Effects of sublethal methylmercury and food stress on songbird energetic performance: metabolic rates, molt and feather quality.

Organisms regularly adjust their physiology and energy balance in response to predictable seasonal environmental changes. Stressors and contaminants have the potential to disrupt these critical seasonal transitions. No studies have investigated how simultaneous exposure to the ubiquitous toxin methylmercury (MeHg) and food stress affects birds' physiological performance across seasons. We quantified several aspects of energetic performance in song sparrows, Melospiza melodia, exposed or not to unpredictable food stress and MeHg in a 2×2 experimental design, over 3 months during the breeding season, followed by 3 months post-exposure. Birds exposed to food stress had reduced basal metabolic rate and non-significant higher factorial metabolic scope during the exposure period, and had a greater increase in lean mass throughout most of the experimental period. Birds exposed to MeHg had increased molt duration, and increased mass:length ratio of some of their primary feathers. Birds exposed to the combined food stress and MeHg treatment often had responses similar to the stress-only or MeHg-only exposure groups, suggesting these treatments affected physiological performance through different mechanisms and resulted in compensatory or independent effects. Because the MeHg and stress variables were selected in candidate models with a ΔAICc lower than 2 but the 95% confidence interval of these variables overlapped zero, we found weak support for MeHg effects on all measures except basal metabolic rate, and for food stress effects on maximum metabolic rate, factorial metabolic scope and feather mass:length ratio. This suggests that MeHg and food stress effects on these measures are statistically identified but not simple and/or were too weak to be detected via linear regression. Overall, combined exposure to ecologically relevant MeHg and unpredictable food stress during the breeding season does not appear to induce extra energetic costs for songbirds in the post-exposure period. However, MeHg effects on molt duration could carry over across multiple annual cycle stages.

Gabapentin improves neuropathic pain in Minamata disease model rats.

BACKGROUND: Methylmercury (MeHg), the causative agent of Minamata disease, damages the cranial nervous system and causes specific sensory disturbances, especially hypoesthesia, in the extremities. However, recent reports demonstrate that patients with chronic Minamata disease conversely develop neuropathic pain in the lower extremities. Studies on our established Minamata disease model rats showed that MeHg-mediated neurodegeneration might induce neuropathic pain by over time through inducing rewiring with neuronal activation in the somatosensory cortex via microglial activation in the spinal dorsal horn. METHODS: In this study, the effects of gabapentin, a potentially effective treatment for neuropathic pain, was evaluated using this Minamata disease model rats. To further elucidate the mechanism of its medicinal effects, histochemical and biochemical analyses of the nervous system of Minamata disease model rats were conducted. RESULTS: Gabapentin treatment restored the reduction in the pain threshold caused by MeHg exposure in rats. Histochemical and biochemical analyses revealed that gabapentin showed no effect on MeHg-induced neurodegeneration in entire nervous system and microglial activation in the spinal dorsal horn. However, it was shown that gabapentin may reduce excessive synaptogenesis through its antagonist action on the alpha2-delta-1 subunit of calcium channels in the somatosensory cortex. CONCLUSIONS: These results indicate that gabapentin may alleviated neuropathic pain in MeHg poisoning, as typified by Minamata disease, by reversibly modulation synaptic rewiring in the somatosensory cortex.

Distribution of mercury and methylmercury in aquacultured fish in special waters formed by coal mining subsidence.

In China, fence net aquaculture practices have been established in some subsidence waters that have been formed in coal mining subsidence areas. Within this dynamic ecological context, diverse fish species grow continuously until being harvested at the culmination of their production cycle. The purpose of this study was to investigate diverse factors influencing the bioavailability and distribution of mercury (Hg) and methylmercury (MeHg), which have high physiological toxicity in fish, in the Guqiao coal mining subsidence area in Huainan, China. Mercury and MeHg were analyzed in 38 fish samples of eight species using direct mercury analysis (DMA-80) and gas chromatography-cold vapor atomic fluorescence spectrometry (GC-CVAFAS). The analysis results show that the ranges of Hg and MeHg content and methylation rate in the fish were 7.84-85.18 ng/g, 0.52-3.52 ng/g, and 0.81-42.68 %, respectively. Meanwhile, conclusions are also summarized as following: (1) Monophagous herbivorous fish that were fed continuously in fence net aquaculture areas had higher MeHg levels and mercury methylation rates than carnivorous fish. Hg and MeHg contents were affected by different feeding habits of fish. (2) Bottom-dwelling fish show higher MeHg levels, and habitat selection in terms of water depth also partially affected the MeHg content of fish. (3) The effect of fence net aquaculture on methylation of fish in subsidence water is mainly from feed and mercury-containing bottom sediments. However, a time-lag is observed in the physiological response of benthic fishes to the release of Hg from sediments. Our findings provides baseline reference data for the ecological impact of fence net aquaculture in waters affected by soil subsidence induced by coal mining in China. Prevalent environmental contaminants within coal mining locales, notably Hg, may infiltrate rain-induced subsidence waters through various pathways.

