Broken thermometer in foot: a source of mercury poisoning.

A 17-year-old boy was referred after jumping from a ladder onto the ground, crushing a medical thermometer with his right foot. Some days later, he complained of loss of appetite and weakness. A radiograph of the affected foot demonstrated radiopaque densities. Blood and 24-h urine assays for mercury demonstrated toxic levels. Chelation therapy cured the patient dramatically.

Continuous Exposure to Inorganic Mercury Affects Neurobehavioral and Physiological Parameters in Mice.

Contamination with mercury is a real health issue for humans with physiological consequences. The main objective of the present study was to assess the neurotoxicological effect of inorganic mercury: HgCl2. For this, adult mice were exposed prenatally, postnatally, and during the adult period to a low level of the metal, and their behavior and antioxidant status were analyzed. First, we showed that mercury concentrations in brain tissue of treated animals showed significant bioaccumulation, which resulted in behavioral deficits in adult mice. Thus, the treated mice developed an anxiogenic state, as evidenced by open field and elevated plus maze tests. This anxiety-like behavior was accompanied by a decrease in social behavior. Furthermore, an impairment of memory in these treated mice was detected in the object recognition and Y-maze tests. The enzymatic activity of the antioxidant system was assessed in eight brain structures, including the cerebral cortex, olfactory bulb, hippocampus, hypothalamus, mesencephalon, pons, cerebellum, and medulla oblongata. The results show that chronic exposure to HgCl2 caused alterations in the activity of catalase, thioredoxin reductase, glutathione peroxidase, superoxide dismutase, and glutathione S-transferase, accompanied by peroxidation of membrane lipids, indicating a disturbance in intracellular redox homeostasis with subsequent increased intracellular oxidative stress. These changes in oxidative stress were concomitant with a redistribution of essential heavy metals, i.e., iron, copper, zinc, and magnesium, in the brain as a possible response to homeostatic dysfunction following chronic exposure. The alterations observed in overall oxidative stress could constitute the basis of the anxiety-like state and the neurocognitive disorders observed.

Endothelin-1 and angiotensin-II modulate urotensin-II vasoconstriction in rat aorta exposed to mercury.

OBJECTIVES: The aim of this study was to evaluate the possible roles of endothelin-1 and angiotensin-II in urotensin-II vasoconstriction and in endothelial dysfunction induced by mercury. BACKGROUND: Urotensin-II, the most potent vasoactive peptide, is entwined with the cardiovascular diseases and has been labelled as a new pathophysiological biomarker. METHODS: Rat aortic rings were pre-incubated with sb-710411, bq-123, and captopril. Doses of human urotensin-II with increased concentrations were applied in all groups in the presence or absence of mercury chloride. In another set of the experiment, aortic rings were treated with a single dose of mercury chloride in the presence of each of the above blockers. RESULTS: Angiotensin-II and endothelin-1 mediated the vascular responses to the peptide urotensin-II under conditions of both intact endothelium and endothelial impairments induced by mercury. Urotensin-II, angiotensin-II and endothelin-1 significantly participated in vascular responses to mercury chloride. CONCLUSION: The novel finding was that urotensin-II is potentiated under the condition of endothelial dysfunction. Endothelin-1 and angiotensin-II pathways could be heavily exploited in modulating endothelial dysfunction impacts and peptide vascular actions (Tab. 1, Fig. 4, Ref. 30).

Egg turning behavior and incubation temperature in Forster's terns in relation to mercury contamination.

Egg turning behavior is an important determinant of egg hatchability, but it remains relatively understudied. Here, we examined egg turning rates and egg temperatures in Forster's terns (Sterna forsteri). We used artificial eggs containing a data logger with a 3-D accelerometer, a magnetometer, and a temperature thermistor to monitor parental incubation behavior of 131 tern nests. Overall, adults turned their eggs an average (±SD) of 3.8 ± 0.8 turns h-1, which is nearly two times higher than that of other seabirds. Egg turning rates increased with nest initiation date. We also examined egg turning rates and egg temperatures in relation to egg mercury contamination. Mercury contamination has been shown to be associated with reduced egg hatchability, and we hypothesized that mercury may decrease egg hatchability via altered egg turning behavior by parents. Despite the high variability in egg turning rates among individuals, the rate of egg turning was not related to mercury concentrations in sibling eggs. These findings highlight the need for further study concerning the potential determinants of egg turning behavior.

