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Chemosphere Apr 2020Minamata disease in Japan and the large-scale poisoning by methylmercury (MeHg) in Iraq caused wide public concerns about the risk emanating from mercury for human... (Review)
Review
Minamata disease in Japan and the large-scale poisoning by methylmercury (MeHg) in Iraq caused wide public concerns about the risk emanating from mercury for human health. Nowadays, it is widely known that all forms of mercury induce toxic effects in mammals, and increasing evidence supports the concern that environmentally relevant levels of MeHg could impact normal biological functions in wildlife. The information of mechanism involved in mercurial toxicity is growing but knowledge gaps still exist between the adverse effects and mechanisms of action, especially at the molecular level. A body of data obtained from experimental studies on mechanisms of mercurial toxicity in vivo and in vitro points to that disruption of the antioxidant system may play an important role in the mercurial toxic effects. Moreover, the accumulating evidence indicates that signaling transduction, protein or/and enzyme activity, and gene regulation are involving in mediating toxic and adaptive response to mercury exposure. We conducted here a comprehensive review of mercurial toxic effects on wildlife and human, in particular synthesized key findings of molecular pathways involved in mercurial toxicity from the cells to human. We discuss the molecular evidence related mercurial toxicity to the adverse effects, with particular emphasis on the gene regulation. The further studies relying on Omic analysis connected to adverse effects and modes of action of mercury will aid in the evaluation and validation of causative relationship between health outcomes and gene expression.
Topics: Animals; Environmental Exposure; Environmental Pollutants; Humans; Japan; Mercury; Mercury Poisoning, Nervous System; Methylmercury Compounds
PubMed: 31881386
DOI: 10.1016/j.chemosphere.2019.125586 -
Neurotoxicology Jul 2023Methylmercury (MeHg) is neurotoxic at high levels and particularly affects the developing brain. One proposed mechanism of MeHg neurotoxicity is alteration of the... (Review)
Review
PURPOSE OF REVIEW
Methylmercury (MeHg) is neurotoxic at high levels and particularly affects the developing brain. One proposed mechanism of MeHg neurotoxicity is alteration of the epigenetic programming. In this review, we summarise the experimental and epidemiological literature on MeHg-associated epigenetic changes.
RECENT FINDINGS
Experimental and epidemiological studies have identified changes in DNA methylation following in utero exposure to MeHg, and some of the changes appear to be persistent. A few studies have evaluated associations between MeHg-related changes in DNA methylation and neurodevelopmental outcomes. Experimental studies reveal changes in histone modifications after MeHg exposure, but we lack epidemiological studies supporting such changes in humans. Experimental and epidemiological studies have identified microRNA-related changes associated with MeHg; however, more research is needed to conclude if these changes lead to persistent and toxic effects.
SUMMARY
MeHg appears to interfere with epigenetic processes, potentially leading to persistent changes. However, observed associations of mercury with epigenetic changes are as of yet of unknown relevance to neurodevelopmental outcomes.
Topics: Humans; Methylmercury Compounds; DNA Methylation; Brain; Neurotoxicity Syndromes; Epigenesis, Genetic
PubMed: 37164037
DOI: 10.1016/j.neuro.2023.05.004 -
The Science of the Total Environment Dec 2022Anthropogenic mercury (Hg) undergoes long-range transport to the Arctic where some of it is transformed into methylmercury (MeHg), potentially leading to high exposure...
Anthropogenic mercury (Hg) undergoes long-range transport to the Arctic where some of it is transformed into methylmercury (MeHg), potentially leading to high exposure in some Arctic inhabitants and wildlife. The environmental exposure of Hg is determined not just by the amount of Hg entering the Arctic, but also by biogeochemical and ecological processes occurring in the Arctic. These processes affect MeHg uptake in biota by regulating the bioavailability, methylation and demethylation, bioaccumulation and biomagnification of MeHg in Arctic ecosystems. Here, we present a new budget for pools and fluxes of MeHg in the Arctic and review the scientific advances made in the last decade on processes leading to environmental exposure to Hg. Methylation and demethylation are key processes controlling the pool of MeHg available for bioaccumulation. Methylation of Hg occurs in diverse Arctic environments including permafrost, sediments and the ocean water column, and is primarily a process carried out by microorganisms. While microorganisms carrying the hgcAB gene pair (responsible for Hg methylation) have been identified in Arctic soils and thawing permafrost, the formation pathway of MeHg in oxic marine waters remains less clear. Hotspots for methylation of Hg in terrestrial environments include thermokarst wetlands, ponds and lakes. The shallow sub-surface enrichment of MeHg in the Arctic Ocean, in comparison to other marine systems, is a possible explanation for high MeHg concentrations in some Arctic biota. Bioconcentration of aqueous MeHg in bacteria and algae is a critical step in the transfer of Hg to top predators, which may be dampened or enhanced by the presence of organic matter. Variable trophic position has an important influence on MeHg concentrations among populations of top predator species such as ringed seal and polar bears distributed across the circumpolar Arctic. These scientific advances highlight key processes that affect the fate of anthropogenic Hg deposited to Arctic environments.
