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Bulletin of the World Health... Feb 2015
Topics: Humans; Methylmercury Compounds; Neurotoxicity Syndromes
PubMed: 25883408
DOI: 10.2471/BLT.14.141911 -
Environmental Pollution (Barking, Essex... Mar 2020China is the largest rice producer and consumer in the world, and mercury (Hg) levels, particularly methylmercury (MeHg), in rice and health exposure risks are public...
China is the largest rice producer and consumer in the world, and mercury (Hg) levels, particularly methylmercury (MeHg), in rice and health exposure risks are public concerns. Total Hg (THg) and MeHg levels in 767 (domestic = 709 and abroad = 58) Chinese commercial rice were investigated to evaluate Hg pollution level, dietary exposures and risks of IHg and MeHg. The mean rice THg and MeHg levels were 3.97 ± 2.33 μg/kg and 1.37 ± 1.18 μg/kg, respectively. The highest daily intake of MeHg and IHg were obtained in younger groups, accounted for 6% of the reference dose-0.1 μg/kg bw/day for MeHg, 0.3% of the provisional tolerance week intake-0.571 μg/kg bw/day for IHg. Residents in Central China and Southern China meet the highest rice Hg exposure, which were more than 7 times of those in Northwest China. Lower concentrations than earlier studies were observed along the implementations of strict policies since 2007. This may indicate that a declining temporal trend of Hg in Chinese grown rice and associated exposures could be obtained with the implementations of strict policies. Though there exist Hg pollution in commercial rice, Hg levels in Chinese commercial rice is generally safe compared with Hg polluted sites. Populations dwelling in China have relatively a quite low and safe MeHg and IHg exposure via the intake of commercial rice. Strict policies contributed to the decrease in THg and MeHg levels in Chinese-grown rice. More attention should be paid to younger groups.
Topics: China; Food Contamination; Humans; Mercury; Methylmercury Compounds; Oryza
PubMed: 31864929
DOI: 10.1016/j.envpol.2019.113706 -
The Journal of Toxicological Sciences 2014The accumulation of methylmercury (MeHg) through the daily consumption of large predatory fish poses potential health risks. MeHg has been found to cause Minamata... (Review)
Review
The accumulation of methylmercury (MeHg) through the daily consumption of large predatory fish poses potential health risks. MeHg has been found to cause Minamata disease, but the full nature of MeHg toxicity remains unclear. Because of its chemical properties, MeHg covalently binds to cellular proteins through their reactive thiols, referred to as S-mercuration, resulting in the formation of protein adducts. In this review, we summarize how the S-mercuration of cellular proteins could be involved in the major mechanisms that have been suggested to underlie MeHg toxicity. Additionally, we introduce our attempts to identify cases of S-mercuration for the research to reveal the true nature of MeHg toxicity.
Topics: Animals; Arginase; Calcium; Cysteine; Glutamic Acid; Glutathione Transferase; Humans; L-Iditol 2-Dehydrogenase; Membrane Proteins; Methylmercury Compounds; Microtubules; Oxidative Stress; Protein Binding; Sulfhydryl Compounds; Superoxide Dismutase; Tubulin
PubMed: 25242398
DOI: 10.2131/jts.39.687 -
The Science of the Total Environment Oct 2016Methylmercury contamination of the environment is an important issue globally, and birds are useful bioindicators for mercury monitoring programs. The available data on... (Review)
Review
Methylmercury contamination of the environment is an important issue globally, and birds are useful bioindicators for mercury monitoring programs. The available data on mercury contamination of birds in western North America were synthesized. Original data from multiple databases were obtained and a literature review was conducted to obtain additional mercury concentrations. In total, 29219 original bird mercury concentrations from 225 species were compiled, and an additional 1712 mean mercury concentrations, representing 19998 individuals and 176 species, from 200 publications were obtained. To make mercury data comparable across bird tissues, published equations of tissue mercury correlations were used to convert all mercury concentrations into blood-equivalent mercury concentrations. Blood-equivalent mercury concentrations differed among species, foraging guilds, habitat types, locations, and ecoregions. Piscivores and carnivores exhibited the greatest mercury concentrations, whereas herbivores and granivores exhibited the lowest mercury concentrations. Bird mercury concentrations were greatest in ocean and salt marsh habitats and lowest in terrestrial habitats. Bird mercury concentrations were above toxicity benchmarks in many areas throughout western North America, and multiple hotspots were