Moisture contents regulate peat water-leachable concentrations of methylmercury, inorganic mercury, and dissolved organic matter from boreal peat soils.

Boreal peatlands are "hotspots" of net methylmercury (MeHg) production and may become drier in the future due to climate change. This study investigates a critical gap by analyzing the nuanced relationship between soil moisture content and the release of MeHg, inorganic mercury (IHg), sulfate (SO42-), and dissolved organic matter (DOM) in a laboratory incubation of boreal peat soils. Dried peat soils exhibited heightened releases of IHg, MeHg, and SO42- during re-wetting events. Both dried and saturated peat soils released more DOM than moist peat soils during re-wetting events, and DOM released from dried soils had higher bioaccessibility than that from the saturated soils (p<0.05). There was an equilibrium of IHg concentrations between peat soils and pore waters, but long-term severe drought may disrupt this equilibrium and then release more IHg to pore waters during re-wetting events. Contrary to expectations, positive relationships between IHg concentrations and SUVA254 did not exist in all treatments. MeHg and SO42- were depleted quickly because there was no external input of Hg and SO42- to this static system. More bioaccessible DOM than aromatic DOM was released from peat soils with different soil moisture contents after 32 weeks during the re-wetting event (p<0.05). These results imply that re-wetting of peat soils after droughts can increase the release of MeHg from peat soils and may also increase net MeHg production due to the release of SO42- and bioaccessible DOM from peat soils, reshaping our understanding of soil moisture's role in mercury dynamics. This novel insight into soil moisture and MeHg dynamics carries significant implications for mitigating mercury contamination in aquatic ecosystems.

Toxicity of methylmercury in aquatic organisms and interaction with environmental factors and coexisting pollutants: A 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.

Economic benefit of ecological remediation of mercury pollution in southwest China 2007-2022.

Methylmercury (MeHg) exposure via rice consumption poses health risk to residents in mercury contaminated areas, such as the Wanshan Hg mining area (WSMA) in southwest China. Making use of the published data for WSMA, this study developed a database of rice MeHg concentrations for different villages in this region for the years of 2007, 2012, 2017, and 2019. The temporal changes of human MeHg exposure, health effects, and economic benefits under different ecological remediation measures were then assessed. Results from this study revealed a decrease of 3.88 µg/kg in rice MeHg concentration and a corresponding reduction of 0.039 µg/kg/d in probable daily intake of MeHg in 2019 compared to 2007 on regional average in the WSMA. Ecological remediation measures in this region resulted in the accumulated economic benefits of $38.7 million during 2007-2022, of which 84 % was from pollution source treatment and 16 % from planting structure adjustment. However, a flooding event in 2016 led to an economic loss of $2.43 million (0.38 % of regional total Gross Domestic Product). Planting structure adjustment generates the greatest economic benefits in the short term, whereas pollution source treatment maximizes economic benefits in the long term and prevents the perturbations from flooding event. These findings demonstrate the importance of ecological remediation measures in Hg polluted areas and provide the foundation for risk assessment of human MeHg exposure via rice consumption.

Dimethylmercury as a Source of Monomethylmercury in a Highly Productive Upwelling System.

Monomethylmercury (MMHg) is a neurotoxicant that biomagnifies in marine food webs, reaching high concentrations in apex predators. To predict changes in oceanic MMHg concentrations, it is important to quantify the sources and sinks of MMHg. Here, we study mercury speciation in the California Current System through cruise sampling and modeling. Previous work in the California Current System has found that upwelling transports mercury-enriched deep waters to productive surface waters. These upwelled waters originate within the California Undercurrent water mass and are subsequently advected as a surface water parcel to the California Current. Between the two major water masses, we find that compared to the California Current, the California Undercurrent contains elevated dissolved total mercury (THg) and dimethylmercury (DMHg) concentrations by 59 and 69%, respectively. We explain that these differences result from losses during advection, specifically scavenging of THg and DMHg demethylation. We calculate a net DMHg demethylation rate of 2.0 ± 1.1% d-1 and build an empirically constrained mass budget model to demonstrate that net DMHg demethylation accounts for 61% of surface MMHg sources. These findings illustrate that DMHg is a significant source of MMHg in this region, challenging the current understanding of the major sources of marine MMHg.

A genome catalogue of mercury-methylating bacteria and archaea from sediments of a boreal river facing human disturbances.