Topics: Arctic Regions; Ecosystem; Environmental Monitoring; Mercury; Methylmercury Compounds; Soil; Water; Water Pollutants, Chemical
PubMed: 35882324
DOI: 10.1016/j.scitotenv.2022.157445 -
International Journal of Molecular... Jun 2022Methylmercury (MeHg) is a widely known environmental pollutant that causes severe neurotoxicity. MeHg-induced neurotoxicity depends on various cellular conditions,... (Review)
Review
Methylmercury (MeHg) is a widely known environmental pollutant that causes severe neurotoxicity. MeHg-induced neurotoxicity depends on various cellular conditions, including differences in the characteristics of tissues and cells, exposure age (fetal, childhood, or adulthood), and exposure levels. Research has highlighted the importance of oxidative stress in the pathogenesis of MeHg-induced toxicity and the site- and cell-specific nature of MeHg-induced neurotoxicity. The cerebellar granule cells and deeper layer cerebrocortical neurons are vulnerable to MeHg. In contrast, the hippocampal neurons are resistant to MeHg, even at high mercury accumulation levels. This review summarizes the mechanisms underlying MeHg-mediated intracellular events that lead to site-specific neurotoxicity. Specifically, we discuss the mechanisms associated with the redox ability, neural outgrowth and synapse formation, cellular signaling pathways, epigenetics, and the inflammatory conditions of microglia.
Topics: Adult; Child; Humans; Mercury; Methylmercury Compounds; Neurons; Neurotoxicity Syndromes; Oxidative Stress
PubMed: 35806222
DOI: 10.3390/ijms23137218 -
The Journal of Toxicological Sciences 2021Methylmercury (MeHg), the causal substrate in Minamata disease, can lead to severe and chronic neurological disorders. The main symptom of Minamata disease is sensory...
Methylmercury (MeHg), the causal substrate in Minamata disease, can lead to severe and chronic neurological disorders. The main symptom of Minamata disease is sensory impairment in the four extremities; however, the sensitivity of individual sensory modalities to MeHg has not been investigated extensively. In the present study, we performed stimulus-response behavioral experiments in MeHg-exposed rats to compare the sensitivities to pain, heat, cold, and mechanical sensations. MeHg (6.7 mg/kg/day) was orally administered to 9-week-old Wistar rats for 5 days and discontinued for 2 days, then administered daily for another 5 days. The four behavioral experiments were performed daily on each rat from the beginning of MeHg treatment for 68 days. The pain sensation decreased significantly from day 11 onwards, but recovered to control levels on day 48. Other sensory modalities were not affected by MeHg exposure. These findings suggest that the pain sensation is the sensory modality most susceptive to MeHg toxicity and that this sensitivity is reversible following discontinuation of the exposure.
Topics: Animals; Hypesthesia; Male; Mercury Poisoning, Nervous System; Methylmercury Compounds; Pain; Rats, Wistar; Rats
PubMed: 34078837
DOI: 10.2131/jts.46.303 -
Neurotoxicology May 2023Methylmercury (MeHg) is a concerning contaminant due to its ubiquity and harmful effects on organisms. Although birds are important models in the neurobiology of vocal... (Review)
Review
Methylmercury (MeHg) is a concerning contaminant due to its ubiquity and harmful effects on organisms. Although birds are important models in the neurobiology of vocal learning and adult neuroplasticity, the neurotoxic effects of MeHg are less understood in birds than mammals. We surveyed the literature on MeHg effects on biochemical changes in the avian brain. Publication rates of papers related to neurology and/or birds and/or MeHg increased with time and can be linked with historical events, regulations, and increased understanding of MeHg cycling in the environment. However, publications on MeHg effects on the avian brain remain relatively low across time. The neural effects measured to evaluate MeHg neurotoxicity in birds changed with time and researcher interest. The measures most consistently affected by MeHg exposure in birds were markers of oxidative stress. NMDA, acetylcholinesterase, and Purkinje cells also seem sensitive to some extent. MeHg exposure has the potential to affect most neurotransmitter systems but more studies are needed for validation in birds. We also review the main mechanisms of MeHg-induced neurotoxicity in mammals and compare it to what is known in birds. The literature on MeHg effects on the avian brain is limited, preventing full construction of an adverse outcome pathway. We identify research gaps for taxonomic groups such as songbirds, and age- and life-stage groups such as immature fledgling stage and adult non-reproductive life stage. In addition, results are often inconsistent between experimental and field studies. We conclude that future neurotoxicological studies of MeHg impacts on birds need to better connect the numerous aspects of exposure from molecular physiological effects to behavioural outcomes that would be ecologically or biologically relevant for birds, especially under challenging conditions.