Rethinking mercury: the role of selenium in the pathophysiology of mercury toxicity.

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.

Vulnerability associated with "symptoms similar to those of mercury poisoning" in communities from Xingu River, Amazon basin.

The Brazilian Amazon is known to be a region with high levels of mercury (Hg) in the environment and studies point to an association between high levels of natural mercury in the mother rock and the vast number of clandestine gold mines. Other studies already report the contamination of fish in this region, as well as high levels of Hg in biological material from environmentally exposed populations. On the other hand, this is one of the least developed regions of the planet and it is necessary to understand the vulnerability factors in these populations that may be intoxicated by this element. The purpose of the present study was to investigate the vulnerability factors in communities from Xingu River-Amazon basin probably exposed to Hg. A cross-selection study in two cities localized in Xingu River was conducted, and the sample contained was 268 individuals. sociodemographic questions, lifestyle, diet habits and health conditions were collated. The majority of the sample was female, between 30 and 59 years old, had less than 3 years of educational level and lived in the local of study more than 240 months. There was regular fish consumption (95.9%), principally carnivorous species (80.5%). The visual problem has a highest prevalence (43.3%) between the health problems and about the symptoms of Hg intoxication, memory loss (42.9%), weakness (35.1%), fatigue (34.3%), mood changes (28.7%) and difficulties in concentration (27.2%) was most reported. The female sex, age over 60, educational level below 3 years of study, did not had flush toilet, smoke and least one chronic non-communicable disease represent higher probability to had symptoms of Hg intoxication. Lack of access to health services, low education level and income evidence the susceptibility of this community to diseases and injuries. The vulnerable groups identified in this study should be a priority in public health and environmental health policies.

Role for apolipoprotein E in neurodegeneration and mercury intoxication.

Mercury intoxication is a serious public health problem and a worldwide concern. The Minamata Convention on Mercury has been signed by 128 countries and endorsed by the World Health Organization with the recommendation of promoting the management of epidemiological information. The Central Nervous System is the main target organ for mercury. Symptoms of intoxication include altered motor coordination, visual and tactile dysfunction and paralysis, caused by neurodegeneration with a key role for oxidative damage. Recently, some studies have demonstrated a correlation between mercury intoxication and isoforms of apolipoprotein E (ApoE). In this review, epidemiological data and hypotheses about the possible molecular mechanisms underlying the association between ApoE and mercury intoxication are assessed. Based on the evidence and the neuropathological changes that the presence of ApoE4 and mercury neurotoxicity have in common, we propose a convergent action of both factors. ApoE4 seems to potentiate the damage caused by mercury. Increased knowledge of this interaction using epidemiological and pre-clinical studies is essential to improve prevention strategies to adequately manage intoxicated patients.

[Molecular genetic aspects of endothelial dysfunction in individuals exposed to mercury].

The article deals with frequency data on polymorphism of candidate genes participating in endothelial dysfunction (EDN1 Lys198Asn, NOS3 T786C, AGT Thrl74Met and AGT Met23SThr) in totality with concentrations of their active substances in individuals exposed to mercury. Findings are changes in levels of nitrogen oxide, endothelin-1, angiotensin II metabolites in examinees including those without cardiovascular diseases. The genetic conditionality is connected with unfavorable genotypes of polymorphic variants - Met235Thr of AGT gene and Lys198Asn of EDNI gene. Changes in levels of biochemical markers of endothelial dysfunction in individuals exposed to mercury indicate serious endothelial function disorders and are not genetically determined processes.

Assessment of the Cardiac Autonomic Nervous System in Mercury-Exposed Individuals via Post-Exercise Heart Rate Recovery.

