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The toxicology of mercury: Current research and emerging trends
... O mercúrio (Hg) é um elemento químico altamente tóxico ao homem e ao meio ambiente (Bjørklund et al., 2017;Gonçalves;Gonçalves, 2004). Na natureza, o Hg pode se apresentar em diversas formas físicas e químicas, entre elas a forma elementar, sais inorgânicos e compostos orgânicos (Clarkson;Vyas;Ballatori, 2007;Franco, 2009). ...
... O metilmercúrio (MeHg), a forma química de Hg mais tóxica para seres vivos, tem a capacidade de bioacumulação e biomagnificação ao longo da cadeia trófica (Almeida et al., 2005;Crespo-López et al., 2005;Gurjão et al., 2010;Hacon et al., 2009;Paula, 2006). Segundo Clarkson (1997) O consenso da literatura científica afirma que a exposição humana ao Hg ocorre por meio do consumo de peixes, amálgamas dentais e vacinas (Bjørklund et al., 2017;Clarkson, 1997;Clarkson;Magos;Myers, 2003;Franco, 2009;Gonçalves;Gonçalves, 2004;Roulet et al., 1998). Na Amazônia, no entanto, estudos têm demonstrado o aumento dos níveis de Hg presentes nos peixes da região, tornando-os a principal fonte de contaminação humana, uma vez que a dieta das comunidades ribeirinhas e indígenas se baseia na ingestão desse tipo de proteína animal (Brito et al., 2017;Franco, 2009;Grotto et al., 2010;Roulet et al., 1998). ...
... Valores elevados de MeHg no corpo humano estão relacionados aos mecanismos de neurotoxidade, incluindo o aumento da produção de radicais livres, causadores do estresse oxidativo, o que poderia resultar em complicações de saúde em médio e longo prazo (Bjørklund et al., 2017;Franco, 2009;Grotto et al., 2010). Nesse contexto, as gestantes representam um grupo de risco, dado que o desenvolvimento fetal pode se tornar comprometido por alterações induzidas pelo Hg (Bjørklund et al., 2017;Faial et al., 2015;Franco, 2009;Rodrigues, 2020). ...
O Mercúrio (Hg) é um metal tóxico capaz de causar efeitos deletérios ao sistema nervoso humano. A intoxicação por Hg durante o período pré-natal e lactacional é considerada um grave problema de saúde pública. Na região amazônica brasileira, esse tipo de contaminação representa uma preocupação particularmente importante devido à alimentação da população local ser baseada na ingestão de peixes, em grande parte, contaminados por metilmercúrio (MeHg). Pesquisas têm demonstrado os benefícios de uma alimentação saudável e de alta qualidade, como alimentos ricos em substâncias antioxidantes, na prevenção ao estresse oxidativo provocado pela exposição crônica ao MeHg. Dessa forma, a hipótese levantada nesse estudo foi a de que a suplementação nutricional baseada em substâncias antioxidantes durante o período gestacional pode auxiliar na diminuição dos níveis de MeHg sérico e, assim, contribuir para atenuar possíveis agravos de saúde à mãe e ao bebê. O objetivo desse artigo foi descrever os efeitos da suplementação nutricional com substâncias antioxidantes em gestantes expostas ao Hg na Amazônia brasileira nos anos 2019 a 2024. Trata-se de uma Revisão Sistemática da Literatura (RSL). A pesquisa dos artigos foi realizada em três bases de dados: LILACS, PubMed e SciELO, utilizando a opção de busca avançada de artigos publicados em qualquer idioma nos últimos cinco anos. O estudo não encontrou artigos sobre os efeitos da suplementação nutricional com substâncias antioxidantes em gestantes expostas ao Hg na Amazônia brasileira. Esta constatação reforça a necessidade de investigar a ação das substâncias antioxidantes durante a gestação de mulheres em exposição crônica ao Hg na Amazônia Legal.
... The severity of mercury's toxic effects on the body depends on several critical factors. These factors include the chemical structure of the mercury that is ingested, the exposure route, and the mercury concentration upon exposure (Wu et al. 2024;Bjørklund et al. 2017). Due to these factors, mercury has the potential to affect multiple systems in the body, including the vascular (Poznyak et al. 2021;Genchi et al. 2017), neuronal (Basu et al. 2023;Philibert et al. 2022;Cariccio et al. 2019), adipose cells (Tinkov et al. 2021;Kaczor-Kamińska et al. 2020;Rizzetti et al. 2019) respiratory, gastrointestinal, renal, and endocrine systems (Unsal 2018). ...
... Mercury can bind to several enzymes that contain cysteine, such as manganesesuperoxide dismutase (Mn-SOD), arginase I, sorbitol dehydrogenase, and δ-aminolevulinate dehydratase. The high affinity of Hg-compounds to sulfhydryl (-SH) groups has been reported in numerous studies (Ajsuvakova et al. 2020;Bjørklund et al. 2017). Enzymes play a crucial role in catalyzing biochemical reactions necessary for supporting life. ...
... A review by Bjørklund et al. (2017) highlighted mercury's interactions with microtubules and membrane transport proteins. Mercury binds cysteine residues, affecting tubulin and leading to microtubule depolymerization. ...
Mercury is widely known for its detrimental effects on living organisms, whether in its elemental or bonded states. Recent comparative studies have shed light on the biochemical implications of mercury ingestion, both in low, persistent concentrations and in elevated acute dosages. Studies have presented models that elucidate how mercury disrupts healthy cells. Mercury’s unique ability to interfere with crucial enzymatic processes at deposition sites is a vital feature of these models. The strong affinity for the sulfhydryl moieties of enzyme catalytic sites leads to enzyme inactivation through permanent covalent modifications. This inactivation can have catastrophic effects on an organism’s metabolic functions. Moreover, it has been found that mercury’s binding to sulfhydryl moieties is highly nonspecific and can occur in various ways. This review aimed to explore the effects of mercury on a broad spectrum of enzymes with a specific focus on how these alterations can detrimentally affect several metabolic pathways.
... Annually, approximately 200 tons of mercury are emitted into the atmosphere in ASGM areas of the Amazon, and on a global scale, annual Hg emissions correspond to 27% of the total released worldwide (Galvis 2020). Hg can be found in several chemical forms in the environment, including elemental/metallic form (Hg 0 ), inorganic form (Hg + , Hg ++ ), and organic forms, in which methylmercury (MeHg) is the most cited (Bjørklund et al. 2017). The elemental and inorganic forms reach the human body mainly by inhaling the compound volatilized during its burning, and MeHg contamination occurs primarily by ingesting contaminated animal tissues (UNEP 2019), including invertebrates (Ramos-Filho et al. 2025;Rodrigues et al. 2022), fishes (Rodrigues et al. 2024), elasmobranchs , and chelonians (Nery et al. 2025). ...
... After burning, volatilized mercury is released in its elementary form (Hg 0 ) into the air, which can reach long distances from its place of emission (Bjørklund et al. 2017), and its particles reach the land and water surface according to Hg is condensed. Elemental mercury can also pass through oxidative reactions and interact with elements like chlorine, sulfur, or oxygen, leading to its transformation into inorganic mercury (Hg 2+ ) (Seigneur et al. 1994). ...
In the Amazon, gold is predominantly found in alluvial deposits, so miners use liquid mercury (Hg) to process this metal, occasionally contaminating rivers, lakes, aquatic organisms, and humans, including Indigenous communities that depend on natural resources. This systematic review aimed to analyze the potential health risks associated with Hg levels found in biological samples from Indigenous populations and animals consumed by these populations in the Amazon biome. A search was carried out to find articles between July and September 2024 using the following databases: Scopus, PubMed, ScienceDirect, and Web of Science. Levels of mercury were found in hair and urine in Indigenous communities from Amazon, such as Colombia, which had the highest average in one of the communities analyzed in hair (22.2 ± 1.7 µg g⁻¹). Studies revealed averages above the safe levels in hair established by the World Health Organization, of 6 µg g⁻¹, in three countries (Brazil, Colombia, and Peru). The levels in wild animals were lower than those found in fish, mainly carnivores, where five species had Hg levels above the limit of 1 ppm established for predatory fish (Pygocentrus nattereri, Platynematichthys notatus, Boulengerella cuvieri, Ageneiosus brevifilis, and Cichla ocellaris). Assessments of neurological manifestations of mercury (Hg) poisoning were carried out in Brazil (Yanomami and Munduruku villages) and Peru (Maizal, Cacoatal, and Yomibato villages). Therefore, it is essential for the countries within the Amazon region to work together on protecting Indigenous territories in order to prevent these activities from further endangering the survival of these vulnerable populations.
Graphic Abstract
... Mercury is a highly toxic heavy metal with severe impacts on human health and ecosystems even at trace levels [6]. It is well known for its bioaccumulation in the food chain and persistence in the environment [7]. ...
The green synthesis of blue fluorescent carbon nanodots (CNDs) from apricot kernel shells via a hydrothermal method was successfully executed. The interaction of the synthesized CNDs with various cations was systematically investigated using fluorescence spectroscopy. Fluorescence measurements were performed to evaluate the interaction of CNDs with 36 different cations, including Li⁺, Na⁺, K⁺, Be²⁺, Mg²⁺, Ca²⁺, Sr²⁺, Ba²⁺, Sc³⁺, Y³⁺, Ti⁴⁺, V⁵⁺, Cr³⁺, Mo⁶⁺, W⁶⁺, Mn²⁺, Fe³⁺, Co²⁺, Ni²⁺, Cu²⁺, Ag⁺, Zn²⁺, Cd²⁺, B³⁺, Al³⁺, Tl⁺, As⁵⁺, Se²+, NH₄⁺, Au³⁺, Sb³⁺, Sn⁴⁺, Bi³⁺, Hg²⁺, Pd²⁺, and Pb²⁺. Among these, the CNDs exhibited exceptional selectivity and sensitivity as a fluorescent probe for the detection of Hg²⁺ ions. The working range for Hg²⁺ detection was established as 35–95 µM, with a detection limit of 14.0 µM and a quantification limit of 41.4 µM. The method was validated and successfully applied to tap water and river water, demonstrating the practical utility of CNDs derived from apricot seed shells for environmental monitoring and analytical applications.
... For example, Sb has been shown to exert toxic effects through oxidative stress and mitochondrial dysfunction, both of which are processes that can alter miRNA expression profiles [41]. Hg, especially in its organic forms, is a strong nerve poison that can disrupt the way genes are controlled, including miRNAs that play a role in brain development and immune system function [42]. Similarly, chronic As exposure has been linked to altered expression of miRNAs associated with carcinogenesis, inflammation, and cardiovascular dysfunction [43]. ...
The objectives of this study comprise the identification of key miRNAs and their target genes associated with severe tolerance in individuals exposed to aluminum and welding fumes, and the elucidation of the underlying regulatory mechanisms. In this study, the levels of seven miRNAs (hsa-miR-19a-3p, hsa-miR-130b-3p, hsa-miR-25-3p, hsa-miR-363-3p, hsa-miR-92a-3p, hsa-miR-24-3p, and hsa-miR-19b-3p) were analyzed using both hsa-miR-16-5p and RNU6 (U6 snRNA) as reference miRNAs to validate normalization reliability. The qRT-PCR method was used on blood serum samples from 16 workers who were exposed to aluminum, 16 workers who were exposed to welding fumes, and 16 healthy controls who were not exposed to aluminum or welding fumes. We determined heavy metal levels from serum samples of workers exposed to aluminum and welding fumes and control groups using the ICP-OES method. The expression levels of hsa-miR-19a-3p and hsa-miR-19b-3p in aluminum-exposed and control groups were found to be statistically significant (p < 0.05). When workers exposed to welding fumes were compared with the those in the control groups, the expression levels of hsa-miR-19a-3p, hsa-miR-130b-3p, hsa-miR-92a-3p, and hsa-miR-24-3p were observed to be statistically significant (p < 0.05). This study shows that the identification of miRNAs and target genes in different biological functions and pathways plays an important role in understanding the molecular mechanisms of responses to heavy metal toxicity. We share the view that the study will make a significant contribution to the literature in that seven candidate miRNAs can be used as possible biomarkers for exposure to aluminum and welding fumes in humans.
... In many regions, dentists continue to use dental amalgams, which primarily consist of elemental mercury. 44 Inorganic mercury (mercury salts) has been identified in products such as laxatives, cosmetics, teething powders, diuretics, and antiseptics. It can also form as a result of the metabolism of elemental mercury vapor or methylmercury (MeHg). ...
Mercury is a dangerous and toxic contaminant that poses significant threats to both the environment and human health. Consequently, lowering mercury levels to meet drinking water standards has become a priority. Covalent organic frameworks (COFs) are porous materials with adjustable structures that are easy to design and synthesize, and they have garnered significant attention. COFs present a crucial solution for the urgent removal of mercury from water due to their outstanding properties, including high adsorption capacity, excellent photocatalytic performance, tunable porosity, and high stability and reusability. This review aims to discuss the latest advancements regarding the toxicity of mercury and its chemical forms, as well as the synthesis methods for COFs. For the first time, we introduce COFs and their applications in mercury removal, detailing the current challenges and issues faced by COF materials in this area. Additionally, we propose future research directions and obstacles to be addressed.
... Conversely, mercury has been identified as a toxic agent that disrupts autophagy. Studies have shown that exposure to methylmercury can induce mitochondrial dysfunction in rat neurons, thereby activating mitochondrial autophagy [26,27]. ...
