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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 -
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 -
Journal of Preventive Medicine and... Nov 2012Methylmercury is a hazardous substance that is of interest with regard to environmental health, as inorganic mercury circulating in the general environment is dissolved... (Review)
Review
Methylmercury is a hazardous substance that is of interest with regard to environmental health, as inorganic mercury circulating in the general environment is dissolved into freshwater and seawater, condensed through the food chain, ingested by humans, and consequently affects human health. Recently, there has been much interest and discussion regarding the toxicity of methylmercury, the correlation with fish and shellfish intake, and methods of long-term management of the human health effects of methylmercury. What effects chronic exposure to a low concentration of methylmercury has on human health remains controversial. Although the possibility of methylmercury poisoning the heart and blood vessel system, the reproductive system, and the immune system is continuously raised and discussed, and the carcinogenicity of methylmercury is also under discussion, a clear conclusion regarding the human health effects according to exposure level has not yet been drawn. The Joint FAO/WHO Expert Committee on Food Additives proposed to prepare additional fish and shellfish intake recommendations for consumers based on the quantified evaluation of the hazardousness of methylmercury contained in fish and shellfish, methylmercury management in the Korea has not yet caught up with this international trend. Currently, the methylmercury exposure level of Koreans is known to be very high. The starting point of methylmercury exposure management is inorganic mercury in the general environment, but food intake through methylation is the main exposure source. Along with efforts to reduce mercury in the general environment, food intake management should be undertaken to reduce the human exposure to methylmercury in Korea.
Topics: Animals; Environmental Exposure; Fishes; Food Chain; Humans; Mercury Poisoning, Nervous System; Methylmercury Compounds; Neurons; Oxidative Stress; Public Health; Reproduction; Thymocytes
PubMed: 23230465
DOI: 10.3961/jpmph.2012.45.6.353 -
Journal of Toxicology and Environmental... 2012Methylmercury (MeHg) is a global environmental pollutant with significant adverse effects on human health. As the major target of MeHg, the central nervous system (CNS)... (Review)
Review
Methylmercury (MeHg) is a global environmental pollutant with significant adverse effects on human health. As the major target of MeHg, the central nervous system (CNS) exhibits the most recognizable poisoning symptoms. The role of the two major nonneuronal cell types, astrocytes and microglia, in response to MeHg exposure was recently compared. These two cell types share several common features in MeHg toxicity, but interestingly, these cells types also exhibit distinct response kinetics, indicating a cell-specific role in mediating MeHg-induced neurotoxicity. The aim of this study was to review the most recent literature and summarize key features of glial responses to this organometal.
Topics: Astrocytes; Environmental Pollutants; Humans; Methylmercury Compounds; Microglia
PubMed: 22852858
DOI: 10.1080/15287394.2012.697840 -
International Journal of Molecular... Mar 2021Methylmercury (MeHg) toxicity is a major environmental concern. In the aquatic reservoir, MeHg bioaccumulates along the food chain until it is consumed by riverine... (Review)
Review
Methylmercury (MeHg) toxicity is a major environmental concern. In the aquatic reservoir, MeHg bioaccumulates along the food chain until it is consumed by riverine populations. There has been much interest in the neurotoxicity of MeHg due to recent environmental disasters. Studies have also addressed the implications of long-term MeHg exposure for humans. The central nervous system is particularly susceptible to the deleterious effects of MeHg, as evidenced by clinical symptoms and histopathological changes in poisoned humans. In vitro and in vivo studies have been crucial in deciphering the molecular mechanisms underlying MeHg-induced neurotoxicity. A collection of cellular and molecular alterations including cytokine release, oxidative stress, mitochondrial dysfunction, Ca and glutamate dyshomeostasis, and cell death mechanisms are important consequences of brain cells exposure to MeHg. The purpose of this review is to organize an overview of the mercury cycle and MeHg poisoning events and to summarize data from cellular, animal, and human studies focusing on MeHg effects in neurons and glial cells. This review proposes an up-to-date compendium that will serve as a starting point for further studies and a consultation reference of published studies.
Topics: Animals; Bioaccumulation; Brain; Humans; Inflammation; Methylmercury Compounds; Microbiota; Neurotoxicity Syndromes
PubMed: 33803585
DOI: 10.3390/ijms22063101 -
Reviews of Environmental Contamination... 2017There are a number of mechanisms by which alkylmercury compounds cause toxic action in the body. Collectively, published studies reveal that there are some similarities... (Review)
Review
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.
Topics: Calcium; Ethylmercury Compounds; Glutathione; Humans; Methylmercury Compounds; Neurotransmitter Agents; Oxidative Stress
PubMed: 27161558
DOI: 10.1007/398_2016_1 -
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 -
The Indian Journal of Medical Research Oct 2008Neurotoxicity induced by methylmercury (MeHg) increases the formation of reactive radicals and accelerates free radical reactions. This review summarizes recent findings... (Review)
Review
Neurotoxicity induced by methylmercury (MeHg) increases the formation of reactive radicals and accelerates free radical reactions. This review summarizes recent findings in the MeHg-induced formation of free radicals and the role of oxidative stress in its neurotoxicity. Oxidative stress on CNS can produce damage by several interacting mechanisms, including mitochondrial damage with increase in intracellular free Ca(2+), activation and inhibition of enzymes, release of excitatory amino acids, metallothioneins expression, and microtubule disassembly. The nature of antioxidants is discussed and it is suggested that antioxidant enzymes and others antioxidants molecules may protect the central nervous system against neurotoxicity caused by MeHg.
Topics: Animals; Antioxidants; Humans; Methylmercury Compounds; Nervous System; Oxidative Stress
PubMed: 19106435
DOI: No ID Found