OBJECTIVE: The aim of this study was to assess exercise heart rate recovery (HRR) indices in mercury-exposed individuals when evaluating their cardiac autonomic function. SUBJECTS AND METHODS: Twenty-eight mercury-exposed individuals and 28 healthy controls were enrolled. All the subjects underwent exercise testing and transthoracic echocardiography. The HRR indices were calculated by subtracting the first- (HRR1), second- (HRR2) and third-minute (HRR3) heart rates from the maximal heart rate. The two groups were evaluated in terms of exercise test parameters, especially HRR, and a correlation analysis was performed between blood, 24-hour urine and hair mercury levels and the test parameters. RESULTS: The mercury-exposed and control groups were similar in age (37.2 ± 6.6 vs. 36.9 ± 9.0 years), had an identical gender distribution (16 females and 12 males) and similar left ventricular ejection fractions (65.5 ± 3.1 vs. 65.4 ± 3.1%). The mean HRR1 [25.6 ± 6.5 vs. 30.3 ± 8.2 beats per min (bpm); p = 0.009], HRR2 (43.5 ± 5.3 vs. 47.8 ± 5.5 bpm; p = 0.010) and HRR3 (56.8 ± 5.1 vs. 59.4 ± 6.3 bpm; p = 0.016) values were significantly lower in the mercury-exposed group than in the healthy controls. However, there were no significant correlations between blood, urine and hair mercury levels and exercise test parameters. CONCLUSIONS: Mercury-exposed individuals had lower HRR indices than normal subjects. In these individuals, mercury exposure measurements did not show correlations with the exercise test parameters, but age did show a negative correlation with these parameters. Therefore, cardiac autonomic functions might be involved in cases of mercury exposure.

Mercuric chloride induced hepatotoxic and hematologic changes in rats: The protective effects of sodium selenite and vitamin E.

This study focuses on investigating the possible protective effect of sodium selenite (Na2SeO3) and/or vitamin E against mercuric chloride (HgCl2)-induced hepatotoxicity in rat. Male rats were given HgCl2 (1 mg/kg body weight (bw)) and HgCl2 plus Na2SeO3 (0.25 mg/kg bw) and/or vitamin E (100 mg/kg bw) daily via gavage for 4 weeks. HgCl2-treated groups had significantly higher white blood cell and thrombocyte counts than the control group. Serum activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, γ-glutamyl-transferase, and lactate dehydrogenase significantly increased and serum levels of total protein, albumin, triglyceride, total cholesterol, and low-density lipoprotein cholesterol significantly decreased in the HgCl2-treated groups compared with control group. Malondialdehyde level significantly increased and superoxide dismutase, catalase, and glutathione peroxidase activities decreased in liver tissue of HgCl2-treated rats. Also, HgCl2 exposure resulted in histopathological changes. Supplementation of Na2SeO3 and/or vitamin E provided partial protection in hematological and biochemical parameters that were altered by HgCl2 As a result, Na2SeO3 and/or vitamin E significantly reduced HgCl2-induced hepatotoxicity, but not protected completely.

Low doses of mercuric chloride cause the main features of anti-nucleolar autoimmunity in female outbred CFW mice.

The growth of the influence of anthropogenic factors aimed on the improvement of human life has its side effect, for example, living organisms receive increasing exposure to toxic mercuric compounds. Experimental data show that mercury (Hg) salts are able to induce systemic autoimmunity in rodents. This Hg-induced autoimmune process (HgIA) is characterized by T cell-dependent polyclonal activation of B lymphocytes, increased level of serum immunoglobulin G1 (IgG1) and immunoglobulin E (IgE), production of antinucleolar autoantibodies (ANoA), and immune complex deposition in multiple organs. HgIA in mice is used as a model of human systemic autoimmune disorders. However, the dose of mercuric chloride (HgCl2) usually used in laboratory mice to induce HgIA is above the allowable limit for everyday levels of Hg exposure in humans. So, we decided to determine the lowest dose of HgCl2 that is able to trigger autoimmunity in outbred Carworth Farms Swiss Webster (CFW) mice not genetically prone to HgIA development. The lowest dose (50 µg/kg body weight (b.w.)/week) was chosen to match the World Health Organization provisional weekly tolerable intake of total Hg for humans. We also tested HgCl2 at 500 and 1500 µg/kg b.w./week (6.5- and 2-fold less than usually used for induction of HgIA in mice). We found that even the lowest dose of Hg resulted in a statistically significant increase in serum level of IgG1 after 8 weeks of treatment. HgCl2 in doses 500 and 1500 µg/kg b.w./week resulted in a significant increase in serum level of IgG1 after 4 weeks of treatment, followed by ANoA production. Sera of HgCl2-treated mice stained the regions in which the major autoantigen in HgIA, fibrillarin, was revealed. These results suggest that low doses of Hg are able to induce the main features of HgIA in genetically heterozygous mice, and that humans chronically exposed to low doses of Hg may be at risk of autoimmunity induction regardless of their genetic background.

