mechanisms of MeHg have not been fully elucidated, and no effective therapeutic and preventive drugs are available to mitigate its toxicity. Recent evidence suggests a reduction in the toxicity of MeHg by natural plant extracts. Scope of review: The aim of this review is to provide an overview of effective natural plant extracts and their putative biochemical mechanisms for blocking gut absorption, enhancing excretion and minimizing toxic effects of MeHg. Major conclusions: Natural plant extracts may act as potential therapeutics in response to MeHg exposure. The roles plant components play in the reduction of MeHg toxicity may be multifaceted including: (1) attenuating neurobehavioral deficits; (2) facilitating demethylation of MeHg to inorganic mercury; (3) reducing MeHg absorption from the gastrointestinal tract; (4) redistributing MeHg to less sensitive target organs and tissues; (5) promoting enterohepatic circulation of MeHg to increase its biliary and intestinal excretion; (6) restoring intracellular redox status. General significance: The possible protective effects of natural plant components contribute to the understanding of mechanisms of MeHg toxicity and to the development of novel therapeutic strategies.
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Organomercurials, especially lipophilic methylmercury and ethylmercury, are the most toxic forms of mercury. Thiol-conjugates of organomercurials can easily cross the cellular membranes, including the blood-brain barrier, and thus cause severe damage to the central nervous system. However, the bacterial resistance to both inorganic mercury (Hg²⁺) and organomercurials is well known. For instance, two strains of the sulfate-reducing bacterium Desulfovibrio desulfuricans show high resistant to methylmercury by virtue of their ability to convert methylmercury into biologically inert HgS, CH4 gas, and dimethylmercury. On the other hand, certain gram-positive and gram-negative bacterial strains with mer operon also display resistance to organomercurials but in a completely different mechanism. The cytosolic organomercurial lyase MerB protein present in these bacteria has an excellent ability to protolytically cleave, otherwise inert, the Hg−C bond of organomercurials and converts them into inorganic mercury (Hg²⁺) and volatile hydrocarbon (RH) products. Interestingly, the mercury-resistant MerB enzyme is absent in higher species like animals and humans. Thus, developing a functional model of MerB with high efficiency to cleave the Hg−C bond of organomercurials under mild conditions will have therapeutic potential to treat patients suffering from methylmercury or ethylmercury poisoning. In this review, we discuss the use of N-heterocyclic-based thiones and selones on the detoxification of mercury-related compounds. Focus is given on how N-heterocyclic-based thiones and selones can suitably be designed to detoxify organomercurials in various ways, similar to that observed in bacteria.
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This paper reports the effects of a placebo-controlled Se-enriched yeast supplementation trial, conducted for 14 months, on arsenism in adult farmers living in a rural community in Inner Mongolia, China. The farmers had been naturally exposed to elevated concentrations of As in drinking water from tube-wells since 1983 but changed to arsenic-free drinking water when the trial began in June 1996. Blood and hair Se and As concentrations were analysed pre-intervention and at the end of the 3rd, 9th and 14th month, while skin lesions were assessed pre-intervention, as well as at the end of the 14th month, using the Arsenism Clinical Criteria established by the Ministry of Health, China. As the trial was a voluntary one, a number of farmers did not routinely have their blood and hair samples taken for analysis. Consequently, the data have been analysed in two categories. Fifty-four farmers from the Se-group and 29 from the placebo-group who were sampled on each occasion were considered as one group, which has been compared with the second group comprising up to a total of 100 farmers in the Se-group and 86 in the placebo-group. Results calculated for those farmers who were sampled on each occasion, showed that at the end of the trial, blood and hair Se concentrations of the Se-group increased from 0.130 to 0.186 g ml–1 and from 0.431 to 0.502 g g–1, respectively, while those of the placebo-groups remained constant. Blood and hair As concentrations of the Se-group decreased from 0.051 to 0.015 g ml–1 and from 2.57 to 0.680 g g–1, respectively, a greater reduction than those in the placebo-group that went from 0.064 to 0.024 g ml–1 and from 2.62 to 1.25 g g–1, respectively. When the data from all patients were examined, the analytical trends were similar. An evaluation of skin lesions in the category who were sampled for hair and blood on each occasion showed that 41.2% of hyperkeratosis, 50.0% of depigmentation and 44.7% of pigmentation in the Se-group improved one or more degrees, while those in the placebo-group improved by only 7.1, 12.0 and 6.7%, respectively. A total of 61.1% of the adults in Se-group improved in one or more type of skin lesion, but only 17.2% improved in the placebo-group. Comparable results were obtained when all the data from both categories of farmers were examined. Results from the trial showed that Se supplementation was more effective for the improvement of adults who were affected by double or triple skin lesions. In the placebo-group, most of the severely affected adults improved in only one kind of skin lesion, but in the Se-group, more adults improved in two or three kinds of skin lesions. Although the trial was limited by its relatively small size, the results have provided some evidence of the usefulness of Se supplementation for people affected by arsenism.