Mercury, a prevalent heavy metal, negatively impacts oocyte maturation. However, the exact mechanism by which methylmercury chloride (MMC) affects this process remains elusive. The present study found that MMC administration triggered meiotic failure in oocytes by disrupting cumulus cell expansion, leading to compromised spindle apparatus and altered chromosomal architecture, which are crucial for oocyte development. This disruption is characterized by abnormal microtubule organization and defective chromosome alignment. Additionally, MMC exposure caused oxidative stress-induced apoptosis due to mitochondrial dysfunction, as indicated by decreased mitochondrial membrane potential, mitochondrial content, mitochondrial DNA copy number, and adenosine triphosphate levels. Proteomic analysis identified 97 differentially expressed proteins, including P62, an autophagy marker. Our results confirmed that MMC induced autophagy, particularly through the hyperactivation of the mitochondrial autophagy to remove damaged and normal mitochondria. The mitochondrial reactive oxygen species (ROS) scavenger Mito-TEMPO alleviated oxidative stress and mitochondrial autophagy levels, suggesting that mitochondrial ROS initiates this autophagic response. Notably, MMC activates mitochondrial autophagy via the monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signal pathway due to mitochondrial dysfunction. In vivo studies in mice revealed that MMC exposure decreased reproductive performance, attributed to excessive mitochondrial autophagy leading to reduced oocyte quality. Overall, these findings demonstrate that MMC exposure impairs oocyte maturation via the hyperactivation of mitochondrial autophagy induced by mitochondrial dysfunction.
... Research on toxicity has garnered substantial attention in the scientific community over time [1,2]. Toxicity studies aim to comprehend the adverse effects of various substances on living organisms, providing insights into the impact of these substances on health and the environment. ...
Various toxic compounds still often contaminate the environment and food of living things to this day. Drosophila is often used as a model organism to study the negative effects of exposure to toxic compounds on organisms. The purpose of this systematic literature review (SLR) is to analyze the distribution, contribution, and gap analysis of studies reporting the effect of toxic compounds on behavior in Drosophila. After conducting a search in the Scopus database, 57 titles that matched the entered search query were obtained. After selection and evaluation step, a total of 19 Scopus indexed articles that met the inclusion and exclusion criteria were successfully collected for analysis. The three countries that most frequently research Drosophila behavior are the US, China, and Nigeria. A total of 5 clusters resulted from the results of bibliometric analysis. Various behavioral studies have included developmental variables, gene expression, to the Circadian clock. Toxic compounds that are often studied generally come from the group of metal compounds. On the other hand, multigenerational studies to analyze the long-term effects of toxic compounds and the plasticity of phenotypic changes into gap analysis have been successfully identified.
... The Hg concentration in seafood is mostly in the form of the more bioavailable and toxic methylmercury (MeHg). The MeHg concentration in marine biota increases with larger sizes, older ages 11 and higher trophic levels 6 , that is, the position in the food web (ranging from 1 (primary) to 5 (high)) 12,13 . Seafood is the second-largest source of animal protein globally and an important source of essential fatty acids, including omega-3; it holds greater importance in providing nutrition to low-and lower-middle-income groups than to wealthier income groups 14 . ...
Seafood consumption is a major pathway for exposure to methylmercury (MeHg), a globally pervasive neurotoxin. Yet, how upstream processes in the seafood value chain influence MeHg exposure remains poorly understood. Here we quantified MeHg in seafood production, trade and consumption in 2019 around the world. We found that countries with seafood-MeHg exposures beyond the recommended threshold by the World Health Organization were predominately high-income countries. These countries experienced a tenfold increase in exposure levels compared with low-income countries, due to greater consumption and long-overlooked higher MeHg concentrations in seafood inherited from production. Notably, 43% of seafood MeHg in production was redistributed through seafood trade, marked by inequality, as exports from high-income to lower-income countries contained higher seafood-MeHg concentrations. These exposures may have resulted in 61,800 global premature deaths and economic losses of around US$2.87 trillion, underscoring the need to change seafood production practices and trade patterns.
... Exposure to Mn can cause neurotoxic effects in children. Exposure to Hg causes adverse effects on the central nervous system in humans (Bjørklund et al., 2017). Exposure to Pb can elevate oxidative stress, increasing the risk of damage to the lungs, brain, liver, and blood vessels. ...
Forest fires, whether natural or anthropogenic, release and mobilize heavy metal(loids) (HM). Following intense rainfall events, soil-bound HM are transported from soil to surface water through surface runoff, leading to water quality deterioration. Pollution and ecological risk indices are effective tools for assessing HM contamination. Most forest fire-affected soils and surface water exhibited a degree of contamination greater than 3 and 8 (high and moderate pollution), with associated high and extremely high ecological risks (165 and 2389, respectively). Pollution indices revealed that soils were highly contaminated with Ni, Cu, Cr, and Pb, while Ni, Cu, Hg, Cd, and As posed significant ecological risks. Surface water was heavily contaminated with Pb, Mn, Al, and Fe, with Ni and V contributing to extremely high ecological risks. This study highlights that trace HM also requires substantial removal efforts to make water potable, with removal efficiencies needed for Sb (94.49%), Be (85.83%), Ba (70.75%), V (68.19%), and Se (65.51%). Fire-affected surface water poses an elevated cancer risk to both children (0.18 and 4.5 × 10–3) and adults (0.39 and 1.53 × 10–3) through oral and dermal exposure, respectively. Children are more vulnerable to dermal cancer and noncancer risks compared to adults. Low-cost treatment methods, such as the application of immobilizing agents combined with compost, straw mulching, and seeding, can be implemented to control soil erosion in forest areas, thereby reducing the transport of soil-bound HM to surface water. These findings can aid government agencies in developing new soil and water quality standards and implementing effective treatment measures.
... The aim to evaluate the capacity of Silicon (SiO 2 NPs and Na 2 SiO 3 ) to remediate Hg contamination in soybean plants also depends on the chemical form of Hg present in the plants, as MeHg is more toxic than Hg(II) (Bjørklund et al. 2017). Through chemical speciation, it was found that Hg was present solely in its ionic form, Hg(II), in both the roots and the aerial parts of the soybean plant. ...
This study aimed to investigate the potential of Silicon (SiO2NPs and Na2SiO3) to mitigate Hg absorption, accumulation, and toxicity in transgenic soybean plants. By analyzing Hg speciation, total Hg content, physiological characteristics, anatomical structures, and the homeostasis of macro (P, S, Ca, K, and Mg) and micro (Cu, Fe, Mn, Zn) nutrients, the impact of Si against Hg-induced stress was assessed. Plants were cultivated under six treatments: water, SiO2NPs, Na2SiO3, Na2SiO3 + HgCl2, SiO2NPs + HgCl2, and HgCl2. The addition of silicon to the soil, both in the form of nanoparticles and in its soluble form, did not negatively impact plant development. SiO2 NPs reduced Hg concentration in roots by 17% (RR) and 29% (INTACTA) and Na2SiO3 by 15% and 37%. In leaves, Hg reductions were 25% with SiO2NPs and 22% with Na2SiO3 for RR variety, while INTACTA showed decreases of 14% and 34%. Only Hg(II) species were found, indicating no Hg methylation in soil or plants. PCA revealed that Hg, alone or with Si, altered nutrient absorption. Morphological analyses showed that SiO2NPs and Na2SiO3 reduced Hg toxicity at the cellular level, highlighting their potential to mitigate heavy metal contamination in crops.
... Due to the toxic effects of Hg, various global organizations, such as Brazil's National Health Surveillance Agency and the Food and Agriculture Organization of the United Nations (FAO), have established permissible limits for Hg concentrations in products, fishing grounds, water, and other foods, as well as daily intake limits [33][34][35][36][37], to prevent potential harm to human health, particularly to the neurological system [55]. In addition to acute cases caused by the absorption of large amounts of mercury, chronic poisoning events are also documented, primarily associated with the ingestion of contaminated food, such as seafood [4]. ...
The marine environment is severely contaminated by anthropogenic activities. Among the pollutants are metals such as mercury (Hg), chromium (Cr), and zinc (Zn), elements commonly found in industrial effluents from steel mills. This study aims to quantify the concentrations of Hg, Cr, and Zn in seafood samples (crab and mussels) and conduct a consumption risk analysis, considering the seasonality and sexual dimorphism of the animals. The samples were collected from traditional fisheries in Itaipu, Niterói, Rio de Janeiro, Brazil. Muscle samples were removed from the animals, which served as the basis for determining Hg, Cr, and Zn levels. Consumption risk assessment was also conducted following the Estimated Monthly Intake and Hazard Quotient (HQ). The quantification results were below the limits set by international regulatory agencies. However, the risk analysis for the population revealed some HQ values above one, particularly for crab consumption.
... Although forest mushrooms contain metallic elements and metalloids beneficial to health, they also accumulate potentially toxic trace elements [29][30][31][32][33][34][35][36][37][38]. One is mercury, categorized as a global pollutant affecting the environment, including humans and animals [39,40]. In Poland, this metal's primary source of emissions is coal-fired power generation. ...
In recent years, the consumption of wild mushrooms in Central Europe has significantly increased. These mushrooms are increasingly recognized as a nutritious, low-calorie, and environmentally friendly food option. They are a valuable source of protein and are rich in vitamins and minerals; however, they can also accumulate toxic elements that may pose risks to human health. This study examined the mercury concentrations in the fruiting bodies of two edible forest mushroom species: Aureoboletus projectellus and Imleria badia. This study took into account the distribution of Hg in the two morphological parts of mushroom fruiting bodies—the caps and the stipes. The total mercury content of the mushroom samples was analyzed using an AMA-254 analyzer. Both mushroom species exhibited higher mercury concentrations in their caps than in their stipes, with levels measuring 0.048 mg·kg⁻¹ dry matter (DM) for Aureoboletus projectellus and 0.055 mg·kg⁻¹ DM for Imleria badia. The mercury content in the stipes was 0.032 mg·kg⁻¹ DM for Aureoboletus projectellus and 0.025 mg·kg⁻¹ DM for Imleria badia. The results obtained indicate that these species do not pose a health risk to consumers in terms of Hg content and can be a valuable addition to the human diet. They are also an indicator of the quality of the forest environment of the central coast of Poland, which should be considered free of mercury pollution.
... Accidental breakage of mercury-containing devices causes mercury vapor inhalation in daily life occasionally. Mercury has toxic effects on several systems, including the neurological, renal, cardiovascular, immune, and endocrine [3,[5][6][7]. Various forms of mercury negatively affect the reproductive health of both sexes [8][9][10]. In women, elevated mercury levels are associated with an increased incidence of infertility, low fertility, menstrual and hormonal disturbances, and adverse pregnancy outcomes. ...
Background
Few studies have been conducted on women of childbearing age with chronic mercury poisoning caused by mercury vapor exposure.
Methods
Occupational exposure, clinical symptoms and signs, laboratory tests, auxiliary examinations, treatment, and follow-up of 31 female workers with chronic mercury poisoning from a mercury thermometer processing factory who received inpatient treatment at our hospital between September 2021 and August 2022 were analyzed.
Results
In 31 female workers of childbearing age (23–43 years) who were chronically exposed to mercury vapor (3–31 months), urinary mercury levels exceeded the normal range. The clinical manifestations were primarily neurological (96.77%). Renal pathology of the two female workers suggested membranous nephropathy in the first stage. Some female workers experienced menstrual abnormalities, anxiety, depression, and sleep disorders. Treatment was mainly chelation therapy supplemented with antioxidants and other symptomatic supportive treatments. All patients achieved good results after discontinuing exposure to mercury vapor and receiving treatment. However, follow-up after discharge revealed that some female workers still had insomnia.
Conclusions
Occupational mercury vapor exposure is hazardous to female workers of childbearing age and increases the risk of adverse effects on their reproductive health. Occupational protection and prevention of mercury exposure in female workers of reproductive age must be emphasized.
... Mercury poisoning is a substantial worldwide public health issue [1]. Despite legislation widely enacted to reduce environmental mercury contamination, some uses, such as mercury amalgamation in illegal mining, persist [24,25]. Illegal mining is the cause of the most mercury release to Amazon water reservoirs, one of the highly endemic areas of MeHg contamination to local communities [25]. ...
Methylmercury (MeHg) is markedly toxic to humans. Our study explores whether MeHg and high‐fat diet (HFD) can impair the intestinal barrier with microbiota dysbiosis in mice. Weanling mice were fed to HFD or standard diet for 40 days. In the last 20 days of diets, mice received either MeHg (20 mg/L) or drinking water. Proximal small intestine, cecum, and hair samples were collected. Villus length, crypt depth, villus/crypt length, mucin2 and lysozyme‐positive cell counts, ZO‐1 and occludin gene expression, and intestinal functional permeability were analyzed to assess the intestinal barrier. Blood samples were drawn to assess lipid parameters. Gut microbiome profiling was conducted with DNA from fecal/cecal samples. In addition, we analyzed ZO‐1 immunofluorescence in the colon and small intestine. HFD increased MDA, Mucin2, and reduced villus height, crypt depth, villus/crypt length, lysozyme(+)‐cell count, and increased intestinal permeability, regardless of MeHg intoxication. MeHg‐HFD combination affected the intestinal barrier, decreasing ZO‐1, occludin, and Nrf2 transcription, and increased permeability. HFD increased total plasma cholesterol and triglycerides. Only MeHg‐HFD reduced microbiome alpha‐diversity along with colonic ZO‐1 immunolabeling loss compared to non‐intoxicated mice fed a control diet. Regardless of diet, the genera Streptococcus, Psychrobacter, Facklamia, and Corynebacterium were severely depleted following MeHg intoxication. Other groups, such as Atopostipes and Jeotgalicoccus, were not altered by MeHg or HFD alone, but were significantly reduced by the combined HFD‐MeHg. Synergistic effects of MeHg‐HFD on the mucosa‐associated microbiota are more pronounced than their individual effects. Our findings suggest that MeHg intoxication does not cause extensive dysbiosis but led to intestinal barrier disruption.
... The primary treatment for mercury toxicity focuses on closely monitoring vital organ function and providing supportive therapy, particularly in cases of acute mercury exposure (Bjørklund et al. 2017). Immediate interventions include administering supplemental oxygen and, in severe cases, mechanical ventilation to stabilize respiratory function (Rafati et al. 2014). ...