identified. Additionally, published toxicity benchmarks established in multiple tissues were summarized and translated into a common blood-equivalent mercury concentration. Overall, 66% of birds sampled in western North American exceeded a blood-equivalent mercury concentration of 0.2 μg/g wet weight (ww; above background levels), which is the lowest-observed effect level, 28% exceeded 1.0 μg/g ww (moderate risk), 8% exceeded 3.0 μg/g ww (high risk), and 4% exceeded 4.0 μg/g ww (severe risk). Mercury monitoring programs should sample bird tissues, such as adult blood and eggs, that are most-easily translated into tissues with well-developed toxicity benchmarks and that are directly relevant to bird reproduction. Results indicate that mercury contamination of birds is prevalent in many areas throughout western North America, and large-scale ecological attributes are important factors influencing bird mercury concentrations.
Topics: Animals; Birds; Canada; Databases, Factual; Environmental Monitoring; Environmental Pollutants; Geographic Information Systems; Methylmercury Compounds; Midwestern United States; Models, Biological; Northwestern United States; Risk Assessment; Southwestern United States; Species Specificity; Tissue Distribution
PubMed: 27093907
DOI: 10.1016/j.scitotenv.2016.03.071 -
Environmental Health Perspectives Aug 1978The available data on the influence of selenium on the toxicity of methylmercury and of methylmercury on selenium as a nutrient and toxic agent are reviewed. Selenium as... (Review)
Review
The available data on the influence of selenium on the toxicity of methylmercury and of methylmercury on selenium as a nutrient and toxic agent are reviewed. Selenium as selenite has a relative protective effect on acute and subacute toxicity of methylmercury in the rat and the quail. The protective mechanism is far from clear. Of special interest is the fact that selenium-treated animals may remain unaffected, even when they have attained tissue mercury levels otherwise associated with toxic effects. Selenite causes some increase of tissue mercury levels in methylmercury-exposed animals. On the other hand, methylmercury induces a remarkable enhancement of organ concentrations of selenium in animals given selenite. The interaction between selenium and methylmercury is in many ways different from that between selenium and inorganic mercury, and also from that between selenium and other metals. Due to the considerable interspecies differences in the toxicity of methylmercury, the available data do not allow conclusions on interactions in man. Practical implications of a possible protective effect of selenium on methylmercury toxicity in humans are discussed.
Topics: Animals; Biotransformation; Drug Interactions; Enzymes; Intestinal Absorption; Methylmercury Compounds; Placenta; Protein Binding; Selenium; Subcellular Fractions
PubMed: 363410
DOI: 10.1289/ehp.782557 -
Journal of Environmental and Public... 2020This report synthesizes and evaluates published scientific literature on the environmental occurrence and biomagnification of mercury with emphasis on the San Francisco... (Review)
Review
This report synthesizes and evaluates published scientific literature on the environmental occurrence and biomagnification of mercury with emphasis on the San Francisco Bay Area (SFBA), California. Mercury forms various compounds, well known for their toxicity in humans and environmental ecosystems. Elemental mercury is transported and distributed by air, water, and sediments. Through the metabolic processes of algae and bacteria, mercury is converted into organic compounds, such as methylmercury (MeHg), which then bioaccumulates up through trophic levels. In fish, it is found primarily in skeletal muscle, while in humans, the primary target organs are the brain and kidneys. Health concerns exist regarding bioaccumulation of mercury in humans. This paper reviews the known anthropogenic sources of mercury contamination, including atmospheric deposition through aerial transport from coal burning power plants, cement production, and residual contaminants of mercury from gold mining, as well as mercury-containing waste from silver amalgams emitted from dental offices into waterways. Although tools exist for measuring mercury levels in hair, breast milk, urine, blood, and feces in humans, current diagnostic tools are inadequate in measuring total mercury load, including deposited mercury in tissues. Additionally, insufficient attention is being paid to potential synergistic impacts of mercury interaction with multipliers such as lead, cadmium, and aluminum. We provide specific data on methylmercury concentrations at different trophic levels, followed by recommendations for reducing the level of mercury in the SFBA in order to protect the health of humans and other species.