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Selenium is of fundamental importance to human health. It is an essential component of several major metabolic pathways, including thyroid hormone metabolism, antioxidant defence systems, and immune function. The decline in blood selenium concentration in the UK and other European Union countries has therefore several potential public health implications, particularly in relation to the chronic disease prevalence of the Western world such as cancer and cardiovascular disease. Ten years have elapsed since recommended dietary intakes of selenium were introduced on the basis of blood glutathione peroxidase activity. Since then 30 new selenoproteins have been identified, of which 15 have been purified to allow characterisation of their biological function. The long term health implications in relation to declining selenium intakes have not yet been thoroughly examined, yet the implicit importance of selenium to human health is recognised universally. Selenium is incorporated as selenocysteine at the active site of a wide range of selenoproteins. The four glutathione peroxidase enzymes (classical GP×1, gastrointestinal GP×2, plasma GP×3, phospholipid hydroperoxide GP×4)) which represent a major class of functionally important selenoproteins, were the first to be characterised. Thioredoxin reductase (TR) is a recently identified seleno-cysteine containing enzyme which catalyzes the NADPH dependent reduction of thioredoxin and therefore plays a regulatory role in its metabolic activity. Approximately 60% of Se in plasma is incorporated in selenoprotein P which contains 10 Se atoms per molecule as selenocysteine, and may serve as a transport protein for Se. However, selenoprotein-P is also expressed in many tissues which suggests that although it may facilitate whole body Se distribution, this may not be its sole function. A second major class of selenoproteins are the iodothyronine deiodinase enzymes which catalyse the 5′5-mono-deiodination of the prohormone thyroxine (T4) to the active thyroid hormone 3,3′5-triiodothyronine (T3). Sperm capsule selenoprotein is localised in the mid-peice portion of spermatozoa where it stabilises the integrity of the sperm flagella. Se intake effects tissue concentrations of selenoprotein W which is reported to be necessary for muscle metabolism. It is of great concern that the health implications of the decline in Se status in the UK over the past two decades have not been systematically investigated. It is well recognised that dietary selenium is important for a healthy immune response. There is also evidence that Se has a protective effect against some forms of cancer; that it may enhance male fertility; decrease cardiovascular disease mortality, and regulate the inflammatory mediators in asthma. The potential influence of Se on these chronic diseases within the European population are important considerations when assessing Se requirement.
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Essential micronutrient selenium is excreted into the urine andor expired after being transformed to methylated metabolites. Monomethylated selenium is excreted into the urine in response to a supply within the required to low-toxic range, whereas tri- and dimethylated selenium increase with excessive supply at a toxic dose. Here we show that the major urinary selenium metabolite within the required to low-toxic range is a selenosugar. The structure of 1beta-methylseleno-N-acetyl-d-galactosamine was deduced from the spectroscopic data and confirmed by chemical synthesis. This metabolite was also detected in the liver, and an additional metabolite increased with inhibition of methylation. The latter metabolite was again a selenosugar conjugated with glutathione instead of a methyl group and was assumed to be a precursor for methylation to the former metabolite. A metabolic pathway for the urinary excretion of selenium, i.e., from the glutathione-S-conjugated selenosugar to the methylated one, was proposed. Urinary monomethylated (selenosugar) and trimethylated selenium can be used as specific indices that increase within the required to low-toxic range and with a distinct toxic dose, respectively.