Mercury (Hg) is a major environmental contaminant significantly impacting human health. As a naturally occurring element, mercury has been extensively mobilized into aquatic and terrestrial ecosystems over thousands of years, largely due to anthropogenic activities such as mining and metal extraction. Acute mercury toxicity causes extensive physiological damage, affecting vital organs including the kidneys, heart, liver, brain, and skin. Phytochemicals, known for their diverse pharmacological properties, have shown promise in mitigating metal-induced toxicities, including mercury. These compounds exhibit protective effects against mercury-induced multi-organ damage through mechanisms such as reactive oxygen species (ROS) scavenging, cyclooxygenase (COX) inhibition, and anti-inflammatory activity. This review explores the therapeutic potential of traditional herbal plants and their phytoconstituents in alleviating mercury-induced toxicity. Key findings highlight several plants with hepatoprotective effects, mitigating necrosis and anatomical distortion in liver cells. Phytochemicals such as quercetin, rutin, salicylic acid, ferulic acid, 6-gingerol, and 6-shogaol play pivotal roles in downregulating molecular pathways activated by mercury exposure. Other bioactive compounds, including acetogenin and gallic acid, exhibit potent antioxidant properties, with mechanisms such as ROS scavenging and inhibition of lipid peroxidation. This review also highlights certain compounds, such as aloe-emodin and gentisic acid, which exhibit potential for mitigating mercury toxicity through mechanisms like inhibiting oxidative stress and enhancing cellular defense pathways. However, these compounds remain underexplored, with no significant studies conducted to evaluate their efficacy against mercury-induced toxicity, presenting a critical area for future research. These findings underscore the potential of phytochemicals as effective agents in combating mercury toxicity through antioxidant mechanisms, cellular signalling regulation, and heavy metal chelation.
... Recent research indicates that the toxic effects of mercury extend far beyond the nervous system and there is evidence of effects on the cardiovascular and immune systems. The World Health Organization (WHO) has recognized mercury as a neurotoxic and immunotoxic substance [80,81]. ...
The European Green Deal attaches great importance to sustainability, including food security, which is also linked to food safety. This is particularly relevant in such a sensitive region as the Mediterranean. The goal of this study was to investigate Rapid Alert System for Food and Feed (RASFF) notifications of hazards reported in 1997–2021 (a 25-year period) in products from northern Mediterranean countries considering products and other variables. A two-way joining cluster analysis was used. The most notable hazards in the latter years of the reported period were as follows: ochratoxin A and pesticide residues in fruits and vegetables imported from Turkey and ethylene oxide in various products, as well as Salmonella in chicken, Listeria in cheese, Escherichia coli in cheese and mussels from France, mercury in swordfish from Spain, and Anisakis in seafood from France and Morocco. The increasing number of notifications of ochratoxin A and pathogenic micro-organisms in recent years may be caused by climate change. This also results in the need to use more pesticides and the appearance of related hazards, i.e., residues of such compounds in food products. It is, therefore, vitally important that border posts and control authorities in particular European Union countries are vigilant.
... Studies on the atmospheric distribution of Hg led to concerns about its potential toxic effects on human health and the ability of MD to transport Hg during dust seasons. Absorbed Hg has dramatic effects on human health due to its prolonged half-life, incomplete metabolism, and interactions with thiol groups in body proteins [28,29,30,31]. Exposure to significant levels of Hg can lead to poisoning, resulting in both acute and chronic illnesses. ...
... Excessive amounts of Hg may lead to various health problems, such as corrosive bronchitis and interstitial pneumonia, and may damage the brain, lung, and kidney tissues of those exposed, as well as damaging the central nervous system through the blood [11,12]. GEM is mainly (~80%) absorbed in human lungs [13] and can spread throughout the body, cross the blood-brain barrier, and accumulate in the central nervous system [14]. Research also shows that the level of GOM absorption in the human body caused by inhalation is approximately 50% lower than that of GEM. ...
In this study, gaseous element mercury (GEM) and gaseous oxidized mercury (GOM) in the atmosphere were continuously observed at a minute resolution from 1 April 2019 to 31 December 2020 in urban Xi’an, the largest central city in Northwestern China. The concentrations of GEM and GOM drastically fluctuated within the ranges of 0.022–297 ng/m³ and 0.092–381 pg/m³, showing average values of 5.78 ± 7.36 ng/m³ and 14.2 ± 20.8 pg/m³, respectively. GEM and GOM showed a decreasing trend of 0.121 ng/m³ and 0.472 pg/m³ per month, respectively, which we believe was mainly caused by anthropogenic sources, especially by a reduction in coal-fired emissions, rather than meteorological factors. The significant positive correlation between GEM and PM2.5, SO2, NO2, and CO, as well as Cr, As, and Pb in PM2.5 also proves that. GEM showed a higher concentration at nighttime than daytime, while an M-shaped diurnal trend was observed for GOM. The hazard quotient of GEM for both males and females decreased at a rate of 0.003 per month, and children aged 2–5 were more sensitive to non-carcinogenic health risks. The changing trends, controlling factors, and human health risks of Hg in the atmosphere are necessary and crucial to study for improving our understanding of the impacts of Hg in Northwestern China.
... [4][5][6] Heavy metals are non-biodegradable and can be transferred through the soil and enriched in the food chain, eventually causing harm to humans. 7 Cd and Hg cause varying degrees of damage to the human liver, kidneys, bones and digestive system, for example, Cd and Hg can cause "Itai-itai disease" and "Minamata disease", [8][9][10][11][12] respectively. Laboratory methods with wide linear range and excellent stability are commonly used to detection Cd and Hg, such as inductively coupled plasma mass spectrometry/optical emission spectrometry (ICP-MS/OES), 13 hydride-generation atomic fluorescence spectrometry (HG-AFS) 14 and graphite furnace atomic absorption spectrometry (GF-AAS). ...
... An important feature of mercury toxicity is the generation of free radicals. 2 The generation of reactive oxygen species (ROS), such as the superoxide anion, singlet oxygen, hydrogen peroxide, and hydroxyl radical, has been one of the underlying agents responsible for tissue damage. 3 Mercury toxicity is also manifested through their interaction with sulfur by reducing molecules containing a free thiol. ...
... Mercury is an exceptionally toxic metal with welldocumented adverse health effects. It is recognized as a primary environmental pollutant, extensively utilized by humans for centuries across several sectors including agriculture, industry and medicine [46,47]. The aforementioned activities generate and release significant quantities of organic mercury. ...
Pollution can be broadly defined as the presence of contaminants or energy sources detrimental to ecosystems and human health. The human organism serves as a valuable indicator of ecosystem contamination. However, understanding physiological disorders and correlating specific contaminants with disease development is a complex and arduous task, necessitating extensive scientific research spanning years or even decades. To facilitate a more rapid and precise understanding of the physiological impairments induced by various contaminants, a comprehensive approach is indispensable. This review proposes a model for such an approach, which involves the systematic collection and analysis of data from ecosystem contamination monitoring, integrated with biomedical data on compromised physiological conditions in humans across different temporal and spatial scales. Given the complexity and sheer volume of data, alongside the imperative for strategic decision-making, this model leverages the capabilities of artificial intelligence (AI) tools. Although this paper exemplifies the model by investigating the effects of contaminants on the human organism, the model is adaptable to all ecosystem components, thereby supporting the conservation of plant and animal species.
... Mercury is present in the environment in a variety of forms, including elemental mercury and as a component of inorganic or organic compounds. Although elemental Hg(0) is not particularly toxic, it is easily oxidized to Hg 2+ , which is both highly reactive and highly toxic [1][2][3]. Despite stringent guidelines and regulations, mercury is released to the environment through various industrial processes and uncontrolled waste disposal [4]. ...
Mercury, a toxic heavy metal produced through both natural and anthropogenic processes, is found in all of Earth’s major systems. Mercury’s bioaccumulation characteristics in the human body have a significant impact on the liver, kidneys, brain, and muscles. In order to detect Hg2+ ions, a highly sensitive and specific fluorescent biosensor has been developed using a novel, modified seven amino acid peptide, FY7. The tyrosine ring in the FY7 peptide sequence forms a 2:1 complex with Hg2+ ions that are present in the water-based sample. As a result, the peptide’s fluorescence emission decreases with higher concentrations of Hg2+. The FY7 peptide’s performance was tested in the presence of Hg2+ ions and other metal ions, revealing its sensitivity and stability despite high concentrations. Conformational changes to the FY7 structure were confirmed by FTIR studies. Simultaneously, we designed a miniaturized setup to support an in-house-developed micro-volume capillary container for volume fluorometry measurements. We compared and verified the results from the micro-volume system with those from the commercial setup. The micro-volume capillary system accommodated only 2.9 µL of sample volume, allowing for rapid, sensitive, and selective detection of toxic mercury (II) ions as low as 0.02 µM.
... have not been studied in detail -likely due to the difficulties associated with such work (Bjørklund et al., 2017;Hoch, 2019). Moreover, their extreme air-and moisture-sensitivity (Witthaut et al., 2023;Prots et al., 2022a;Prots et al., 2022b), call for a specialized preparation methodology. ...
A large variety of chemical and physical properties are exhibited by mercurides and amalgams. In this work, we have successfully examined seven strontium mercurides: SrHg 11 , SrHg 8 , Sr 10 Hg 55 , SrHg 2 , SrHg, Sr 3 Hg 2 , and Sr 3 Hg. The interest in the mercury-rich region is motivated by the large number of mercury-based superconductors that have high mercury content. At the same time, the preparation on the mercury-rich side of the binary phase diagram is experimentally non-trivial, due to the high vapor pressure of mercury and extreme air-sensitivity of mercury-rich compounds. By employing a set of specialized techniques, we were able to discover superconductivity in three mercury-strontium compounds – SrHg 11 ( T c = 3.2 ± 0.3 K, H c 2 = 0.18 ± 0.05 T), SrHg 8 ( T c = 3.0 ± 0.1 K, H c 2 = 0.35 ± 0.02 T), and Sr 10 Hg 55 ( T c = 2.2 ± 0.25 K, H c 2 = 0.54 ± 0.05 T).
Solid sampling-electrothermal vaporization inductively coupled plasma mass spectrometry (SS-ETV-ICP-MS) was proposed for ultra-trace determination of Hg in eye shadow samples. The ETV system was optimized using a heating program, consisting of drying at 80 °C for 20 s and vaporization at 800 °C for 10 s, followed by cooling for 120 s, without a pyrolysis step. The carrier gas flow rate was set to 1.10 L min-1, and sample mass up to 4 mg was analyzed. An alternative external calibration strategy using a standard solution of Hg and magnesium silicate for matrix matching demonstrated good linearity (R2 0.9983) in the range of 5 to 100 pg of Hg. Magnesium silicate enhances analyte transport and acts as a modifier, enabling calibration with aqueous standard solutions and presenting an alternative to certified reference material (CRM). Despite the differences in signal profiles for Hg observed in the eye shadow samples, CRM MESS-3 (Marine Sediment), and the standard solution, the method has good accuracy when the signal was integrated using peak area. Compared to cold vapor inductively coupled plasma mass spectrometry, which needs acid digestion and a ten-fold dilution with a limit of quantification (LOQ) of 0.1 µg g-1 Hg, the SS-ETV-ICP-MS provided a significantly lower LOQ (0.001 µg g-1) and a simplified analytical approach for Hg determination. This approach presents a practical alternative for determining Hg in eye shadows at ultra-trace levels.
Mercury (Hg) contamination in water sources is a critical environmental and public health concern, arising from industrial activities, mining, and improper waste disposal. This study investigates the removal of Hg(II) ions using Fe₃O₄/MgO nanocomposite, a sol–gel-synthesized adsorbent. Structural analysis through X-ray Diffraction (XRD) confirmed the successful formation of cubic Fe₃O₄ and MgO phases, with post-adsorption peak shifts indicating Hg(II) binding. Scanning Electron Microscopy (SEM) revealed a spherical rod-like morphology with an average particle size of 82.9 nm, providing abundant active sites for adsorption. Vibrating Sample Magnetometry (VSM) analysis demonstrated a magnetic saturation value of 11.65 emu·g⁻¹, ensuring easy separation and recovery of the adsorbent. Optimal adsorption conditions were identified as an adsorbent dosage of 0.25 g·L⁻¹, initial Hg(II) concentration of 400 mg·L⁻¹, pH 9, and a 120-min contact time, resulting in a high adsorption capacity of 1554.77 mg·g⁻¹ and 97.17% removal efficiency. Adsorption followed the Langmuir isotherm model, suggesting monolayer adsorption, while kinetic analysis indicated a pseudo-second-order mechanism governed by chemisorption. These findings highlight the potential of Fe₃O₄/MgO as an efficient and recyclable adsorbent for Hg(II) removal in water treatment applications.
The aim of this study was to explore the acute damage caused by acute mercuric chloride poisoning to mice. The mice model of acute mercury (HgCl2) poisoning was prepared by gavage and intraperitoneal injection, respectively. The experimental results showed that the LD50 was about 24 mg/kg for gavage and 4 mg/kg for intraperitoneal injection. On the basis of gavage, there were differences in the time required for water maze and righting reflex tests between groups of mice gavaged with different doses of HgCl2 (p < 0.05); The levels of SOD, MDA, GSH-PX, CRE, BUN, AST and ALT in mice were different from those in the control (Normal saline) group (p < 0.05); The degree of inflammation response under microscope was different in different dose groups after HE staining of liver tissues, and there were differences in the degree of intimal thickening and lumen stenosis in different dose groups after HE staining of kidney tissue; The inductively coupled plasma mass spectrometry (ICP-MS) measured the levels of mercury in mice increased with increasing mercuric chloride concentration, with the accumulation in kidney much higher than that in liver. Based on the results of the study, it was concluded that the damage caused by mercuric chloride to memory, oxidative stress, liver and kidney tissues in mice starts from 4 mg/kg, and the mortality rate of mice reached 100% when the gavage dose was greater than or equal to 32 mg/kg, and the intraperitoneal injection of mercuric chloride produced faster and stronger toxic effects than gavage.
