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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.

Acute mercury vapor poisoning is a rare but fatal toxicological emergency. People are exposed to mercury in daily life by the way of foods, vaccines, antiseptics, ointments, amalgam or occupation. We present here, the clinical picture and management of four members of the same family who were exposed to elemental mercury. Three of the family members were seen in another hospital with malaise, fever, eritematous rash and pulmonary problems. Their questioning revealed the mercury exposure. Having a suspicion of heavy metal intoxication, blood and urine mercury levels were measured and mercury intoxication was diagnosed. On admission to our hospital, two patients already had chelation therapy. In three of them we found three distinct abnormalities: encephalopathy, nephrotic syndrome and polyneuropathy. The fourth family member had minor symptoms. This family is an example for the inhalation exposure resulting from inappropriate handling of liquid mercury. During the first days, flu like illness ensues. Then, severe pulmonary, neurological, renal, hepatic, hematological and dermatological dysfunctions develop. Blood and urine mercury levels should be tested on suspicion, but it must be kept in mind that blood level is unreliable in predicting the severity of mercury toxicity. The priority in the treatment should be removing the patient from the source of exposure. Then British anti-Lewisite, edetate calcium disodium, penicillamine, Sodium 2,3-dimercaptopropane-1-sulfhonate and 2,3-dimercaptosuccinic acid can be used for binding the mercury. We conclude that since mercury-containing devices are present in daily life, physicians must be able to recognize the clinical manifestations and treatment of mercury poisoning.

Introduction: Mercury and mercury salts, including mercurous chloride and mercurous oxide, are prohibited for use in cosmetic products as skin-lightening agents because of their high toxicity. Yet, the public continue to have access to these products., Methods: Reports of skin-lightening cosmetic products containing mercury and cases of mercury poisoning following the use of such products were identified using Medline (1950 - 28 March 2011) with mercury, mercury compounds, mercury poisoning, cosmetics and skin absorption as the subject headings. These searches identified 118 citations of which 31 were relevant., Toxicokinetics: The rate of dermal absorption increases with the concentration of mercury and prior hydration of the skin. The degree of dermal absorption varies with the skin integrity and lipid solubility of the vehicle in the cosmetic products. Ingestion may occur after topical application around the mouth and hand-to-mouth contact. After absorption, inorganic mercury is distributed widely and elimination occurs primarily through the urine and feces. With long-term exposure, urinary excretion is the major route of elimination. The half-life is approximately 1-2 months., Features: The kidneys are the major site of inorganic mercury deposition; renal damage includes reversible proteinuria, acute tubular necrosis and nephrotic syndrome. Gastrointestinal symptoms include a metallic taste, gingivostomatitis, nausea and hypersalivation. Although penetration of the blood-brain barrier by inorganic mercury is poor, prolonged exposure can result in central nervous system (CNS) accumulation and neurotoxicity. Inorganic mercury poisoning following the use of skin-lightening creams has been reported from Africa, Europe, USA, Mexico, Australia and Hong Kong. Nephrotic syndrome (mainly due to minimal change or membranous nephropathy) and neurotoxicity were the most common presenting features. As mercury-containing cosmetic products can contaminate the home, some close household contacts were also reported to have elevated urine mercury concentrations., Assessment: Prevention from further exposure is the first step. Cream users and their close contacts should be evaluated for evidence of mercury exposure, the presence of target organ damage and the need for chelation treatment. Laboratory evaluation of affected subjects should include a complete blood count, serum electrolytes, liver and renal function tests, urinalysis, urine and blood mercury concentrations. Since blood mercury concentrations tend to return to normal within days of exposure, blood samples are useful primarily in short-term, higher-level exposures. Estimation of the urine mercury concentration is the best marker of exposure to inorganic mercury and indicator of body burden. A 24-hour urine for measurement of mercury excretion is preferred; a spot urine mercury concentration should be corrected for creatinine output., Management: Chelation therapy is indicated in patients with features of mercury poisoning and elevated blood and/or urine mercury concentrations. Unithiol (2,3-dimercapto-1-propanesulfonic acid, DMPS) is the preferred antidote though succimer (dimercaptosuccinic acid, DMSA) has also been employed., Conclusions: The use of mercury in cosmetic products should be strictly prohibited. The public should be warned not to use such products as their use can result in systemic absorption and accumulation of mercury causing renal, gastrointestinal and CNS toxicity.