[State of central and peripheral conduction tracts in patients with long-term chronic mercury intoxication].

In connected sample, the authors studied changes in state of peripheral nerves (electroneuromyography) and central afferent conduction tracts (somatosensory evoked potentials) in patients with long-term chronic mercury intoxication. The study helped to reveal negative changes in peripheral and central afferent conduction tracts in the patients with long-term chronic mercury intoxication, more marked in 3 period of the study--demyelination of sensory and motor components of peripheral nerves and longer impulse propagation time in conduction tracts of subcortical and cortical structures of somatosensory brain cortex.

Prenatal exposure to methyl mercury from fish consumption and polyunsaturated fatty acids: associations with child development at 20 mo of age in an observational study in the Republic of Seychelles.

BACKGROUND: Fish is a rich source of n-3 polyunsaturated fatty acids (PUFAs) but also contains the neurotoxicant methyl mercury (MeHg). PUFAs may modify the relation between prenatal MeHg exposure and child development either directly by enhancing neurodevelopment or indirectly through the inflammatory milieu. OBJECTIVE: The objective was to investigate the associations of prenatal MeHg exposure and maternal PUFA status with child development at 20 mo of age. DESIGN: The Seychelles Child Development Study Nutrition Cohort 2 is an observational study in the Republic of Seychelles, a high-fish-eating population. Mothers were enrolled during pregnancy and their children evaluated at 20 mo of age by using the Bayley Scales of Infant Development II (BSID-II), the MacArthur Bates Communicative Development Inventories (CDI), and the Infant Behavior Questionnaire-Revised. There were 1265 mother-child pairs with complete data. RESULTS: Prenatal MeHg exposure had no direct associations with neurodevelopmental outcomes. Significant interactions were found between MeHg and PUFAs on the Psychomotor Developmental Index (PDI) of the BSID-II. Increasing MeHg was associated with lower PDI but only in children of mothers with higher n-6/n-3. Among mothers with higher n-3 PUFAs, increasing MeHg was associated with improved PDI. Higher maternal docosahexaenoic acid (DHA) was associated with improved CDI total gestures (language development) but was significantly adversely associated with the Mental Development Index (MDI), both with and without MeHg adjustment. Higher n-6:n-3 ratios were associated with poorer scores on all 3 CDI outcomes. CONCLUSIONS: We found no overall adverse association between prenatal MeHg exposure and neurodevelopmental outcomes. However, maternal PUFA status as a putative marker of the inflammatory milieu appeared to modify the associations of prenatal MeHg exposure with the PDI. Increasing DHA status was positively associated with language development yet negatively associated with the MDI. These findings may indicate the existence of an optimal DHA balance with respect to arachidonic acid for different aspects of neurodevelopment.

Toxicant exposure and bioaccumulation: a common and potentially reversible cause of cognitive dysfunction and dementia.

Juxtaposed alongside the ongoing rise in the incidence and prevalence of dementia, is the surge of recent research confirming widespread exposure and bioaccumulation of chemical toxicants. Evidence from sources such as the Centers for Disease Control reveals that most people have accrued varying degrees of assorted toxic pollutants including heavy metals, flame retardants, and pesticide residues within their bodies. It has been well established that many of these toxicants have neurodegenerative as well as neurodevelopmental impact as a result of various pathophysiologic mechanisms including neuronal mitochondrial toxicity and disruption of neurotransmitter regulation. Elimination of stockpiled toxicants from the body may diminish adverse toxicant impact on human biology and allow restoration of normal physiological function. Incorporating a review of medical literature on toxicant exposure and dementia with a case history of a lead-exposed individual diagnosed with dementia, this paper will discuss a much overlooked and potentially widespread cause of declining brain function and dementia.

Mercury poisoning as a cause of intracranial hypertension.