Triazole, a heterocyclic organic molecule containing nitrogen, exhibits strong coordination abilities with various metal ions. Several synthetic techniques, including Claisen-Schmidt condensation, Huisgen-1,3-dipolar cycloaddition reaction (CuAAC), Pellizzari synthesis, Einhorn-Brunner synthesis, Dimroth rearrangement and Boulton-Katritzky Rearrangement have been employed to synthesize triazole derivatives. Experimental and spectroscopic investigations have demonstrated that triazole possesses a high binding affinity for heavy metal ions such as Pb²⁺, Hg²⁺, Cd²⁺, Cu²⁺ and Al³⁺. The increasing environmental pollution caused by the uncontrolled discharge of heavy metal ions into water bodies and open spaces poses a serious threat to ecosystem and public health. To address this issue, a cost-effective and efficient chemosensor based on triazole has been developed for selective detection of toxic heavy metal ions. Notably, triazole exhibits fluorescence quenching or enhancement upon interaction with the Hg²⁺ ions, attributed to changes in its absorption and emission spectra upon coordination. This unique photophysical behaviour makes triazole-based probes valuable tools for monitoring Hg²⁺ ions in environmental and biological samples. This review provides a comprehensive overview of triazole-based fluorescent chemosensors for Hg²⁺ ions detection, covering advancements made between 2010–2025. The study highlights the high specificity, excellent sensitivity, and low detection limits of these sensors, emphasizing their potential for practical applications in environmental monitoring and analytical chemistry.
Mercury and explosives are well-known hazards that affect the environment and threaten society. Mercury generally exists as inorganic mercuric (Hg²⁺) salts, and its detection via fluorometric response is highly notable. Likewise, mainstream explosives contains a nitro (−NO2) moiety as a functional unit, and numerous reports have quantified them using fluorescence quenching. Among the available literature, there are still noticeable concerns about the environmental and biological applicability of luminescent pyrene derivaives-tunedfluorometric detection of Hg²⁺ and explosives. In the presence of Hg²⁺ ions, pyrene derivatives tend to form excimers, which can be tuned to the chelation-enhanced fluorescence (CHEF), photo-induced electron transfer (PET), or fluorescence resonance energy transfer (FRET), etc., to exhibit “Turn-On” or “Turn-Off” fluorescence responses. On the other hand, π-π stacking of emissive pyrene-derivatives may lead to J- or H-type aggregation via self-excimers (Py-Py*), which has been found to be quenched/enhanced by explosive hazards. In fact, −NO2-containing explosives interact with pyrene derivatives, leading to exceptional fluorescence quenching or enhancement. This review details the use of pyrene derivatives toward the sensing of Hg²⁺ and explosives with demonstrated applications. Further, the design requirements, sensory mechanisms, advantages, limitations, and the future scope of using the reported pyrene derivatives in Hg²⁺ and explosives sensing are discussed.
Heavy metals represent a class of pollutants detected at concentrations lower than 10 ppm in different matrices that are intensively monitored due to having a major impact on human health. Industrial activities including mining, agriculture, and transport, determine their presence in different environments. Corrosion phenomena of various installations, volcanic eruptions, or atmospheric deposition on the soil surface and in water can contaminate the respective environments. Atmospheric pollutants in the form of suspended dust particles with diameters below 10 microns are predominantly composed of different metallic species from Cd, Cr, Cu, Ni, etc. This paper presents a review of the main sources and types of heavy metals present in the atmosphere in the composition of particulate matter (PM), highlighting the main mechanisms of occurrence and detection techniques, including the impact on bio-geo-chemical processes in the soil and food chain, in close correlation with their impact on environment and human health. The purpose of this review is to highlight the current level of knowledge regarding the global situation of heavy metals in PM and to identify gaps as targets for future research.
The spatial and temporal variability of Hg, As, and Sb contents were assessed in stream sediments across the Fiora River catchment (Italy), which drains the dismissed Monte Amiata Mining District, the 3rd largest Hg producer worldwide. Mercury, As, and Sb concentrations of samples collected in 2022 along Fiora River tributaries were compared to data collected in 1985 after mine decommissioning. In 2022, the Fiora River showed downstream magnification of Hg pollution, close to the outflow into the Mediterranean Sea. At several sampling sites, concentrations are above the Italian safety limit of 1 mg/kg (up to 3300 mg/kg). Arsenic and Sb concentrations are high in the mid-catchment tributaries (up to 84 and 79 mg/kg, respectively). The river contributes to the pollutant budget of the Mediterranean Sea, and showed low resilience to Hg pollution in the period 1985–2022, whereas for As and Sb some attenuation occurred. The mass loads of Hg, As, and Sb discharged into the Mediterranean Sea from the Fiora River are at least 0.9, 2.2, and 1.8 t/y respectively. The estimated potential sediment-bound Hg flux from the whole Monte Amiata district to the Mediterranean Sea (1.2–6.6 t/y) is in the same range of that calculated for the Idrija district, highlighting the pivotal role of the Mt. Amiata district on the Mediterranean Sea pollution.
In the current research project, a highly sensitive biosensor responding to mercury (Hg) was developed by cloning merR, merT, and merP genes of mercury operon from a native bacteria of Hg polluted soils and Green Fluorescent Protein-uv (GFP-uv) reporter gene that shows green fluorescence under UV light driven by the Hg inducible merR promoter. Hg resistant bacteria have been isolated from the Hg polluted soil of Oak Ridge Reservation site (Tennessee). The bacteria have been identified by 16S rDNA sequencing. Eight Hg resistant bacterial (VMI-WS-ORR-1 to VMI-WS-ORR-11) strains have been isolated and identified as Pseudomonas jessenii and Pseudomonas migulae strains. The bacteria were screened for Hg resistance through the
determination of minimum inhibitory concentration (MIC) using Bioscreen C Pro automated microbiology growth curve analysis system. The growth patterns of these bacteria in the presence of various concentrations of Hg revealed that these bacterial strains were able to tolerate concentrations ranging from 10-20 ppm of Hg. In this study, VMI-WS-ORR-11, a strain with a 99.13% identity to Pseudomonas miguale showed Hg MIC of 20 ppm which is higher than the previously reported Pseudomonas strains. The merR, merT, and merP genes of mercury operon were isolated by PCR from this strain and cloned into the pACYC vector using Gibson Assembly. In the GFP-uv reporter containing plasmid ((pSmart), the GFP-uv gene promoter was replaced with merR promoter through in situ mutagenesis. Then, both plasmids were transformed into DH5α E. coli cells to develop whole cell Hg biosensor. The developed Hg biosensor working conditions were optimized by testing at different conditions in minimal M9 medium supplemented with 4% glucose and antibiotics. This biosensor started detection of Hg at the range of 0.02-0.2 µM and 0.04-0.3 µM concentrations after 4 h of incubation with starting cell density of 0.5 and 0.7 OD. It showed the optimum Hg detection after 12 h of incubation. The testing with environmental samples such as lake, spring and sea waters and soil samples, this biosensor also detected Hg in these samples. The selectivity of this Hg biosensor was tested with various metals at the 0.05 µM concentration and the results indicated that it showed highest selectivity to Hg. In conclusion, this new Hg biosensor found to be highly sensitive, Hg selective and cost effective without need for any substrate or specialized instruments for Hg detection.
Contaminant body burdens are determined by complex interactions between contaminant inputs into the environment, local ecological dynamics, and organismal ontogeny. Although a naturally occurring element, mercury (Hg) is a potent neurotoxin, commonly assessed in contaminant body burdens. Anthropogenic activity has impacted its spatial distribution, resulting in regional ‘hotspots’ with elevated Hg concentrations. Due to the propensity of methylated Hg to bioaccumulate within individuals over time and biomagnify across trophic levels, long-lived apex predators can carry substantial body burdens in affected ecosystems. Still, the role of an organism's ontogeny and habitat in shaping individual Hg concentrations, especially within and across species, is not well understood. We assessed total Hg, carbon (δ13C), and nitrogen (δ15N) isotopic ratios in whole blood samples (n = 133) across three distinct habitats in the Southeastern U.S. to investigate how size and dietary shifts in the American alligator (Alligator mississippiensis) influence Hg accumulation. Mercury concentrations were approximately 8-fold higher in alligators inhabiting the Okefenokee Swamp, Georgia (mean = 0.62 mg/kg) compared to those inhabiting coastal habitats (Jekyll Island, Georgia and Yawkey Wildlife Center, South Carolina). Whereas individual size and nitrogen isotope signatures generally displayed positive relationships with Hg concentrations, model selection approaches revealed these relationships varied across populations, likely in response to site-specific differences in environmental Hg concentrations and life history attributes of the alligators. Collectively, our findings demonstrate that although Hg concentrations in A. mississippiensis are highly influenced by differences between sites, diet and body size can sometimes additionally affect individual variation within populations, suggesting that organismal ontogeny interacts with site-specific contamination and ecological factors to affect Hg body burdens.
This study aims to investigate the effects of mercury (Hg) toxicity on the fetal brain. Methylmercury (MeHg) is widely recognized for its severe toxic effects on the developing embryonic nervous system compared to mature neurons. Studies show that immature neurons are more vulnerable to Hg toxicity. Furthermore, maternal nutrition plays a critical role in fetal brain development. From this perspective, this review aims to address the definition of Hg, its metabolism in the human body, and the effects and mechanisms of action related to its toxicity, emphasizing the impact on the health of pregnant women and the fetal brain. The influence of daily fish consumption during pregnancy was also discussed, particularly in the Amazon region, where fish consumption is high and is an essential source of exposure to Hg. The review presents guidelines for the consumption of fish in pregnant women's diet, aiming to promote their health and reduce fetal exposure to Hg.
Background
Heavy metals and trace elements are considered as environmental pollutants that pose serious risks to public health as they are nonbiodegradable and remain in the ecosystem. It has been documented that they are neurotoxic, and their levels in hair samples can be used as a biomarker of exposure, indicating their levels in soft tissues. Multiple sclerosis (MS) is considered one of the most common chronic neurodegenerative diseases. Its pathogenesis is complex and multifactorial, and there is interaction between genetic and environmental factors.
Aim
The aim of this study is to compare the levels of some heavy metals and trace elements in hair samples of children with MS with those of healthy controls to investigate their possible association with the onset of MS.
Patients and methods
A total of 30 children with MS and 30 healthy children were investigated. Using inductively coupled plasma atomic emission spectrometry, we analyzed 21 elements in hair samples from MS patients and a healthy control group.
Results
Zn, Cr, Ba, Mg, Mn, Se, Sr, and V were significantly higher in hair samples from children with MS. While Hg, B, and As were only detected in cases, there was no significant difference in the level of Al, Ag, Ca, Cd, Cu, Fe, Ni, Pb, P, and Na between cases and controls.
Conclusion
Zn, Cr, Ba, Mg, Mn, Se, Sr, and V were significantly higher in hair samples from children with MS. There was no significant difference in levels of Al, Ag, Ca, Cd, Cu, Fe, Ni, Pb, P, and Na between cases and controls.
Background
Chronic kidney disease (CKD) is an important public health problem. Although cross-sectional studies have identified many heavy metals/trace elements associated with reduced kidney function, prospective studies are needed to determine the pathogenic role of these elements in the development and progression of CKD.
Methods
To explore the association between baseline urinary heavy metal/trace element concentrations and long-term impaired kidney function (IKF)/CKD, as well as the incidence of rapid decline in kidney function in a population-based exploratory prospective study, we mean age 51.9 years at baseline) whose urinary trace elements concentrations have been determined by inductively coupled plasma mass spectrometry (ICP-MS). IKF was defined by a reduced estimated glomerular filtration rate (eGFR) between 60-90 mL/min/1.73 m2, and CKD was defined as an eGFR<60 mL/min/1.73 m2. Rapid eGFR decline was defined as a decrease≥3 mL/min/1.73 m2 /year.
Results
Over a mean follow-up of 12.5 years, 123 participants (2.6%) experienced rapid decline in kidney function, and 1455 (31.7%) developed IKF or CKD. After adjusting for covariates including baseline eGFR, we found that urinary vanadium (HR=1.07, 1.03-1.12), cobalt (HR=1.69, 1.21-2.37), nickel (HR=1.19, 1.08-1.3), copper (HR=1.03, 1.01-1.06), selenium (HR=1.33, 1.02-1.73), molybdenum (HR=1.48, 1.2-1.82) and iodine (HR=1.1, 1.02-1.2) were associated with an increased risk of new incident IKF or CKD cases during the follow-up. Also, urinary copper (OR=1.12, 1.04-1.21), silver (OR=1.83, 1-3.35), molybdenum (OR=1.02, 1.01-1.04) and cadmium (OR=1.05, 1.01-1.09) were associated with an increased risk of rapid eGFR decline.
Conclusion
In the general population, several urinary heavy metals/trace elements are associated with a rapid decline in kidney function or new cases of IKF/CKD.
Heavy metals are naturally occurring components of the Earth’s crust and persistent environmental pollutants. Human exposure to heavy metals occurs via various pathways, including inhalation of air/dust particles, ingesting contaminated water or soil, or through the food chain. Their bioaccumulation may lead to diverse toxic effects affecting different body tissues and organ systems. The toxicity of heavy metals depends on the properties of the given metal, dose, route, duration of exposure (acute or chronic), and extent of bioaccumulation. The detrimental impacts of heavy metals on human health are largely linked to their capacity to interfere with antioxidant defense mechanisms, primarily through their interaction with intracellular glutathione (GSH) or sulfhydryl groups (R-SH) of antioxidant enzymes such as superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione reductase (GR), and other enzyme systems. Although arsenic (As) is believed to bind directly to critical thiols, alternative hydrogen peroxide production processes have also been postulated. Heavy metals are known to interfere with signaling pathways and affect a variety of cellular processes, including cell growth, proliferation, survival, metabolism, and apoptosis. For example, cadmium can affect the BLC-2 family of proteins involved in mitochondrial death via the overexpression of antiapoptotic Bcl-2 and the suppression of proapoptotic (BAX, BAK) mechanisms, thus increasing the resistance of various cells to undergo malignant transformation. Nuclear factor erythroid 2-related factor 2 (Nrf2) is an important regulator of antioxidant enzymes, the level of oxidative stress, and cellular resistance to oxidants and has been shown to act as a double-edged sword in response to arsenic-induced oxidative stress. Another mechanism of significant health threats and heavy metal (e.g., Pb) toxicity involves the substitution of essential metals (e.g., calcium (Ca), copper (Cu), and iron (Fe)) with structurally similar heavy metals (e.g., cadmium (Cd) and lead (Pb)) in the metal-binding sites of proteins. Displaced essential redox metals (copper, iron, manganese) from their natural metal-binding sites can catalyze the decomposition of hydrogen peroxide via the Fenton reaction and generate damaging ROS such as hydroxyl radicals, causing damage to lipids, proteins, and DNA. Conversely, some heavy metals, such as cadmium, can suppress the synthesis of nitric oxide radical (NO·), manifested by altered vasorelaxation and, consequently, blood pressure regulation. Pb-induced oxidative stress has been shown to be indirectly responsible for the depletion of nitric oxide due to its interaction with superoxide radical (O2·−), resulting in the formation of a potent biological oxidant, peroxynitrite (ONOO⁻). This review comprehensively discusses the mechanisms of heavy metal toxicity and their health effects. Aluminum (Al), cadmium (Cd), arsenic (As), mercury (Hg), lead (Pb), and chromium (Cr) and their roles in the development of gastrointestinal, pulmonary, kidney, reproductive, neurodegenerative (Alzheimer’s and Parkinson’s diseases), cardiovascular, and cancer (e.g. renal, lung, skin, stomach) diseases are discussed. A short account is devoted to the detoxification of heavy metals by chelation via the use of ethylenediaminetetraacetic acid (EDTA), dimercaprol (BAL), 2,3-dimercaptosuccinic acid (DMSA), 2,3-dimercapto-1-propane sulfonic acid (DMPS), and penicillamine chelators.