Lead, cadmium, mercury, and arsenic, often referred to as "heavy metals", are toxic for wildlife, experimental animals, and humans. While experimental animal and human occupational studies with high exposure levels generally support an adverse role for these metals in human reproductive outcomes, information on the effects of low, environmentally-realistic exposure levels of these metals on male reproductive outcomes is limited. We review the literature on effects of exposure to low levels of these metals on measures of male fertility (semen quality and reproductive hormone levels) and provide supporting evidence from experimental and occupational studies. Potentially modifying effects of genetic polymorphisms on these associations are discussed. A brief review of the literature on the effects of three trace metals, copper, manganese, and molybdenum, that are required for human health, yet may also cause adverse reproductive effects, follows. Overall, there were few studies examining the effects of exposure to low levels of these metals on male reproductive health. For all metals, there were several well-designed studies with sufficient populations appropriately adjusted for potential confounders and many of these reported harmful effects. However, many studies lacked sufficient numbers of participants to be able to detect differences in outcomes between exposed and non-exposed individuals, did not clearly identify the source and characteristics of the participants, and did not control for other exposures that could alter or contribute to the outcomes. The evidence for the effects of low exposure was strongest for cadmium, lead, and mercury and less certain for arsenic. The potential modifying effects of genetic polymorphisms has not been fully explored. Additional studies on the reproductive effects of these toxic ubiquitous metals on male reproduction are required to expand the knowledge base and to resolve inconsistencies.

Case Report: A 36-year-old jewelry producer presented with tremor, slurred speech, lethargy, headache, and incoordination. On examination he had a coarse tremor of the outstretched hands and protruded tongue, slurred speech, "Hatter's shakes" handwriting, impaired heel-toe walking and heel-shin coordination, mild dysdiadochokinesis, and constricted visual fields to confrontation. The patient received four 5-day courses of oral 2,3-dimercapto-1-propanesulfonate (30 mg/kg/day), which was associated with substantial objective clinical improvement and the excretion of 99,406 microg mercury., Conclusion: We recommend that the administration of 2,3-dimercapto-1-propanesulfonate should be considered in symptomatic patients who have been exposed to mercury vapor and who have supporting analytical confirmation of the diagnosis.

Introduction: Intravenous injection of mercury has seldom been reported, especially in cases of attempted suicide, and is associated with variable clinical outcomes., Case Report: A young woman came to our attention after self-injecting and ingesting mercury drawn from 37 thermometers. The patient suffered lung embolization complicated by adult respiratory distress syndrome (ARDS), toxic dermatitis, anemia, mild hepato-renal impairment, and died after 30 days. Mercury was monitored in biological fluids (blood, plasma, urine, and bronchoalveolar fluid) to study its toxicokinetics and to evaluate dose-effect relationships. Its urinary clearance significantly increased after a chelation challenge test with meso-2,3-dimercaptosuccinic acid (DMSA) (median values of 2.48 and 8.85 before and after the test, respectively, p < 0.05)., Conclusions: Mercury poisoning by intravenous injection is a clinical emergency, potentially leading to death. When injected, the element has a very slow clearance, mainly renal. Our data do not allow any conclusion about the effectiveness of chelation therapy.

Objective: To investigate the suitability of measurements of mercury (Hg) concentration as a means of identifying patients with health complaints attributed to dental amalgam., Methods: Hg in erythrocytes, plasma, urine, and saliva was determined in 27 patients complaining about health problems attributed to amalgam, 27 healthy volunteers with amalgam fillings, and 27 healthy amalgam-free volunteers., Results: Concentrations of inorganic mercury in blood and of total mercury in urine and saliva differed significantly between individuals with amalgam fillings and amalgam-free volunteers, but not between symptomatic patients and healthy volunteers with amalgam fillings. Urine Hg levels tended to be better correlated with blood than with saliva data. Levels of organic Hg were equal in all groups., Conclusion: Concentrations of total and inorganic mercury in body fluids do not distinguish between asymptomatic amalgam bearers and those who suffer from a poorly defined syndrome of multiple nonspecific symptoms.

Background: Although mercury is toxic, few studies have measured exposure in children who handled elemental mercury briefly. In 2004, a student spilled approximately 60 milliliters of mercury at a Nevada school. Within 12 hours, all students were removed from the source of exposure. We conducted an exposure assessment at the school., Methods: We administered questionnaires and obtained urine samples from students. Using two-sample t-tests, we compared urine mercury levels from students who self-reported exposure to mercury levels of other students., Results: Two-hundred students participated, including 55/62 (89%) who were decontaminated. The students' geometric mean urine mercury level was 0.36 microg/L (95% confidence interval 0.32-0.40 microg/L). The student who brought the mercury to school was the only one to have an elevated urine mercury level (11.4 microg/L)., Conclusion: Despite environmental contamination, mercury exposure may have been minimized because of rapid identification of the elemental mercury spill and decontamination.