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It has been suggested that mercury, a highly reactive heavy metal with no known physiologic activity, increases the risk of cardiovascular disease. Because fish intake is a major source of exposure to mercury, the mercury content of fish may counteract the beneficial effects of its n-3 fatty acids. In a case-control study conducted in eight European countries and Israel, we evaluated the joint association of mercury levels in toenail clippings and docosahexaenoic acid (C22:6n-3, or DHA) levels in adipose tissue with the risk of a first myocardial infarction among men. The patients were 684 men with a first diagnosis of myocardial infarction. The controls were 724 men selected to be representative of the same populations. The average toenail mercury level in controls was 0.25 microg per gram. After adjustment for the DHA level and coronary risk factors, the mercury levels in the patients were 15 percent higher than those in controls (95 percent confidence interval, 5 to 25 percent). The risk-factor-adjusted odds ratio for myocardial infarction associated with the highest as compared with the lowest quintile of mercury was 2.16 (95 percent confidence interval, 1.09 to 4.29; P for trend=0.006). After adjustment for the mercury level, the DHA level was inversely associated with the risk of myocardial infarction (odds ratio for the highest vs. the lowest quintile, 0.59; 95 percent confidence interval, 0.30 to 1.19; P for trend=0.02). The toenail mercury level was directly associated with the risk of myocardial infarction, and the adipose-tissue DHA level was inversely associated with the risk. High mercury content may diminish the cardioprotective effect of fish intake.
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This study investigated the effects of a single dose of intravenously administered sodium 2,3-dimercaptopropane-1-sulfonate (DMPS) on the essential elements copper, zinc, and selenium in human blood and urine. The possible role of dental amalgam was also addressed. Eighty individuals, divided in four groups according to the presence or absence of dental amalgam fillings and symptoms self-related to such fillings, were given DMPS (2 mg/kg body wt) and 500 mL Ringer’s acetate intravenously. Urine and blood were collected prior to the injection, and thereafter at intervals over a 24-h period. Cu, Zn, and Se concentrations were determined by atomic absorption spectrometry methods. A statistically significant increase in the concentrations of Cu and Zn in urine was observed 30 and 120 min after the DMPS injection compared to the preinjection concentrations. The concentrations of Se were not affected. The cumulated excretion over 24 h after DMPS injection constitutes only from 0.1% to 0.7% of the body content of these elements. There was no effect of different amalgam statuses on Cu and Zn excretion. We found a temporary decrease (4–7%) in the concentrations of Cu, Zn, and Se in blood 15 and 30 min after DMPS, but this seems to be the result of dilution factors. Administration of a single dose of DMPS does not affect the body stores of the essential elements Cu, Zn, and Se.
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Selenium-enriched yeast (Se-yeast) is a common form of Se used to supplement the dietary intake of this important trace mineral. However, its availability within the European Union is under threat, owing to concerns expressed by the European Community (EC) Scientific Committee on Food that Se-yeast supplements are poorly characterised and could potentially cause the build up of Se in tissues to toxic levels. The present review examines the validity of these concerns. Diagrams of the biosynthesis and metabolism of Se compounds show which species can be expected to occur in Se-yeast preparations. Se-yeast manufacture is described together with quality-control measures applied by reputable manufacturers. The way in which speciation of Se-yeast is achieved is explained and results on amounts of Se species in various commercial products are tabulated. In all cases described, selenomethionine is the largest single species, accounting for 54-74 % of total Se. Se-yeast is capable of increasing the activity of the selenoenzymes and its bioavailability has been found to be higher than that of inorganic Se sources in all but one study. Intervention studies with Se-yeast have shown the benefit of this form in cancer prevention, on the immune response and on HIV infection. Of about one dozen supplementation studies, none has shown evidence of toxicity even up to an intake level of 800 microg Se/d over a period of years. It is concluded that Se-yeast from reputable manufacturers is adequately characterised, of reproducible quality, and that there is no evidence of toxicity even at levels far above the EC tolerable upper intake level of 300 microg/d.