Pyridine, N-containing heterocyclic organic compound, displays strong coordination capabilities with various metal ions. It can be synthesized through various methods, such as Friedlander synthesis, heterocumulene synthesis, cross-coupling reactions, the Radziszewski reaction, Bonnemann cyclization, as well as cobalt-catalyzed synthesis. Experimental and spectroscopic analyses have demonstrated a strong binding affinity between pyridine and several heavy metal ions, including Pb²⁺, Hg²⁺, and Cd²⁺ ions. The escalating environmental pollution caused by the disposal of heavy metal ions in rivers, open air, and water reservoirs poses a significant threat to both ecosystem and human health. To address these environmental challenges, a cost-effective and easily synthesized chemosensor has been prepared for identifying toxic heavy metal ions in various samples. Pyridine’s photophysical properties make it an effective sensor for detecting Hg²⁺ ions, displaying fluorescence quenching or enhancement in their presence. The coordination between pyridine and Hg²⁺ ions lead to shifts in the absorption spectra. The pyridine-based sensor has been evaluated for its sensitivity, selectivity, and detection limits under different experimental conditions. Pyridine’s solubility and environmental stability make it applicable for real-time detection, making pyridine probes valuable tool for monitoring toxic Hg²⁺ ions in the environment. The results demonstrate that the pyridine-based chemosensor exhibits good selectivity and sensitivity for targeting Hg²⁺ ions, with detection limits within acceptable ranges. This review (from years 2011 to 2023) emphasizes the preparation of various substituted pyridine compounds as selective, sensitive, and specific sensors for real-time detection of Hg²⁺ ions.
Schematic representation of sulphydryl functionalization of MXene and selective sensing of mercury ions.
Mercury (Hg), hexavalent chromium (Cr (VI)), and selenium (Se) are significant environmental pollutants found in various forms in the environment, with diverse sources and adverse health effects. This book consists of three chapters.Chapter I focuses on Hg, recognized as one of the most hazardous heavy metals. Its extensive release from both natural and anthropogenic sources. Natural sources include volcanic eruptions and weathering of rocks, while significant anthropogenic sources contributing to mercury pollution include mining, industrial processes, and the combustion of fossil fuels. Hg exists in various forms such as elemental mercury, mercuric sulfide, and methylmercury, with each form having different environmental behaviors and toxicities. Remediation techniques for mercury-contaminated soils include thermal desorption, electrokinetic extraction, soil washing, chemical stabilization, phytoremediation, and microbial methods.Chapter II adresses chromium, which occurs in two states: Trivalent chromium (Cr(III)) and hexavalent chromium (Cr(VI)), with Cr(VI) being more harmful and associated with occupational carcinogenesis. Cr(VI) is primarily released from industrial processes such as chrome plating, stainless steel production, and leather tanning. Occupational exposure to Cr(VI) can lead to various health issues, including respiratory problems and increased cancer risk. Remediation methods for Cr (VI) encompass bioremediation and phytoremediation.Chapter III discusses Se, an essential trace element for living organisms, offering health benefits at low concentrations but posing significant environmental and health hazards at elevated levels. Natural sources of Se contamination include weathering of rocks and volcanic eruptions, while human activities such as metal smelting, coal-fired power plants, and agricultural drainage also contribute significantly. Se toxicity is predominantly associated with its inorganic forms, Se(IV) and Se(VI), which are highly mobile and bioavailable, leading to contamination of water, air, and soil. Remediation approaches for selenium, including membrane technology, phytoremediation, in situ bio-reduction, electro-coagulation (EC), adsorption, electrochemical technique, electrokinetics and the use of weak magnetic fields.Overall, this book presents sources of Hg, Cr (VI), and Se, their toxicity, and numerous remediation techniques.
Methyl mercury (MeHg) has the highest toxicity among the derivative of the organic mercury compounds. Rate of accumulation of MeHg in the body is very high because it is soluble in lipids. The ability of methyl mercury binds to proteins in the body causing MeHg to penetrate the blood-brain barrier easily, so that it can quickly disrupt the central nervous system and speed up nerve cell damage. This paper reported the effect of methyl mercury on the number of microglia cells and expression of iNOS in the brains of Rattus norvegicus. In this study, rats were divided into two groups: a control group with no exposure of MeHg and groups of rats exposed with MeHg at a dose of 0.6 mg/kg BW/day given orally for 21 days. Number of microglia cells is investigated using silver nitrate staining method and iNOS expression is determined by immunohistochemistry methods. The results showed that exposure with MeHg in a dose of 0.6 mg/kgBW can increase the number of microglia cells and iNOS expression respectively as mush as 151.63% and 918.08%
Autism spectrum disorder (ASD) is a neurodevelopmental disorder that can cause significant social, communication and behavioral challenges. Environmental contribution to ASD is due in large part to the sensitivity of the developing brain to external exposures such as lead (Pb), and mercury (Hg) as toxic heavy metals or due to a poor detoxification ability as the phenotype of this disorder. Selenium (Se) as an antioxidant element that counteracts the neurotoxicity of Hg, and Pb, presumably through the formation of nontoxic complexes. In the present study, Pb, Hg, and Se were measured in red blood cells (RBCs) of 35 children with ASD and 30 age- and gender-matched healthy control children using atomic absorption spectrometry. Receiver Operating Characteristics (ROC) analysis of the obtained data was performed to measure the predictive value of their absolute and relative concentrations. The obtained data demonstrates a significant elevation of Hg and Pb together with a significant decrease in the Se levels in RBCs of patients with ASD when compared to the healthy controls. The ratios of Se to both Pb and Hg were remarkably altered, being indicative of heavy metal neurotoxicity in patients with ASD. In conclusion, the present study indicates the importance of Se for prevention and/or therapy of heavy metal neurotoxicity.
The aim of this study was to evaluate the association of blood lead, mercury, and cadmium concentrations with developmental delays and to explore the association of these concentrations with the health status of children. This study recruited 89 children with developmental delays and 89 age- and sex-matched children with typical development. Their health status was evaluated using the Pediatric Quality of Life (PedsQL) Inventory for health-related quality of life (HRQOL) and the Pediatric Outcomes Data Collection Instrument for function. Family function was also evaluated. Blood lead, mercury, and cadmium concentrations were measured using inductively coupled mass spectrometry. The children with developmental delays had a considerably poorer HRQOL, lower functional performance and family function, and a higher blood lead concentration than those with typical development. The blood lead concentration had a significantly positive association with developmental delays [odds ratio (OR) = 1.54, p < 0.01] in a dose-response manner, and it negatively correlated with PedsQL scores (regression coefficient: −0. 47 to −0.53, p < 0.05) in all the children studied. The higher blood cadmium concentration showed a significantly positive association with developmental delays (OR = 2.24, for >1.0 μg/L vs. <0.6 μg/L, p < 0.05). The blood mercury concentration was not associated with developmental delays and health status.
Mercury contamination in the water bodies of developing countries is a serious concern due to its toxicity, persistence, and bioaccumulation. Vembanad, a tropical backwater lake situated at the southwest coast of India, is the largest Ramsar site in southern India. The lake supports thousands of people directly and indirectly through its resources and ecosystem services. It is highly polluted with toxic pollutants such as heavy metals, as it receives effluent discharges from Kerala’s major industrial zone. In the present study, water, pore water, sediment, and fish samples collected from Vembanad Lake were analysed for total mercury (THg) and methyl mercury (MHg) contents. The maximum concentrations of THg and MHg in surface water samples were31.8 and 0.21 ng/L, respectively, and those in bottom water samples were 206 and 1.22 ng/L, respectively. Maximum concentration of THg in surface sediment was observed during monsoon season (2850 ng/g) followed by that in the pre-monsoon season (2730 ng/g) and the post-monsoon season (2140 ng/g). The highest sediment concentration of MHg (202.02 ng/g) was obtained during monsoon season. The spatial variation in the mercury contamination clearly indicates that the industrial discharge into the Periyar River is a major reason for pollution in the lake. The mercury pollution was found to be much higher in Vembanad Lake than in other wetlands in India. The bioaccumulation was high in carnivorous fishes, followed by benthic carnivores. The THg limit in fish for human consumption (0.5 mg/kg dry wt.) was exceeded for all fish species, except for Glossogobius guiris and Synaptura orientalis. The concentration of THg was five times higher in Megalops cyprinoides and four times higher in Gazza minuta. Significant variation was observed among species with different habits and habitats. Overall, risk assessment factors showed that the mercury levels in the edible fishes of Vembanad Lake can pose serious health impacts to the human population.
All types of dental amalgams contain mercury, which partly is emitted as mercury vapor. All types of dental amalgams corrode after being placed in the oral cavity. Modern high copper amalgams exhibit two new traits of increased instability. Firstly, when subjected to wear/polishing, droplets rich in mercury are formed on the surface, showing that mercury is not being strongly bonded to the base or alloy metals. Secondly, high copper amalgams emit substantially larger amounts of mercury vapor than the low copper amalgams used before the 1970s. High copper amalgams has been developed with focus on mechanical strength and corrosion resistance, but has been sub-optimized in other aspects, resulting in increased instability and higher emission of mercury vapor. This has not been presented to policy makers and scientists. Both low and high copper amalgams undergo a transformation process for several years after placement, resulting in a substantial reduction in mercury content, but there exist no limit for maximum allowed emission of mercury from dental amalgams. These modern high copper amalgams are nowadays totally dominating the European, US and other markets, resulting in significant emissions of mercury, not considered when judging their suitability for dental restoration.
Celiac disease (CD) is an autoimmune disease with increasing prevalence in the USA. CD leads to decreased absorption of many nutrients including certain divalent metals. On the other hand, recent cross-sectional studies suggest the associations between trace heavy metal exposure and autoimmunity. We aimed to determine if there is an association between CD autoimmunity and blood levels of heavy metals in the general US population. We used nationally representative data from National Health and Nutrition Examination Survey, 2009-2012. Our study comprised 3643 children (ages 6-17 years) and 11,040 adults (age ≥18 years). Children with CD seropositivity had significantly lower blood lead (0.56 versus 0.80 μg/dL, P = 0.001) and mercury levels (0.47 versus 0.64 μg/L, P = 0.001). In the linear regression model, CD seropositivity was associated with lower levels of blood lead and mercury in children (β = -0.14, P = 0.03 for lead and β = -0.22, P = 0.008 for mercury), but not in adults. These findings of CD-heavy metals association are, to our knowledge, novel, and we conclude that decreased levels of heavy metals in blood are most likely a consequence of CD in the US children.
The paper’s objective was to estimate weekly Hg intake from fish meals based on intervention research. Total Hg (THg) concentrations in blood and hair samples collected from men (n = 67) from an intervention study as well as muscular tissues of fresh and after heat-treating fish were determined using the thermal decomposition amalgamation atomic absorption spectrometry method (TDA-AAS) using direct mercury analyzer (DMA-80). The mean of the estimated weekly intake (EWI) was estimated at 0.62 μg/kg bw/week in the range 0.36–0.96 μg/kg body weight (bw) /week through the consumption of 4 edible marine fish species every day (for 10 days) by the participants from the intervention research in Lodz, Poland. The Hg intake in the volunteers in our intervention study accounted for 38.6% of the provisional tolerable weekly intake (PTWI) (1.6 μg/kg bw, weekly) value. The average Hg concentration in the analyzed fish ranged from 0.018 ± 0.006 mg/kg wet weight (Gadus chalcogrammus) to 0.105 ± 0.015 mg/kg wet weight (Macruronus magellanicus). The results for the average consumers were within PTWI of methylmercury (MeHg). Moreover, the average concentration of Hg in the selected fish after heat treatment did not exceed the maximum permitted concentrations for MeHg (MPCs = 0.5 mg/kg wet weight) in food set by the European Commission Regulation (EC/1881/2006). Hence, the risk of adverse effects of MeHg for the participants is substantially low.
Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder that affects social, communication, and behavioral development. Recent evidence supported but also questioned the hypothetical role of compounds containing mercury (Hg) as contributors to the development of ASD. Specific alterations in the urinary excretion of porphyrin-containing ring catabolites have been associated with exposure to Hg in ASD patients. In the present study, the level of urinary porphyrins, as biomarkers of Hg toxicity in children with ASD, was evaluated, and its correlation with severity of the autistic behavior further explored. A total of 100 children was enrolled in the present study. They were classified into three groups: children with ASD (40), healthy controls (40), and healthy siblings of the ASD children (20). Children with ASD were diagnosed using DSM-IV-TR, ADI-R, and CARS tests. Urinary porphyrins were evaluated within the three groups using high-performance liquid chromatography (HPLC), after plasma evaluation of mercury (Hg) and lead (Pb) in the same groups. Results showed that children with ASD had significantly higher levels of Hg, Pb, and the porphyrins pentacarboxyporphyrin, coproporphyrin, precoproporphyrin, uroporphyrins, and hexacarboxyporphyrin compared to healthy controls and healthy siblings of the ASD children. However, there was no significant statistical difference in the level of heptacarboxyporphyrin among the three groups, while a significant positive correlation between the levels of coproporphyrin and precoproporphyrin and autism severity was observed. Mothers of ASD children showed a higher percentage of dental amalgam restorations compared to the mothers of healthy controls suggesting that high Hg levels in children with ASD may relate to the increased exposure to Hg from maternal dental amalgam during pregnancy and lactation. The results showed that the ASD children in the present study had increased blood Hg and Pb levels compared with healthy control children indicating that disordered porphyrin metabolism might interfere with the pathology associated with the autistic neurologic phenotype. The present study indicates that coproporphyrin and precoproporhyrin may be utilized as possible biomarkers for heavy metal exposure and autism severity in children with ASD.