Methyl mercury, a toxic compound, is produced by anaerobic microbes and magnifies in aquatic food webs, affecting the health of animals and humans. The exploration of mercury methylators based on genomes is still limited, especially in the context of river ecosystems. To address this knowledge gap, we developed a genome catalogue of potential mercury-methylating microorganisms. This was based on the presence of hgcAB from the sediments of a river affected by two run-of-river hydroelectric dams, logging activities and a wildfire. Through the use of genome-resolved metagenomics, we discovered a unique and diverse group of mercury methylators. These were dominated by members of the metabolically versatile Bacteroidota and were particularly rich in microbes that ferment butyrate. By comparing the diversity and abundance of mercury methylators between sites subjected to different disturbances, we found that ongoing disturbances, such as the input of organic matter related to logging activities, were particularly conducive to the establishment of a mercury-methylating niche. Finally, to gain a deeper understanding of the environmental factors that shape the diversity of mercury methylators, we compared the mercury-methylating genome catalogue with the broader microbial community. The results suggest that mercury methylators respond to environmental conditions in a manner similar to the overall microbial community. Therefore, it is crucial to interpret the diversity and abundance of mercury methylators within their specific ecological context.

Mercury-induced toxicity: Mechanisms, molecular pathways, and gene regulation.

Mercury is a well-known neurotoxicant for humans and wildlife. The epidemic of mercury poisoning in Japan has clearly demonstrated that chronic exposure to methylmercury (MeHg) results in serious neurological damage to the cerebral and cerebellar cortex, leading to the dysfunction of the central nervous system (CNS), especially in infants exposed to MeHg in utero. The occurrences of poisoning have caused a wide public concern regarding the health risk emanating from MeHg exposure; particularly those eating large amounts of fish may experience the low-level and long-term exposure. There is growing evidence that MeHg at environmentally relevant concentrations can affect the health of biota in the ecosystem. Although extensive in vivo and in vitro studies have demonstrated that the disruption of redox homeostasis and microtube assembly is mainly responsible for mercurial toxicity leading to adverse health outcomes, it is still unclear whether we could quantitively determine the occurrence of interaction between mercurial and thiols and/or selenols groups of proteins linked directly to outcomes, especially at very low levels of exposure. Furthermore, intracellular calcium homeostasis, cytoskeleton, mitochondrial function, oxidative stress, neurotransmitter release, and DNA methylation may be the targets of mercury compounds; however, the primary targets associated with the adverse outcomes remain to be elucidated. Considering these knowledge gaps, in this article, we conducted a comprehensive review of mercurial toxicity, focusing mainly on the mechanism, and genes/proteins expression. We speculated that comprehensive analyses of transcriptomics, proteomics, and metabolomics could enhance interpretation of "omics" profiles, which may reveal specific biomarkers obviously correlated with specific pathways that mediate selective neurotoxicity.

Elevated CO2 exacerbates the risk of methylmercury exposure in consuming aquatic products: Evidence from a complex paddy wetland ecosystem.

Elevated CO2 levels and methylmercury (MeHg) pollution are important environmental issues faced across the globe. However, the impact of elevated CO2 on MeHg production and its biological utilization remains to be fully understood, particularly in realistic complex systems with biotic interactions. Here, a complete paddy wetland microcosm, namely, the rice-fish-snail co-culture system, was constructed to investigate the impacts of elevated CO2 (600 ppm) on MeHg formation, bioaccumulation, and possible health risks, in multiple environmental and biological media. The results revealed that elevated CO2 significantly increased MeHg concentrations in the overlying water, periphyton, snails and fish, by 135.5%, 66.9%, 45.5%, and 52.1%, respectively. A high MeHg concentration in periphyton, the main diet of snails and fish, was the key factor influencing the enhanced MeHg in aquatic products. Furthermore, elevated CO2 alleviated the carbon limitation in the overlying water and proliferated green algae, with subsequent changes in physico-chemical properties and nutrient concentrations in the overlying water. More algal-derived organic matter promoted an enriched abundance of Archaea-hgcA and Deltaproteobacteria-hgcA genes. This consequently increased the MeHg in the overlying water and food chain. However, MeHg concentrations in rice and soil did not increase under elevated CO2, nor did hgcA gene abundance in soil. The results reveal that elevated CO2 exacerbated the risk of MeHg intake from aquatic products in paddy wetland, indicating an intensified MeHg threat under future elevated CO2 levels.

Degradation of organic mercury in high salt environments by a marine aerobic bacterium Alteromonas macleodii KD01.