Topics: Animals; Methylmercury Compounds; Acetylcholinesterase; Brain; Oxidative Stress; Neurotoxicity Syndromes; Birds; Mammals
PubMed: 37059311
DOI: 10.1016/j.neuro.2023.04.004 -
Biological & Pharmaceutical Bulletin 2023Methylmercury (MeHg) is the causal substrate of Minamata disease and a major environmental toxicant. MeHg is widely distributed, mainly in the ocean, meaning its... (Review)
Review
Methylmercury (MeHg) is the causal substrate of Minamata disease and a major environmental toxicant. MeHg is widely distributed, mainly in the ocean, meaning its bioaccumulation in seafood is a considerable problem for human health. MeHg has been intensively investigated and is known to induce inflammatory responses and neurodegeneration. However, the relationship between MeHg-induced inflammatory responses and neurodegeneration is not understood. In the present review, we first describe recent findings showing an association between inflammatory responses and certain MeHg-unrelated neurological diseases caused by neurodegeneration. In addition, cell-specific MeHg-induced inflammatory responses are summarized for the central nervous system including those of microglia, astrocytes, and neurons. We also describe MeHg-induced inflammatory responses in peripheral cells and tissue, such as macrophages and blood. These findings provide a concept of the relationship between MeHg-induced inflammatory responses and neurodegeneration, as well as direction for future research of MeHg-induced neurotoxicity.
Topics: Humans; Methylmercury Compounds; Neurotoxicity Syndromes; Inflammation; Astrocytes; Central Nervous System
PubMed: 37661394
DOI: 10.1248/bpb.b23-00075 -
Neurotoxicology Mar 2024
Topics: Animals; Methylmercury Compounds; Cohort Studies; Seafood; Fishes; Seychelles; Food Contamination
PubMed: 38367819
DOI: 10.1016/j.neuro.2024.02.004 -
Environmental Science & Technology Apr 2023Methylmercury (MeHg) is a potent neurotoxin and has great adverse health impacts on humans. Organisms and sunlight-mediated demethylation are well-known detoxification...
Methylmercury (MeHg) is a potent neurotoxin and has great adverse health impacts on humans. Organisms and sunlight-mediated demethylation are well-known detoxification pathways of MeHg, yet whether abiotic environmental components contribute to MeHg degradation remains poorly known. Here, we report that MeHg can be degraded by trivalent manganese (Mn(III)), a naturally occurring and widespread oxidant. We found that 28 ± 4% MeHg could be degraded by Mn(III) located on synthesized Mn dioxide (MnO) surfaces during the reaction of 0.91 μg·L MeHg and 5 g·L mineral at an initial pH of 6.0 for 12 h in 10 mM NaNO at 25 °C. The presence of low-molecular-weight organic acids (e.g., oxalate and citrate) substantially enhances MeHg degradation by MnO via the formation of soluble Mn(III)-ligand complexes, leading to the cleavage of the carbon-Hg bond. MeHg can also be degraded by reactions with Mn(III)-pyrophosphate complexes, with apparent degradation rate constants comparable to those by biotic and photolytic degradation. Thiol ligands (cysteine and glutathione) show negligible effects on MeHg demethylation by Mn(III). This research demonstrates potential roles of Mn(III) in degrading MeHg in natural environments, which may be further explored for remediating heavily polluted soils and engineered systems containing MeHg.
Topics: Humans; Manganese; Methylmercury Compounds; Mercury; Oxidants; Cysteine
PubMed: 36995950
DOI: 10.1021/acs.est.3c00532 -
The Science of the Total Environment Sep 2024Mercury is a hazardous heavy metal that is distributed worldwide in aquatic ecosystems. Methylmercury (MeHg) poses significant toxicity risks to aquatic organisms,... (Review)
Review
Mercury is a hazardous heavy metal that is distributed worldwide in aquatic ecosystems. Methylmercury (MeHg) poses significant toxicity risks to aquatic organisms, primarily through bioaccumulation and biomagnification, due to its strong affinity for protein thiol groups, which results in negative effects even at low concentrations. MeHg exposure can cause various physiological changes, oxidative stress, neurotoxicity, metabolic disorders, genetic damage, and immunotoxicity. To assess the risks of MeHg contamination in actual aquatic ecosystems, it is important to understand how MeHg interacts with environmental factors such as temperature, pH, dissolved organic matter, salinity, and other pollutants such as microplastics and organic compounds. Complex environmental conditions can cause potential toxicity, such as synergistic, antagonistic, and unchanged effects, of MeHg in aquatic organisms. This review focuses on demonstrating the toxic effects of single MeHg exposure and the interactive relationships between MeHg and surrounding environmental factors or pollutants on aquatic organisms. Our review also recommends further research on biological and molecular responses in aquatic organisms to better understand the potential toxicity of combinational exposure.
Topics: Methylmercury Compounds; Aquatic Organisms; Water Pollutants, Chemical; Animals; Environmental Monitoring
PubMed: 38823721
DOI: 10.1016/j.scitotenv.2024.173574