Clinical manifestations of methylmercury (MeHg) intoxication include cerebellar ataxia, concentric constriction of visual fields, and sensory and auditory disturbances. The symptoms depend on the site of MeHg damage, such as the cerebellum and occipital lobes. However, the underlying mechanism of MeHg-induced tissue vulnerability remains to be elucidated. In the present study, we used a rat model of subacute MeHg intoxication to investigate possible MeHg-induced blood-brain barrier (BBB) damage. The model was established by exposing the rats to 20-ppm MeHg for up to 4 weeks; the rats exhibited severe cerebellar pathological changes, although there were no significant differences in mercury content among the different brain regions. BBB damage in the cerebellum after MeHg exposure was confirmed based on extravasation of endogenous immunoglobulin G (IgG) and decreased expression of rat endothelial cell antigen-1. Furthermore, expression of vascular endothelial growth factor (VEGF), a potent angiogenic growth factor, increased markedly in the cerebellum and mildly in the occipital lobe following MeHg exposure. VEGF expression was detected mainly in astrocytes of the BBB. Intravenous administration of anti-VEGF neutralizing antibody mildly reduced the rate of hind-limb crossing signs observed in MeHg-exposed rats. In conclusion, we demonstrated for the first time that MeHg induces BBB damage via upregulation of VEGF expression at the BBB in vivo. Further studies are required in order to determine whether treatment targeted at VEGF can ameliorate MeHg-induced toxicity.
Human exposure to mercury is still a major public health concern. In this context, children have a higher susceptibility to adverse neurological mercury effects, compared to adults with similar exposures. Moreover, there exists a marked variability of personal response to detrimental mercury action, in particular among population groups with significant mercury exposure. New scientific evidence on genetic backgrounds has raised the issue of whether candidate susceptibility genes can make certain individuals more or less vulnerable to mercury toxicity. In this review, the aim is to evaluate a new genetic dimension and its involvement in mercury risk assessment, focusing on the important role played by relevant polymorphisms, located in attractive gene targets for mercury toxicity. Existing original articles on epidemiologic research which report a direct link between the genetic basis of personal vulnerability and different mercury repercussions on human health will be reviewed. Based on this evidence, a careful evaluation of the significant markers of susceptibility will be suggested, in order to obtain a powerful positive “feedback” to improve the quality of life. Large consortia of studies with clear phenotypic assessments will help clarify the “window of susceptibility” in the human health risks due to mercury exposure.
In this study we investigated the additive effect of mercury on the brain mitochondrial
dysfunction in experimental autoimmune encephalomyelitis (EAE) model. Experimental
animals (female C57BL/6 mice) are divided into four groups (n = 8); control, Hg, EAE,
EAE with Hg. EAE model of MS induced by injecting myelin oligodendrocyte glycoprotein
(MOG). Neurobehavioral alterations are recorded and then mice were sacrificed at day 28
and brain mitochondria were isolated and mitochondrial toxicity parameters including
mitochondrial swelling, reactive oxygen species (ROS) formation, collapse of mitochondrial
membrane potential (MMP) and cytochrome c release were measured. Our results showed
that repeated treatment of mercury following induction of EAE in mice significantly increased
the neurobehavioral scores, as well as mitochondrial toxicity through ROS formation,
mitochondrial swelling, collapse of MMP and cytochrome c release. Our findings proved that
repeated exposure with mercury accelerates progression of MS through mitochondrial damage
related to oxidative stress and finally apoptosis.
Background
Transport of methylmercury (MeHg) across the blood-brain barrier towards the brain side is well discussed in literature, while ethylmercury (EtHg) and inorganic mercury are not adequately characterized regarding their entry into the brain. Studies investigating a possible efflux out of the brain are not described to our knowledge. Methods
This study compares, for the first time, effects of organic methylmercury chloride (MeHgCl), EtHg-containing thiomersal and inorganic Hg chloride (HgCl2) on as well as their transfer across a primary porcine in vitro model of the blood-brain barrier. ResultsWith respect to the barrier integrity, the barrier model exhibited a much higher sensitivity towards HgCl2 following basolateral incubation (brain-facing side) as compared to apical application (blood-facing side). These HgCl2 induced effects on the barrier integrity after brain side incubation are comparable to that of the organic species, although MeHgCl and thiomersal exerted much higher cytotoxic effects in the barrier building cells. Hg transfer rates following exposure to organic species in both directions argue for diffusion as transfer mechanism. Inorganic Hg application surprisingly resulted in a Hg transfer out of the brain-facing compartment. Conclusions
In case of MeHgCl and thiomersal incubation, mercury crossed the barrier in both directions, with a slight accumulation in the basolateral, brain-facing compartment, after simultaneous incubation in both compartments. For HgCl2, our data provide first evidence that the blood-brain barrier transfers mercury out of the brain.
All dental amalgam fillings contain approximately 50 % elemental mercury by weight. Concerns about health risks due to continual emissions of mercury vapor from this tooth restorative material have been addressed by dentists, scientists, and government authorities worldwide and have resulted in a range of recommended practices and regulations. By reviewing articles collected by a literature search of the International Academy of Oral Medicine and Toxicology (IAOMT) database and the PubMed database, we identify health risks associated with dental mercury amalgam. We present the science of potential harm as applicable to the general population, pregnant women, fetuses, children, and dental professionals. We specifically address genetic predispositions, mercury allergies, Alzheimer’s disease, multiple sclerosis, amyotrophic lateral sclerosis, and other health conditions pertinent to dental mercury exposure. We conclude that reviews and studies of dental amalgam mercury risk should assess biocompatibility with special consideration for all populations and all risk factors.
Mercury, in both its elemental and bonded states, is noted for its negative effects on biological organisms. Recent anthropogenic and environmental disasters have spurred numerous comparative studies. These studies attempted to detail the biochemical implications of mercury ingestion, in low, persistent concentrations as well as elevated acute dosages. The studies propose models for mercuric action on healthy cells; which is centered on the element’s disruption of key enzymatic processes at deposition sites. Mercury’s high affinity for the sulfhydryl moieties of enzyme catalytic sites is a common motif for enzyme inactivation. These permanent covalent modifications inactivate the enzyme, thereby inducing devastating effects on an organism’s metabolic functions. Mercury has been shown to be highly nonspecific in its binding to sulfhydryl moieties, and highly varied in terms of how it is encountered by living organisms. This review focuses on mercury’s effects on a wide swath of enzymes, with emphasis on how these alterations deleteriously affect several metabolic pathways.
The objective of the study was to investigate hair trace elements content in children suffering from autism spectrum disorder (ASD). A total of 74 ASD children and 74 sex- and age-matched controls divided into two age groups (2-4 and 5-9 years) were investigated. Hair trace elements content was assessed using inductively coupled plasma mass spectrometry. A general cohort of ASD children was characterized by 29 %, 41 %, and 24 % lower hair levels of chromium (Cr), iodine (I), and vanadium (V), respectively, whereas the level of selenium (Se) exceeded the respective control values by 31 %. In ASD children aged 2-4 years hair Cr, I and V content was 68 %, 36 % and 41 % lower than in the controls. Older ASD children were characterized by 45 % increase in hair Se levels. In a general cohort of ASD children hair beryllium (Be) and tin (Sn) levels were 50 % and 34 % lower than the control values. In the first age group (2-4 years) of ASD children 34 %, 42 %, and 73 % lower levels of arsenic (As), boron (B), and Be were detected. In the second age group of ASD children only a nearly significant 25 % decrease in hair lead (Pb) was detected. Surprisingly, no significant group difference in hair mercury (Hg), zinc (Zn), and copper (Cu) content was detected. Generally, the results of the present study demonstrate that children with ASD are characterized by lower values in hair of not only essential but also toxic trace elements.
In the 1970s, a woman who was then in her thirties contacted her doctor with intermittent respiratory ailments, increasing fatigue, agitation and visual disturbances. She developed a complex array of symptoms involving multiple organ systems. More than 30 years would pass before the likely cause of the symptoms was identified.
Our patient had acute work-related symptoms that are typical of harmful exposure to mercury, but more than 30 years went by before she received a probable diagnosis. The case history serves as a reminder of the importance of asking whether symptoms arise or worsen when the patient is at work. On suspicion of work-related symptoms, there should be a low threshold for referral to a specialist for diagnostic clarification and to an occupational health specialist for evaluation of exposure.
That mercury exposure can cause visual impairment is not well known. Testing of colour vision and neurological testing including visually evoked potentials should be carried out upon suspicion of visual impairment in persons that have been exposed to mercury.
In our patient the chronification of symptoms and development of permanent disability could probably have been avoided had her exposure been stopped earlier. Although the use of mercury in dental fillings has now been banned in Norway (since 2008), similar arrays of symptoms may occur upon exposure to other toxic substances, such as lead or organic solvents.
The patient has consented to the publication of this article.
Alzheimer’s disease (AD) is a neurodegenerative disorder presenting one of the biggest healthcare challenges in developed countries. No effective treatment exists. In recent years the main focus of AD research has been on the amyloid hypothesis, which postulates that extracellular precipitates of beta amyloid (Aβ) derived from amyloid precursor protein (APP) are responsible for the cognitive impairment seen in AD. Treatment strategies have been to reduce Aβ production through inhibition of enzymes responsible for its formation, or to promote resolution of existing cerebral Aβ plaques. However, these approaches have failed to demonstrate significant cognitive improvements. Intracellular rather than extracellular events may be fundamental in AD pathogenesis. Selenate is a potent inhibitor of tau hyperphosphorylation, a critical step in the formation of neurofibrillary tangles. Some selenium (Se) compounds e.g. selenoprotein P also appear to protect APP against excessive copper and iron deposition. Selenoproteins show anti-inflammatory properties, and protect microtubules in the neuronal cytoskeleton. Optimal function of these selenoenzymes requires higher Se intake than what is common in Europe and also higher intake than traditionally recommended. Supplementary treatment with N-acetylcysteine increases levels of the antioxidative cofactor glutathione and can mediate adjuvant protection. The present review discusses the role of Se in AD treatment and suggests strategies for AD prevention by optimizing selenium intake, in accordance with the metal dysregulation hypothesis. This includes in particular secondary prevention by selenium supplementation to elderly with mild cognitive impairment.
Chelation Therapy in the Treatment of Metal Intoxication presents a practical guide to the use of chelation therapy, from its basic chemistry, to available chelating antidotes, and the application of chelating agents. Several metals have long been known to be toxic to humans, and continue to pose great difficulty to treat. These challenges pose particular problems in industrial settings, with lead smelting known to be associated with hemopoietic alterations and paralyses, and the inhalation of mercury vapor in mercury mining being extremely detrimental to the central nervous system. Clinical experience has demonstrated that acute and chronic human intoxications with a range of metals can be treated efficiently by administration of chelating agents. Chelation Therapy in the Treatment of Metal Intoxication describes the chemical and biological principles of chelation in the treatment of these toxic metal compounds, including new chelators such as meso-2,3-dimercaptosuccinic acid (DMSA) and D,L-2,3-dimercapto-1-propanesulfonic acid (DMPS).
This study focuses on the extent of zinc (Zn), copper (Cu), cadmium (Cd), cobalt (Co), manganese (Mn), lead (Pb), mercury (Hg), and arsenic (As) bioaccumulation in edible muscles of Caspian kutum (Rutilus frisii kutum), in both male and female sexes at Noor and Babolsar coastal regions from the southern basin of Caspian Sea. These values were compared with the WHO and the UNFAO safety standards regarding the amount of the abovementioned heavy metals in fish tissues (mg/kg ww). Results showed that the accumulation of these elements (except for Zn) was not significantly different between sexes of male and female in Babolsar coastal regions (P > 0.05). In the other hand, accumulation of Hg and As at edible muscles of Caspian kutum has significant difference between two sexes of male and female in Noor coastal regions (P < 0.05), the female had higher concentration than the male. Furthermore, it was not significantly correlated with sex and rivers in length and weight of fish (R
2 < 0.50; P > 0.05). Based on the results, the concentration of heavy metals in the studied fish tissues proved to be significantly lower than international standards (P < 0.05), so its consumption is not a threat to the health of consumers.
Background:
The protective effect of a diet supplemented by the Amazonian fruit Euterpe oleracea (EO) against methylmercury (MeHg) toxicity in rat retina was studied using electroretinography (ERG) and biochemical evaluation of oxidative stress.
Method:
Wistar rats were submitted to conventional diet or EO-enriched diet for 28 days. After that, each group received saline solution or 5 mg/kg/day of MeHg for 7 days. Full-field single flash, flash and flicker ERGs were evaluated in the following groups: control, EO, MeHg, and EO+MeHg. The amplitudes of the a-wave, b-wave, photopic negative response from rod and/or cone were measured by ERGs as well as the amplitudes and phases of the fundamental component of the sine-wave flicker ERG. Lipid peroxidation was determined by thiobarbituric acid reactive species.
Results:
All ERG components had decreased amplitudes in the MeHg group when compared with controls. EO-enriched food had no effect on the non-intoxicated animals. The intoxicated animals and those that received the supplemented diet presented significant amplitude reductions of the cone b-wave and of the fundamental flicker component when compared with non-intoxicated control. The protective effect of the diet on scotopic conditions was only observed for bright flashes eliciting a mixed rod and cone response. There was a significant increase of lipid peroxidation in the retina from animals exposed to MeHg and EO-supplemented diet was able to prevent MeHg-induced oxidative stress in retinal tissue.