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L'injection de trs petites quantits de slnite de sodium, administres simultanment ou 1 h aprs l'intoxication par le sublim corrosif, en abaisse considrablement la toxicit: les rats blancs intoxiqus par une dose ltale de sublime corrosif survivent sous l'effet du slnite dans un % important et les lsions typiques des reins et d'autres organes n'apparaissent pas.
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Mercuric chloride (10 μmole/kg body weight) injected every day into mice showed an inhibitory effect on GSH peroxidase, a selenoenzyme, in the kidney on Days 4 and 8. The simultaneous administration of the same dose of sodium selenite provided complete protection against the reduction of the enzyme activity induced by Hg in spite of the fact that the kidneys of these animals accumulated nearly twice as much as Hg as those of mice receiving Hg alone. Hg given alone resulted in a atomic ratio of 10.9 in the kidney with GSH peroxidase inhibition. Little GSH peroxidase inhibition occurred in the liver or kidney when Hg was given with Se. In these cases ratios were much lower, ranging from 1.0 to 2.2. The maximum concentration of Hg ion which showed no inhibitory effect on purified GSH peroxidase of rabbit erythrocytes was 10−5m. This concentration was higher than the final concentration of Hg in a test tube assaying the activity of GSH peroxidase in vivo. It is probable that deficiency of available Se due to its increased binding to Hg in the kidney resulted in the reduced activity of GSH peroxidase in that organ.
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The thioredoxin (Trx) system, involving redox active Trxs and thioredoxin reductases (TrxRs), sustain a number of important Trx-dependent pathways. These redox active proteins support several processes crucial for cell function, cell proliferation, antioxidant defense, and redox-regulated signaling cascades. Methylmercury (MeHg) is an important environmental toxicant that has a high affinity for thiol groups and can cause oxidative stress. The Trx system is the major system responsible for maintaining the redox state of cells and this function involves thiol reduction mediated by selenol groups in TrxRs. MeHg has a great affinity to thiols and selenols, thus the potential toxic effects of MeHg on TrxR inhibition were determined in the current study. A single administration of MeHg (1, 5, and 10 mg/Kg) caused a marked inhibition of kidney TrxR activity, while significant inhibition was observed in the liver after exposure to 5 and 10 mg/Kg of MeHg. TrxR activity was determined 24 h after MeHg. In the brain, MeHg did not inhibit TrxR activity. In vitro exposure to MeHg indicated that MeHg inhibits cerebral (IC(50), 0.158 μM), hepatic (IC(50), 0.071 μM), and renal TrxR activity (IC(50), 0.078 μM). The results presented herein demonstrated for the first time that renal and hepatic TrxRs can serve as an in vivo target for MeHg. This study suggests that MeHg can bind to selenocysteine residues present in the catalytic site of TrxR, in turn causing enzyme inhibition that can compromise the redox state of cells.
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Dietary selenium (Se) status is inversely related to vulnerability to methylmercury (MeHg) toxicity. Mercury exposures that are uniformly neurotoxic and lethal among animals fed low dietary Se are far less serious among those with normal Se intakes and are without observable consequences in those fed Se-enriched diets. Although these effects have been known since 1967, they have only lately become well understood. Recent studies have shown that Se-enriched diets not only prevent MeHg toxicity, but can also rapidly reverse some of its most severe symptoms. It is now understood that MeHg is a highly specific, irreversible inhibitor of Se-dependent enzymes (selenoenzymes). Selenoenzymes are required to prevent and reverse oxidative damage throughout the body, particularly in the brain and neuroendocrine tissues. Inhibition of selenoenzyme activities in these vulnerable tissues appears to be the proximal cause of the pathological effects known to accompany MeHg toxicity. Because Hg's binding affinities for Se are up to a million times higher than for sulfur, its second-best binding partner, MeHg inexorably sequesters Se, directly impairing selenoenzyme activities and their synthesis. This may explain why studies of maternal populations exposed to foods that contain Hg in molar excess of Se, such as shark or pilot whale meats, have found adverse child outcomes, but studies of populations exposed to MeHg by eating Se-rich ocean fish observe improved child IQs instead of harm. However, since the Se contents of freshwater fish are dependent on local soil Se status, fish with high MeHg from regions with poor Se availability may be cause for concern. Further studies of these relationships are needed to assist regulatory agencies in protecting and improving child health.