Topics: Animals; Ecosystem; Environmental Monitoring; Environmental Pollutants; Humans; Mercury; Mercury Poisoning; Metals, Heavy; Methylmercury Compounds; San Francisco
PubMed: 33014081
DOI: 10.1155/2020/8184614 -
Toxicology Mechanisms and Methods Jan 2024Mercury is a ubiquitous environmental contaminant and can be found in inorganic (Hg, Hg and Hg) and organic forms (chiefly CHHg or MeHg). The main route of human,... (Review)
Review
Mercury is a ubiquitous environmental contaminant and can be found in inorganic (Hg, Hg and Hg) and organic forms (chiefly CHHg or MeHg). The main route of human, mammals and bird exposure occurs predatory fish ingestion. Occupational exposure to Hg (and Hg) can also occur; furthermore, in gold mining areas the exposure to inorganic Hg can also be high. The toxicity of electrophilic forms of Hg (EHg) is mediated by disruption of thiol (-SH)- or selenol (-SeH)-containing proteins. The therapeutic approaches to treat methylmercury (MeHg), Hg and Hg are limited. Here we discuss the potential use of ebselen as a potential therapeutic agent to lower the body burden of Hg in man. Ebselen is a safe drug for humans and has been tested in clinical trials (for instance, brain ischemia, noise-induce hearing loss, diabetes complications, bipolar disorders) at doses varying from 400 to 3600 mg per day. Two clinical trials with ebselen in moderate and severe COVID are also approved. Ebselen can be metabolized to an intermediate with -SeH (selenol) functional group, which has a greater affinity to electrophilic Hg (EHg) forms than the available thiol-containing therapeutic agents. Accordingly, as observed and rodent models Ebselen exhibited protective effects against MeHg, indicating its potential as a therapeutic agent to treat MeHg overexposure. The combined use of ebselen with thiol-containing molecules (e.g. N-acetylcysteine and enaramide)) is also commented, because they can have synergistic protective effects against MeHg.
Topics: Animals; Humans; Mercury; Methylmercury Compounds; Azoles; Sulfhydryl Compounds; Mammals
PubMed: 37731353
DOI: 10.1080/15376516.2023.2258958 -
Environmental Health Perspectives Oct 2002Intracellular concentrations of essential metals are normally maintained within a narrow range, whereas the nonessential metals generally lack homeostatic controls. Some... (Review)
Review
Intracellular concentrations of essential metals are normally maintained within a narrow range, whereas the nonessential metals generally lack homeostatic controls. Some of the factors that contribute to metal homeostasis have recently been identified at the molecular level and include proteins that mediate import of essential metals from the extracellular environment, those that regulate delivery to specific intracellular proteins or compartments, and those that mediate metal export from the cell. Some of these proteins appear highly selective for a given essential metal; however, others are less specific and interact with multiple metals, including toxic metals. For example, DCT1 (divalent cation transporter-1; also known as NRAMP2 or DMT1) is considered to be a major cellular uptake mechanism for Fe(2+) and other essential divalent metals, but this protein also mediates uptake of Cd(2+), Pb(2+), and possibly of other toxic divalent metals. The ability of nonessential metals to interact with binding sites for essential metals is critical for their ability to gain access to specific cellular compartments and for their ability to disrupt normal biochemical or physiological functions. Another major mechanism by which metals traverse cell membranes and produce cell injury is by forming complexes whose overall structures mimic those of endogenous molecules. For example, it has long been known that arsenate and vanadate can compete with phosphate for transport and metabolism, thereby disrupting normal cellular functions. Similarly, cromate and molybdate can mimic sulfate in biological systems. Studies in our laboratory have focused on the transport and toxicity of methylmercury (MeHg) and inorganic mercury. Mercury has a high affinity for reduced sulfhydryl groups, including those of cysteine and glutathione (GSH). MeHg-l-cysteine is structurally similar to the amino acid methionine, and this complex is a substrate for transport systems that carry methionine across cell membranes. Once MeHg has entered the cell, some of it binds to GSH, and the resulting MeHg-glutathione complex appears to be a substrate for proteins that mediate cellular export of glutathione S-conjugates, including the apically located MRP2 (multidrug resistance-associated protein 2) transporter, a member of the adenosine triphosphate-binding cassette protein superfamily. Because other toxic metals also form complexes with endogenous molecules, comparable mechanisms may be involved in their membrane transport and disposition.