Conclusion:
These findings open up perspectives for the use of diets supplemented with EO as a protective strategy against visual damage induced by MeHg.
Hippocampal neurogenesis-related structural damage, particularly that leading to defective adult cognitive function, is considered an important risk factor for neurodegenerative and psychiatric diseases. Normal differentiation of neurons and glial cells during development is crucial in neurogenesis, which is particularly sensitive to the environmental toxicant methylmercury (MeHg). However, the exact effects of MeHg on hippocampal neural stem cell (hNSC) differentiation during puberty remain unknown. This study investigates whether MeHg exposure induces changes in hippocampal neurogenesis and whether these changes underlie cognitive defects in puberty. A rat model of methylmercury chloride (MeHgCl) exposure (0.4 mg/kg/day, PND 5-PND 33, 28 days) was established, and the Morris water maze was used to assess cognitive function. Primary hNSCs from hippocampal tissues of E16-day Sprague-Dawley rats were purified, identified, and cloned. hNSC proliferation and differentiation and the growth and morphology of newly generated neurons were observed by MTT and immunofluorescence assays. MeHg exposure induced defects in spatial learning and memory accompanied by a decrease in number of doublecortin (DCX)-positive cells in the dentate gyrus (DG). DCX is a surrogate marker for newly generated neurons. Proliferation and differentiation of hNSCs significantly decreased in the MeHg-treated groups. MeHg attenuated microtubule-associated protein-2 (MAP-2) expression in neurons and enhanced the glial fibrillary acidic protein (GFAP)-positive cell differentiation of hNSCs, thereby inducing degenerative changes in a dose-dependent manner. Moreover, MeHg induced deficits in hippocampus-dependent spatial learning and memory during adolescence as a consequence of decreased generation of DG neurons. Our findings suggested that MeHg exposure could be a potential risk factor for psychiatric and neurodegenerative diseases.
Tachykinins (substance P, neurokinin A, and neurokinin B) are pro-inflammatory neuropeptides that may play an important role in some autoimmune neuroinflammatory diseases, including autism spectrum disorder (ASD). Mercury (Hg) is a neurotoxicant, and potentially one of the main environmental triggers for ASD as it induces neuroinflammation with a subsequent release of neuropeptides. This is the first study to explore the potentially causal relationship between levels of serum neurokinin A and blood mercury (BHg) in children with ASD. Levels of serum neurokinin A and BHg were measured in 84 children with ASD, aged between 3 and 10 years, and 84 healthy-matched children. There was a positive linear relationship between the Childhood Autism Rating Scale (CARS) and both serum neurokinin A and BHg. ASD children had significantly higher levels of serum neurokinin A than healthy controls (P < 0.001). Increased levels of serum neurokinin A and BHg were respectively found in 54.8 % and 42.9 % of the two groups. There was significant and positive linear relationship between levels of serum neurokinin A and BHg in children with moderate and severe ASD, but not in healthy control children. It was found that 78.3 % of the ASD patients with increased serum levels of neurokinin A had elevated BHg levels (P < 0.001). Neuroinflammation, with increased levels of neurokinin A, is seen in some children with ASD, and may be caused by elevated BHg levels. Further research is recommended to determine the pathogenic role of increased levels of serum neurokinin A and BHg in ASD. The therapeutic role of tachykinin receptor antagonists, a potential new class of anti-inflammatory medications, and Hg chelators, should also be studied in ASD.
Seafood consumption during pregnancy is thought to be beneficial for child neuropsychological development, but to our knowledge no large cohort studies with high fatty fish consumption have analyzed the association by seafood subtype. We evaluated 1,892 and 1,589 mother-child pairs at the ages of 14 months and 5 years, respectively, in a population-based Spanish birth cohort established during 2004-2008. Bayley and McCarthy scales and the Childhood Asperger Syndrome Test were used to assess neuropsychological development. Results from multivariate linear regression models were adjusted for sociodemographic characteristics and further adjusted for umbilical cord blood mercury or long-chain polyunsaturated fatty acid concentrations. Overall, consumption of seafood above the recommended limit of 340 g/week was associated with 10-g/week increments in neuropsychological scores. By subtype, in addition to lean fish, consumption of large fatty fish showed a positive association; offspring of persons within the highest quantile (>238 g/week) had an adjusted increase of 2.29 points in McCarthy general cognitive score (95% confidence interval: 0.42, 4.16). Similar findings were observed for the Childhood Asperger Syndrome Test. Beta coefficients diminished 15%-30% after adjustment for mercury or long-chain polyunsaturated fatty acid concentrations. Consumption of large fatty fish during pregnancy presents moderate child neuropsychological benefits, including improvements in cognitive functioning and some protection from autism-spectrum traits.
Aims Currently, the spectrum of pathological manifestations associated with cadmium-induced testicular toxicity is poorly understood. Thus, we investigated the impact of cadmium (Cd) exposure on testicular mineral bioavailability, activity of antioxidant enzymes, testicular structure and germ cells ultrastructure Main methods Cadmium chloride was administered in a single dose to thirty rats equally randomized into five groups: Saline, 0.9% NaCl; Cd1 – Cd4, 0.67, 0.74, 0.86 and 1.1 mg Cd/kg. Seven days after Cd exposure, animals were euthanized and testes were collected for biochemical analysis, as well as light, scanning and transmission electron microscopy. Key findings Cadmium exposure induced dose-dependent testicular toxicity. Tubular and intertubular compartments were targets of Cd and calcium (Ca) deposits, marked structural and ultrastructural pathologic remodeling, and a reduced distribution of iron, selenium, magnesium, copper, zinc and total protein. Despite upregulation in antioxidant enzyme activities (i.e. catalase [CAT] and superoxide dismutase [SOD]), morphologic and molecular testis damage such as protein oxidation was not prevented, especially with higher doses of Cd. As non-degenerated tissue areas also presented Ca deposits, Ca imbalance was not only a consequence but also a cause of Cd-induced testis toxicity and germ cell death Significance Taken together, our findings indicated that Cd exposition induced dose-dependent testicular dystrophic calcification, which was associated with increased antioxidant enzymes activity and protein oxidation, mineral imbalance, germ cell calcification and death in rats. Although increased CAT and SOD activity represents a counter-regulatory reaction to cadmium-induced toxicity, this reaction is insufficient to prevent testicular pathological remodeling.
A highly sensitive and selective fluorescence method of quantitative detection for mercury in soil was developed using non-labeled molecular beacon (MB), single-stranded nucleic acid (ssDNA) and fluorescent dye Hoechst 33258. In this analytical method, the loop of MB was designed to be a sequence that was complementary to the ssDNA with multiple T-T mismatches, the stem of MB was completely designed as C-G base pairs, and both ends of the MB are not modified by any fluorophore and quencher. In the absence of Hg²⁺, the interaction between Hoechst 33258 and the MB was very weak, and the fluorescence signal of Hoechst 33258 was very low. In the presence of Hg²⁺, the MB and ssDNA with multiple T-T mismatches formed a double-stranded nucleic acid (dsDNA) via the T-Hg²⁺-T coordination structure which provided binding sites for Hoechst 33258. Then Hoechst 33258 binded to A-T base pairs of dsDNA, and the fluorescence intensity of Hoechst 33258 was significantly enhanced. Thus, a highly sensitive fluorescence quantitative detection method for Hg²⁺ can be realized. In this strategy, the optimal determination conditions for Hg²⁺ were a buffer solution pH of 8.2, an incubated temperature of 50°C, an incubated time of 5 min and NaCl of 60 mmol L⁻¹. Under the optimum conditions, the fluorescence intensity of Hoechst 33258 exhibited a good linear dependence on the concentration of Hg²⁺ in the range of 5 × 10⁻⁹ – 400 × 10⁻⁹ mol L⁻¹. The fitted regression equation was ΔI = 2.1084C – 8.9587 with a correlation coefficient of 0.9943 (R²), and the detection limit of this method was 3 × 10⁻⁹ mol L⁻¹ (3σ). The proposed method had a high selection; the common substances in soil such as Ca²⁺, Mg²⁺, Mn²⁺, Fe³⁺, Cu²⁺, Pb²⁺, Al³⁺, K⁺, Na⁺, Ni²⁺, Cd²⁺, Cr³⁺, SiO3²⁻, Cl⁻, PO4³⁻, NH4⁺ and S²⁻ had no interference to the detection of mercury. The proposed method had a high accuracy, and it was applied to detect mercury of ten different types of soil; the recoveries were 97.65 – 103.22%. In addition, the proposed method had a low background emission, fast detection speed and low detection cost.
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Despite the distance from large anthropogenic emission sources, toxic mercury is transported via the atmosphere and oceans to the Southern Ocean. Seawater samples were collected at selected stations and were analysed for total mercury (HgT) (8 stations), dissolved gaseous mercury (DGM) (62 stations) and methylmercury (12 stations) during winter (Weddell Sea), spring (Weddell Sea) and summer (Amundsen and Ross Seas) in the Southern Ocean. The HgT distribution in water columns was found to not vary significantly with depth. In the Weddell Sea the average column concentration was higher in spring (2.6 ± 1.3 pM, 2 stations) than in winter (2.0 ± 1.0 pM, 6 stations). We hypothesize that the seasonal HgT increase is due to atmospheric deposition of particulate Hg(II) formed during atmospheric mercury depletion events (AMDEs), as well as the addition of inorganic mercury species from melting sea ice and snow. Furthermore, HgT concentrations found in this study were significantly higher than previously measured in the Southern Ocean (Cossa et al., 2011), which was hypothesized to be due to seasonal variations in atmospheric deposition.
Manganese (Mn) is the fifth most abundant metal on earth. Although it is a well understood essential trace
element, in excess, Mn is neurotoxic. Initial toxic symptoms associated with Mn are of psychiatric nature and
are clinically defined as locura manganica. Neurological signs of Mn toxicity include dystonia, progressive
bradykinesia, and disturbance of gait, slurring, and stuttering of speech with diminished volume. Studies
indicate that children who ingested Mn in the drinking water (WMn) at or above a level of 0.241 mg/L for a
minimum of three years performed more poorly in school as measured by mastery of language, mathematics,
and in their overall grade average. The Mn-exposed children also performed more poorly on a battery of
neurobehavioral tests. It was also found a significant association between higher WMn and lower cognitive
performance, verbal function, and full-scale intelligence quotient (IQ) scores. Young children appear to make up a vulnerable group in exposed populations. Toxicity of WMn is a problem particularly in areas of industrial
waste or where Mn is leaching from the soil into public drinking water. Practical and cost-effective approaches are available to remove Mn from drinking water. It is crucial to protect developing brains against Mn toxicity.
Owing to advances in modern medicine, life expectancies are lengthening and leading to an increase in the population of older individuals. The aging process leads to significant alterations in many organ systems, with the kidney being particularly susceptible to age-related changes. Within the kidney, aging leads to ultrastructural changes such as glomerular and tubular hypertrophy, glomerulosclerosis, and tubulointerstitial fibrosis, which may compromise renal plasma flow (RPF) and glomerular filtration rate (GFR). These alterations may reduce the functional reserve of the kidneys, making them more susceptible to pathological events when challenged or stressed, such as following exposure to nephrotoxicants. An important and prevalent environmental toxicant that induces nephrotoxic effects is mercury (Hg). Since exposure of normal kidneys to mercuric ions might induce glomerular and tubular injury, aged kidneys, which may not be functioning at full capacity, may be more sensitive to the effects of Hg than normal kidneys. Age-related renal changes and the effects of Hg in the kidney have been characterized separately. However, little is known regarding the influence of nephrotoxicants, such as Hg, on aged kidneys. The purpose of this review was to summarize known findings related to exposure of aged and diseased kidneys to the environmentally relevant nephrotoxicant Hg.
In this study we examined the independent self assembly of metal-binding in C-terminal Cys- rich region of a type 1 metallothionein (MT) isoform from rice (OsMTI-1b). To this end the N-terminal of OsMTI-1b (C-OsMTI-1b) was heterologously expressed in Escherichia coli as fusion protein with glutathione-S-transferase (GST). As compared with control (The E. coli cells containing pET41a without gene), transgenic E. coli cells expressing GST-C-OsMTI-1b accumulated more Ni(2+), Cd(2+), and Zn(2+) from culture medium and showed increased tolerance against these metals. The recombinant GST-C-OsMTI-1b was purified using affinity chromatography. According to in vitro assays the protein GST-C-OsMTI-1b was able to form complexes with Ni(2+), Cd(2+) and Zn(2+). These results demonstrate the formation of independent metal-thiolate cluster at C-terminal Cys-rich region of OsMTI-1b without participation of N-terminal Cys-rich region.
Selenium (Se) nanoparticles are often synthesized by anaerobes. However, anaerobic bacteria cannot be directly applied for bioremediation of contaminated top soil which is generally aerobic. In this study, a selenite-reducing bacterium, Citrobacter freundii Y9, demonstrated high selenite reducing power and produced elemental nano-selenium nanoparticles (nano-Se⁰) under both aerobic and anaerobic conditions. The biogenic nano-Se⁰ converted 45.8-57.1% and 39.1-48.6% of elemental mercury (Hg⁰) in the contaminated soil to insoluble mercuric selenide (HgSe) under anaerobic and aerobic conditions, respectively. Addition of sodium dodecyl sulfonate enhanced Hg⁰ remediation, probably owing to the release of intracellular nano-Se⁰ from the bacterial cells for Hg fixation. The reaction product after remediation was identified as non-reactive HgSe that was formed by amalgamation of nano-Se⁰ and Hg⁰. Biosynthesis of nano-Se⁰ both aerobically and anaerobically therefore provides a versatile and cost-effective remediation approach for Hg⁰-contaminated surface and subsurface soils, where the redox potential often changes dramatically.