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The ability of selenium compounds to modify profoundly the toxicity of both organic and inorganic mercury compounds has previously been demonstrated in experimental animals. Other earlier analytical data on tuna and marine mammals showed that natural levels of mercury and selenium are strongly correlated. In this paper the authors report an approximately molar ratio for these elements in certain human organs following exposure to high levels of inorganic mercury. The results to date clearly demonstrate an approximately 1:1 molar ratio for those organs which accumulate and retain mercury strongly, namely, thyroid, pituitary, and kidney. The same effect is also seen in brain samples, with different sections of the same brain all displaying a near molar ratio. Since selenium, as an essential trace element, will normally be present in at least typical physiological levels, whereas mercury in non exposed persons should only approach insignificant amounts, a molar ratio will only be observed for rather elevated values. Even slightly increased mercury levels, however, seem capable of raising the selenium content; the ratio of the increments over normal levels approaches the molar ratio in many cases. The 1:1 molar ratio naturally suggests a direct Hg Se linkage, though at this stage one can only speculate about the nature of the group or complex and its mode of attachment. Keeping in mind that the time between death and termination of exposure in the professionally exposed subjects varied greatly, it seems that the effect is both accumulative (as in the case of marine mammals and tuna) and retentive. This emphasizes the strength of the Hg Se interaction and suggests their removal from biological turnover. Thus in general it seems that the effect can occur where mercury is present as the methyl (tuna) or the inorganic form (marine mammals and man), and whether selenium is relatively abundant in the diet or not.
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The mean dietary selenium intake in Finland increased from 40 to 100 micrograms/d in 1987 because of the addition in 1985 of selenium to fertilizers. A selenium-supplementation study was performed in 1987 on the same men as were followed in a 1981 study that had a similar design (200 micrograms Se/d). Selenite and selenate, but not selenium yeast increased platelet glutathione peroxidase (GSHPx) activity by 30% compared with placebo, much less than the 70% found in the previous study. Selenium yeast and selenite increased plasma selenium after 11 wk from 1.39 mumol/L to peak values of 2.15 and 1.58 mumol/L, respectively. Only yeast selenium was incorporated into red cells. From a regression plot based on present and literature data, it was estimated that the plasma selenium concentration needed to achieve maximal platelet GSHPx activity was 1.25-1.45 mumol/L. At the present selenium intake in Finland, 100 micrograms/d, GSHPx activity is saturated in plasma and red cells and almost saturated in platelets.
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As an index of lipid peroxidation, thiobarbituric acid (TBA)-reactive substances in the liver, kidney, and serum, and hydrocarbons (ethane and pentane) in the exhalation of rats injected subcutaneously with 10 mg/kg/day of methylmercuric chloride (MMC) were determined. Formation of TBA-reactive substances in the liver and kidney of rats was significantly increased 4 and 2 days after initial injection of MMC, respectively. The result for serum was similar to that for the kidney. The maximum ethane production in the exhaled gases was observed 4 days after initial injection of MMC, and thereafter decreased slowly. Pentane production was significantly increased 5 days after initial injection of MMC, and thereafter continued to increase. Glutathione peroxidase activity and amount of vitamin C in the liver were depleted 4 days after initial injection of MMC; vitamin E was not depleted. In the kidney, significant decreases of glutathione peroxidase activity and vitamin C content were also seen 4 days after initial injection of MMC, but vitamin E content was unaltered. Thus, a clear increase of lipid peroxidation as determined by measurement of TBA-reactive substances in tissues and of hydrocarbons in the exhaled gases of rats after MMC treatment was demonstrated, though there was a lag phase of several days before the increase of lipid peroxidation. It is suggested that the significant increase of lipid peroxide formation may be a result of depletion of defending factors against lipid peroxidation.