Topics: Animals; Biological Transport; Cell Membrane; Glutathione; Humans; Mercury; Metals; Methylmercury Compounds; Structure-Activity Relationship
PubMed: 12426113
DOI: 10.1289/ehp.02110s5689 -
The Tohoku Journal of Experimental... Feb 2002The interaction between mercury and selenium may involve a variety of toxicologically and biochemically distinct processes. In this paper, the interaction between... (Review)
Review
The interaction between mercury and selenium may involve a variety of toxicologically and biochemically distinct processes. In this paper, the interaction between inorganic mercury and sodium selenite, the interaction most extensively studied, as well as the interaction between methylmercury (MeHg) and selenium, the interaction perhaps most significant for non-occupational human populations, will be discussed. It has been shown that the former interaction can be understood as a modification of the kinetic behavior of inorganic mercury by selenite, but this interaction may occur only under very limited conditions. On the other hand, the mechanism of the latter interaction is largely unknown, and kinetic modification appears to play only a minor role. An interaction between MeHg and seleno-proteins or a possible interaction between the inorganic mercury, resulting from the demethylation of MeHg, and the selenium may be important. Compared to the experimental findings, little evidence of the toxicological modification of MeHg by selenium was obtained in epidemiological studies.
Topics: Animals; Humans; Mercury; Methylmercury Compounds; Selenium
PubMed: 12498318
DOI: 10.1620/tjem.196.71 -
[The effects of methylmercury on health in children and adults; national and international studies].Nutricion Hospitalaria Nov 2014The benefit of fish consumption in children and adults is well-known. However, it has been pointed out that excessive methylmercury intake due to consumption of... (Review)
Review
The benefit of fish consumption in children and adults is well-known. However, it has been pointed out that excessive methylmercury intake due to consumption of contaminated fish leads to neurological toxicity in children, affecting cognitive function, memory, visual-motor function and language. After the intoxications in Minamata and Iraq, wide-ranging epidemiological studies were carried out in New Zealand, the Faroe Islands and the Seychelles and international recommendations were established for fish consumption in pregnant women and small children. In Spain, the Childhood and Environmental project (INMA, its Spanish acronym) has studied the effects of diet and the environment on fetal and childhood development in different geographic areas of Spain. National and international sudies have demonstrated that mercury concentrations are mainly dependent on fish consumption, although there are variations among countries which can be explained not only by the levels of fish consumption, but also by the type or species of fish that is consumed, as well as other factors. Although the best documented adverse effects of methylmercury are the effects on nervous sytem development in fetuses and newborns, an increasing number of studies indicate that cognitive function, reproduction and, especially, cardiovascular risk in the adult population can also be affected. However, more studies are necessary in order to confirm this and establish the existance of a causal relationship.
Topics: Adult; Animals; Female; Fishes; Humans; Infant; Infant, Newborn; Mercury Poisoning; Methylmercury Compounds; Pregnancy; Seafood
PubMed: 25365002
DOI: 10.3305/nh.2014.30.5.7728