Soil mercury (Hg) contamination is a major factor that affects agricultural yield and food security. Hydrogen sulfide (H2S) plays multifunctional roles in mediating a variety of responses to abiotic stresses. The effects of exogenous H2S on rice (Oryza sativa var ‘Nipponbare’) growth and metabolism under mercuric chloride (HgCl2) stress were investigated in this study. Either 100 or 200 μM sodium hydrosulfide (NaHS, a donor of H2S) pretreatment improved the transcription of bZIP60, a membrane-associated transcription factor, and then enhanced the expressions of non-protein thiols (NPT) and metallothioneins (OsMT-1) to sequester Hg in roots and thus inhibit Hg transport to shoots. Meanwhile, H2S promoted seedlings growth significantly even in the presences of Hg and superoxide dismutase (SOD, EC 1.15.1.1) or catalase (CAT, EC 1.11.1.6) inhibitors, diethyldithiocarbamate (DDC) or 3-amino-1,2,4-triazole (AT). H2S might act as an antioxidant to inhibit or scavenge reactive oxygen species (ROS) productions for maintaining the lower MDA and H2O2 levels, and thereby preventing oxidative damages. All these results indicated H2S effectively alleviated Hg toxicity by sequestering it in roots or by regulating ROS in seedlings and then thus significantly promoted rice growth.
The autism spectrum is highly variable, both behaviorally and neurodevelopmentally. Broadly speaking, four related factors contribute to this variability: (1) genetic processes, (2) environmental events, (3) gene × environment interactions, and (4) developmental factors. Given the complexity of the relevant processes, it appears unlikely that autism spectrum atypicalities can be attributed to any one causal mechanism. Rather, the development of neural atypicality reflects an interaction of genetic and environmental risk factors. As the individual grows, changes in neural atypicality, consequent variation in behavior, and environmental response to that behavior may become linked in a positive feedback loop that amplifies deviations from the typical developmental pattern. WIREs Cogn Sci 2017, 8:e1426. doi: 10.1002/wcs.1426
This article is categorized under: Neuroscience > Clinical Neuroscience
Neuroscience > Development
Vaccines are prophylactics used as the first line of intervention to prevent, control and eradicate infectious diseases. Young children (before the age of six months) are the demographic group most exposed to recommended/mandatory vaccines preserved with Thimerosal and its metabolite ethylmercury (EtHg). Particularly in the less-developed countries, newborns, neonates, and young children are exposed to EtHg because it is still in several of their pediatric vaccines and mothers are often immunized with Thimerosal-containing vaccines (TCVs) during pregnancy. While the immunogenic component of the product has undergone more rigorous testing, Thimerosal, known to have neurotoxic effects even at low doses, has not been scrutinized for the limit of tolerance alone or in combination with adjuvant-Al during immaturity or developmental periods (pregnant women, newborns, infants, and young children). Scientific evidence has shown the potential hazards of Thimerosal in experiments that modeled vaccine-EtHg concentrations. Observational population studies have revealed uncertainties related to neurological effects. However, consistently, they showed a link of EtHg with risk of certain neurodevelopment disorders, such as tic disorder, while clearly revealing the benefits of removing Thimerosal from children’s vaccines (associated with immunological reactions) in developed countries. So far, only rich countries have benefited from withdrawing the risk of exposing young children to EtHg. Regarding Thimerosal administered to the very young, we have sufficient studies that characterize a state of uncertainty: the collective evidence strongly suggests that Thimerosal exposure is associated with adverse neurodevelopmental outcomes. It is claimed that the continued use of Thimerosal in the less-developed countries is due to the cost to change to another preservative, such as 2-phenoxyethanol. However, the estimated cost increase per child in the first year of life is lower than estimated lifetime cost of caring for a child with a neurodevelopmental disorder, such tic disorder. The evidence indicates that Thimerosal-free vaccine options should be made available in developing countries.
Autoimmune diseases result from an interplay of genetic predisposition and factors which stimulate the onset of disease. Mercury (Hg), a well-established toxicant, is an environmental factor reported to be linked with autoimmunity. Hg exists in several chemical forms and is encountered by humans in dental amalgams, certain vaccines, occupational exposure, atmospheric pollution and seafood. Several studies have investigated the effect of the various forms of Hg, including elemental (Hg?), inorganic (iHg) and organic mercury (oHg) and their association with autoimmunity. In vitro studies using peripheral blood mononuclear cells (PBMC) from healthy participants have shown that methylmercury (MeHg) causes cell death at lower concentrations than iHg albeit exposure to iHg results in a more enhanced pro-inflammatory profile in comparison to MeHg. In vivo research utilising murine models susceptible to the development of metal-induced autoimmunity report that exposure to iHg results in a lupus-like syndrome, whilst mice exposed to MeHg develop autoimmunity without the formation of immune complexes. Furthermore, lower concentrations of IgE are detected in MeHg-treated animals in comparison with those treated with iHg. It appears that, oHg has a negative impact on animal models with existing autoimmunity. The research conducted on humans in this area is diverse in study design and the results are conflicting. There is currently no evidence to implicate a role for Hg? exposure from dental amalgams in the development or perpetuation of autoimmune disease, apart from some suggestion of individual sensitivity. Several studies have consistently shown a positive correlation between iHg exposure and serum autoantibody concentrations in gold miners, although the clinical impact of iHg remains unknown. Furthermore, a limited number of studies have reported individuals with autoimmune disease have higher concentrations of blood Hg compared to healthy controls. In summary, it appears that iHg perpetuates markers of autoimmunity to a greater extent than oHg, albeit the impact on clinical outcomes in humans is yet to be elucidated.
Selenium (Se) is highly abundant in marine foods traditionally consumed by Inuit of Nunavik (Northern Quebec, Canada) and accordingly, their Se intake is among the highest in the world. However, little is known regarding the biological implications of this high Se status in this Arctic indigenous population. We used a method combining affinity chromatography and inductively coupled plasma-mass spectrometry with quantification by post-column isotope dilution to determine total Se levels and concentrations of Se-containing proteins in archived plasma samples of Inuit adults who participated to the 2004 Nunavik Inuit Health Survey (N = 852). Amounts of mercury (Hg) associated with Se-containing proteins were also quantified. Results show that glutathione peroxidase 3 (GPx3), selenoprotein P (SelP) and selenoalbumin (SeAlb) represented respectively 25%, 52% and 23% of total plasma Se concentrations. In addition, small amounts of Hg co-eluted with each Se-containing protein and up to 50% of plasma Hg was associated to SelP. Total plasma Se concentrations (median = 139 μg L− 1; interquartile range (IQR) = 22.7 μg L− 1) were markedly lower and less variable than whole blood Se concentration (median = 261 μg L− 1, IQR = 166 μg L− 1). A non linear relation was observed between whole blood Se and plasma Se levels, with plasma Se concentrations leveling off at approximately 200 μg L− 1, whereas 16% and 3% of individuals exhibited whole blood concentrations higher than 500 μg L− 1 and 1000 μg L− 1, respectively. In contrast, a linear relationship was previously reported in communities consuming Brazil nuts which are rich Se, mainly present as selenomethionine. This suggests that a different selenocompound, possibly selenoneine, is present in the Arctic marine food chain and accumulates in the blood cellular fraction of Inuit.
Environmental exposure to methylmercury (MeHg) during development is of concern because it is easily incorporated in children’s body both pre- and post-natal, it acts at several levels of neural pathways (mitochondria, cytoskeleton, neurotransmission) and it causes behavioral impairment in child. We evaluated the effects of prolonged exposure to 10–600 nM MeHg on primary cultures of mouse cortical (CCN) and of cerebellar granule cells (CGC) during their differentiation period. In addition, it was studied if prenatal MeHg exposure correlated with altered antioxidant defenses and cofilin phosphorylation in human placentas (n = 12) from the INMA cohort (Spain).
There are a number of mechanisms by which alkylmercury compounds cause toxic action in the body. Collectively, published studies reveal that there are some similarities between the mechanisms of the toxic action of the mono-alkyl mercury compounds methylmercury (MeHg) and ethylmercury (EtHg). This paper represents a summary of some of the studies regarding these mechanisms of action in order to facilitate the understanding of the many varied effects of alkylmercurials in the human body. The similarities in mechanisms of toxicity for MeHg and EtHg are presented and compared. The difference in manifested toxicity of MeHg and EtHg are likely the result of the differences in exposure, metabolism, and elimination from the body, rather than differences in mechanisms of action between the two.
In treatment of metal poisonings, the top priorities should be prevention of further uptake, decreased absorption from the gastrointestinal tract, and general supportive therapy focusing on the maintenance of respiration, circulation, water and electrolyte balance, and control of cerebral function. Elimination of the absorbed poison can be facilitated by diuresis, hemodialysis, or exchange transfusion. Chelating agents counteract the effects of an absorbed toxic metal by displacing the metal from its receptor site into urine or a tissue where it cannot exert toxic effects. Chelation therapy is indicated in the treatment of metal poisonings, metal storage diseases, and to aid the elimination of some radionuclides. Chelators may also have toxic effects, for example, by depletion of essential metals or by the reallocation of toxic metals to other vulnerable tissues. Use and misuse of chelators are discussed in this chapter. Dimercaprol (BAL), the classical but now a rather outdated chelator with high toxicity, competes with protein thiol groups for arsenic and some other metals. Today its less toxic analogs Dimaval (DMPS) and Succimer (DMSA) are used in the treatment of intoxications by arsenic, mercury, bismuth, and lead. The previous use of intravenous calcium EDTA, may redistribute lead to the brain after acute or chronic poisoning, and is therefore not recommended. Due to its serious side effects, the use of EDTA in atherosclerotic diseases is contraindicated. Penicillamine and trientine have proven to be effective in the treatment of copper accumulation and in the management of Wilson’s disease. Deferoxamine is the treatment of choice in acute iron poisoning. It can also be used in the treatment of transfusional siderosis, preferably in combination with deferiprone or deferasirox, the new oral agents that can mobilize intracellular iron from liver and heart. Derivatives of DTPA as aerosol have been used to decrease the lung deposits of inhaled plutonium.
Mercury vapor is highly toxic to the human body. The present study aimed to investigate the occurrence of neuropsychological dysfunction in former workers of fluorescent lamps factories that were exposed to mercury vapor (years after cessation of exposure), diagnosed with chronic mercurialism, and to investigate the effects of such exposure on the Autonomic Nervous System (ANS) using the non-invasive method of dynamic pupillometry. The exposed group and a control group matched by age and educational level were evaluated by the Beck Depression Inventory and with the computerized neuropsychological battery CANTABeclipse - subtests of working memory (Spatial Span), spatial memory (Spatial Recognition Memory), visual memory (Pattern Recognition Memory) and action planning (Stockings of Cambridge). The ANS was assessed by dynamic pupillometry, which provides information on the operation on both the sympathetic and parasympathetic functions. Depression scores were significantly higher among the former workers when compared with the control group. The exposed group also showed significantly worse performance in most of the cognitive functions assessed. In the dynamic pupillometry test, former workers showed significantly lower response than the control group in the sympathetic response parameter (time of 75% of pupillary recovery at 10cd/m(2) luminance). Our study found indications that are suggestive of cognitive deficits and losses in sympathetic autonomic activity among patients occupationally exposed to mercury vapor.
Multiple formins regulate microtubule (MTs) arrays, but whether they function individually or in a common pathway is unknown. Lysophosphatidic acid (LPA) stimulates the formation of stabilized detyrosinated MTs (Glu MTs) in NIH3T3 fibroblasts through RhoA and the formin mDia1. Here we show that another formin, INF2, is necessary for mDia1-mediated induction of Glu MTs and regulation of MT dynamics, and that mDia1 could be bypassed by activating INF2. INF2 localized to MTs after LPA treatment in an mDia1-dependent fashion, suggesting that mDia1 regulates INF2. Mutants of either formin that disrupt their interaction failed to rescue MT stability in cells depleted of the respective formin and the mDia1 interacting protein IQGAP1 regulated INF2's localization to MTs and the induction of Glu MTs by either formin. The N-terminus of IQGAP1 associated with the C-terminus of INF2 directly, suggesting the possibility of a tripartite complex stimulated by LPA. Supporting this, the interaction of mDia1 and INF2 was induced by LPA and dependent on IQGAP1. Our data highlight a unique mechanism of formin action in which mDia1 and INF2 function in series to stabilize MTs and point to IQGAP1 as a scaffold that facilitates the activation of one formin by another.
Aluminum (Al) is present in the daily life of humans, and the incidence of Al contamination increased in recent years. Long-term excessive Al intake induces neuroinflammation and cognition impairment. Neuroinflammation alter density of dendritic spine, which, in turn, influence cognition function. However, it is unknown whether increased neuroinflammation is associated with altered density of dendritic spine in Al-treated rats. In the present study, AlCl3 was orally administrated to rat at 50, 150 and 450 mg/kg for 90d. We examined the effects of AlCl3 on the cognition function, density of dendritic spine in hippocampus of CA1 and DG region and the mRNA levels of IL-1β, IL-6, TNF-α, MHC II, CX3CL1 and BNDF in developing rat. These results showed exposure to AlCl3 lead to increased mRNA levels of IL-1β, IL-6, TNF-α and MCH II, decreased mRNA levels of CX3CL1 and BDNF, decreased density of dendritic spine and impaired learning and memory in developing rat. Our results suggest AlCl3 can induce neuroinflammation that may result in loss of spine, and thereby leads to learning and memory deficits.
Governmental agencies (www.epa.gov/mercury) and the scientific community have reported on the high toxicity due to mercury. Indeed, exposure to mercury can cause severe injury to the central nervous system and kidney in humans. Beyond its recognized toxicity, little is known regarding the molecular mechanisms involved in the actions of this heavy metal. Mercury has been also observed to form insoluble fibrous protein aggregates in the cell nucleus. We used D. discoideum to evaluate micronuclei formation and, since mercury is able to induce oxidative stress that could bring to protein aggregation, we assessed nuclear protein carbonylation by Western Blot. We observed a significant increase in micronuclei formation and 14 carbonylated proteins were identified. Moreover, we used isotope-coded protein label (ICPL) and mass spectrometry analysis of proteins obtained by lysis of purified nuclei, before of tryptic digestion to quantify nuclear proteins affected by mercury. In particular, we examined the effects of mercury that associate a classical genotoxic assay to proteomic effects into the nucleus. The data present direct evidences for mercury genotoxicity, nuclear protein carbonylation, quantitative change in core histones, and the involvement of pseudouridine synthase in mercury toxicity. © 2016 Wiley Periodicals, Inc. Environ Toxicol, 2016.