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Binding of equimolar mercury (Hg) and selenium (Se) to a specific plasma protein in the detoxification of Hg was studied in vitro by the HPLC/inductively coupled argon plasma-mass spectrometry (ICP-MS) method with use of an enriched stable isotope. Hg and 82Se became co-eluted with endogenous 78Se on a size exclusion column by incubation of 0-200 microM HgCl2 and 82Se-enriched selenite with rat serum in the presence of glutathione at 37 degrees C for 10 min. The endogenous 78Se peak was the most abundant plasma Se-containing protein, and it showed the affinity to heparin, indicating it to be selenoprotein P (Sel P). The 82Se/endogenous Se ratio of (Hg-Se)-Sel P complex changed with doses of HgCl2 and 82Se-enriched selenite and amounted to more than 100, suggesting that more than 1,000 units of (Hg-Se) bind to Sel P based on the fact that there are 10 selenocysteinyl residues per Sel P. These results indicate that equimolar Hg and Se bind to Sel P to form the {(Hg-Se)n}m-Sel P complex, where n is the number of Hg-Se complexes and m the number of binding sites in Sel P.
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The present study was undertaken to determine if in vitro exposure to mercuric chloride produces reactive oxygen species (ROS) in the synaptosomes prepared from various regions of rat brain. The effects of in vivo exposure to mercury on antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities in different regions of rat brain were also investigated. Adult male Sprague-Dawley (CD) rats were dosed with 0, 1, 2.0 or 4.0 mg HgCl2/kg body weight, for 7 days. One week after the last dose, animals were sacrificed by decapitation, their brains were removed and dissected and frozen in dry ice prior to measuring the activities of these enzymes. The results demonstrated that in vitro exposure to mercury produced a concentration-dependent increase of ROS in different regions of the rat brain. In vivo exposure to mercury produced a significant decrease of total SOD, Cu, Zn-SOD and Mn-SOD activities in the cerebellum of rats treated with different doses of mercury. SOD activity did not vary significantly in cerebral cortex and brain stem. GPx activity declined in a dose-dependent manner in the cerebellum with a significant reduction in animals receiving the 4 mg HgCl2/kg body weight. The activity of GPx increased in the brain stem while unchanged in the cerebral cortex. The results demonstrate that inorganic mercury decreased SOD activity significantly in the cerebellum while GPx activity was affected in both cerebellum and brain stem. Therefore, it can be concluded that oxidative stress may contribute to the development of neurodegenerative disorders caused by mercury intoxication.
Exogenous and endogenous oxidants constantly cause oxidative damage to DNA. Since the reactive oxidants itself are not suitable for analysis, oxidized bases like 8-hydroxy-2'-deoxyguanosine (8OHdG) are used as biomarkers for oxidative stress, either in cellular DNA or as elimination product in urine. A simple, fast and robust analytical procedure is described for urinary 8OHdG as an indicator of oxidative damage in humans. The adduct was purified from human urine by applying a single solid-phase extraction step on LiChrolut EN. After evaporation of the eluate, the residue was resolved and an aliquote was injected into a HPLC system with a triple quadrupole mass spectrometer. The limit of detection was 0.2 ng ml(-1) (7 fmol absolute) when using one product ion as quantifier and two further product ions as qualifier. The coefficient of variation was 10.1% (n=5 at 2.8 ng ml(-1) urine). The sample throughput was about 50 samples a day. Thus, this method is more sensitive and much faster than the common method using HPLC with electrochemical detection. The results of a study with nine volunteers investigated at six time-points each over 5 days are presented. The mean excretion of 8OHdG was 2.1 ng mg(-1) creatinine (range 0.17-5.9 ng mg(-1) creatinine; 4 of 53 samples were below the LOD). A relatively large intra- (relative SD 66%) and inter-individual (relative SD 71%) variation in urinary 8OHdG excretion rates was found.