Mercury poisoning is a rare but fatal toxicologic emergency. Neurologic manifestations involving the central nervous system are seen usually with chronic mercury intoxication. The most commonly seen complaints are headache, tremor, impaired cognitive skills, weakness, muscle atrophy, and paresthesia. Here, we present a male patient who was chronically exposed to elemental mercury and had papilledema and intracranial hypertension without parenchymal lesion in the central nervous system. A 12-year-old male patient was referred to our emergency room because of severe fatigue, generalized muscle pain and weakness, which was present for a month. Physical examination revealed painful extremities, decreased motor strength and the lack of deep tendon reflexes in lower extremities. He had mixed type polyneuropathy in his electromyography. Whole blood and 24-hour urinary mercury concentrations were high. A chelation therapy with succimer (dimercaptosuccinic acid) was started on the fourth day of his admission. On the seventh day of his admission, he developed headache and nausea, and bilateral papilledema and intracranial hypertension were detected on physical examination. Acetazolamide was started and after 1 month of treatment, the fundi examination was normal. The patient stayed in the hospital for 35 days and was then discharged with acetazolamide, vitamin B6, gabapentin, and followed as an outpatient. His clinical findings were relieving day by day. Although headache is the most common symptom in mercury poisoning, the clinician should evaluate the fundus in terms of intracranial hypertension.

Effect of low-level prenatal mercury exposure on neonate neurobehavioral development in China.

BACKGROUND: This study aimed to assess the effects of low-level prenatal mercury exposure on neonate neurobehavioral development in China. METHODS: In total, 418 mother-neonate pairs were included in the study. Maternal urine, hair, and blood samples and cord blood samples were used to document prenatal exposure to mercury. The Neonatal Behavioral Neurological Assessment was used to estimate neurobehavioral development in the neonates at 3 days of age. RESULTS: Total mercury level was significantly higher in cord blood than that in maternal blood. A strong correlation was found between total mercury levels in maternal blood and those in cord blood (r = 0.7431; P < 0.0001). Trend analysis revealed that mothers who consumed more fish had higher blood and cord blood mercury levels (all P < 0.0001). Significant differences were also found between male and female cord blood mercury levels among groups with different fish consumption frequencies (all P < 0.0001). Cord blood mercury level was significantly associated with total Neonatal Behavioral Neurological Assessment scores (ß = 0.03; standard error = 0.01; P = 0.0409), passive muscle tone (odds ratio = 1.07; 95% confidence interval = 1.12-1.13; P = 0.0071), and active muscle tone (odds ratio = 1.06; 95% confidence interval = 1.01-1.11; P = 0.0170) scores after adjustment, respectively. CONCLUSIONS: Neonatal neurodevelopment was associated with prenatal exposure to mercury. Women with high mercury levels should avoid intake seafood excessively during pregnancy. Long-term effects of exposure to mercury on childhood development need to be further explored.

Clinical manifestation and management of intravenous mercury injection: a case report.

Intentional self-injection of metallic mercury case report is presented. A 22 year old man with a past medical history of ethylene glycol suicidal poisoning was admitted to a Acad. N. Kipshidze Central University Clinic in Tbilisi, four months after deliberate intravenous injection of an unknown quantity of metallic mercury from several thermometers into his antecubital vein. After 2 months of asymptomatic period, the patient began to complain of pain and tremor in limbs, fatigue and skin rash. CT scan of the thorax and the abdomen confirmed multiple small opacities of metallic density in both lungs, liver and right kidney. After the procedure the patient was transferred to the toxicology center in Baku, Azerbaijan for chelation therapy. On arrival no biochemical abnormalities in hepatic or renal function or clinical pulmonary malfunction were detected, despite presence of slight symptoms of erethism, tremor mercuralis, knee joints arthralgia and lower extremities weakness. Chelation therapy with intramuscular injection of Unithiol (DMPS) was started in dose of 20mg/kg/day. After one month of chelation therapy, mercury blood concentration slowly decreased from initially 134 microgram/L to 105 microgram/L. This case report demonstrates mild acute toxicity following intravenous administration of unknown amounts of elemental mercury. Because of chelation therapy can remove approximately 1 mg of mercury per day the patient was recommended further long-term DMPS treatments under the control blood mercury levels. It is concluded that clinical manifestations of intravenous elemental mercury intoxication may be delayed despite significant increase in blood mercury level.

[Quantitative estimation of the health status dynamics of persons occupationally exposed to mercury vapor: a remote period of intoxication].

The article presents the results of the dynamic clinical observation for persons suffered from occupational chronic mercury intoxication in the remote post-exposure period of the disease. The estimation of the dynamics of syndrome manifestations of chronic mercury intoxication and co-morbidity are presented. The important role of mercury exposure load as a predictor of deterioration of actual health of the patients in the remote period of intoxication is demonstrated.