Mercury (Hg), particularly organic mercury, poses a global concern due to its pronounced toxicity and bioaccumulation. Bioremediation of organic mercury in high-salt wastewater faces challenges due to the growth limitations imposed by elevated Cl- and Na+ concentrations on microorganisms. In this study, an isolated marine bacterium Alteromonas macleodii KD01 was demonstrated to degrade methylmercury (MeHg) efficiently in seawater and then was applied to degrade organic mercury (MeHg, ethylmercury, and thimerosal) in simulated high-salt wastewater. Results showed that A. macleodii KD01 can rapidly degrade organic mercury (within 20 min) even at high concentrations (>10 ng/mL), volatilizing a portion of Hg from the wastewater. Further analysis revealed an increased transcription of organomercury lyase (merB) with rising organic mercury concentrations during the exposure process, suggesting the involvement of mer operon (merA and merB). These findings highlight A. macleodii KD01 as a promising candidate for addressing organic mercury pollution in high-salt wastewater.

Global survey of hgcA-carrying genomes in marine and freshwater sediments: Insights into mercury methylation processes.

Mercury (Hg) methylation is a microbially mediated process that produces methylmercury (MeHg), a bioaccumulative neurotoxin. A highly conserved gene pair, hgcAB, is required for Hg methylation, which provides a basis for identifying Hg methylators and evaluating their genomic composition. In this study, we conducted a large-scale omics analysis in which 281 metagenomic freshwater and marine sediment samples from 46 geographic locations across the globe were queried. Specific objectives were to examine the prevalence of Hg methylators, to identify horizontal gene transfer (HGT) events involving hgcAB within Hg methylator communities, and to identify associations between hgcAB and microbial biochemical functions/genes. Hg methylators from the phyla Desulfobacterota and Bacteroidota were dominant in both freshwater and marine sediments while Firmicutes and methanogens belonging to Euryarchaeota were identified only in freshwater sediments. Novel Hg methylators were found in the Phycisphaerae and Planctomycetia classes within the phylum Planctomycetota, including potential hgcA-carrying anammox metagenome-assembled genomes (MAGs) from Candidatus Brocadiia. HGT of hgcA and hgcB were identified in both freshwater and marine methylator communities. Spearman's correlation analysis of methylator genomes suggested that in addition to sulfide, thiosulfate, sulfite, and ammonia may be important parameters for Hg methylation processes in sediments. Overall, our results indicated that the biochemical drivers of Hg methylation vary between marine and freshwater sites, lending insight into the influence of environmental perturbances, such as a changing climate, on Hg methylation processes.

Organ-specific mercury stable isotopes, speciation and particle measurements reveal methylmercury detoxification processes in Atlantic Bluefin Tuna.

Identifying metabolism and detoxification mechanisms of Hg in biota has important implications for biomonitoring, ecotoxicology, and food safety. Compared to marine mammals and waterbirds, detoxification of MeHg in fish is understudied. Here, we investigated Hg detoxification in Atlantic bluefin tuna Thunnus thynnus using organ-specific Hg and Se speciation data, stable Hg isotope signatures, and Hg and Se particle measurements in multiple tissues. Our results provide evidence for in vivo demethylation and biomineralization of HgSe particles, particularly in spleen and kidney. We observed a maximum range of 1.83‰ for δ202Hg between spleen and lean muscle, whereas Δ199Hg values were similar across all tissues. Mean percent methylmercury ranged from 8% in spleen to 90% in lean muscle. The particulate masses of Hg and Se were higher in spleen and kidney (Hg: 61% and 59%, Se: 12% and 6%, respectively) compared to muscle (Hg: 2%, Se: 0.05%). Our data supports the hypothesis of an organ-specific, two-step detoxification of methylmercury in wild marine fish, consisting of demethylation and biomineralization, like reported for waterbirds. While mass dependent fractionation signatures were highly organ specific, stable mass independent fractionation signatures across all tissues make them potential candidates for source apportionment studies of Hg using ABFT.

Total mercury, methylmercury, and their possible controlling factors in soils of typical coastal wetlands in China.

Coastal wetland soils play a critical role in the global mercury (Hg) cycle, serving as both an important repository for total mercury (THg) and a hotspot for methylmercury (MeHg) production. This study investigated Hg pollution in soils dominated by Phragmites australis (PA) and Spartina alterniflora (SA) across five representative China's coastal wetlands (Yellow River (YR), Linhong River (LHR), Yangtze River (CJR), Min River (MR), and Nanliu River (NLR)). The THg concentrations ranged from 16.7 to 446.0 (96.3 ± 59.3 ng g-1, dw), while MeHg concentrations varied from 0.01 to 0.81 (0.12 ± 0.12 ng g-1, dw). We further evaluated Hg risk in these wetlands using potential ecological risk index (Er) and geographical enrichment factor (Igeo). Most wetlands exhibited low to moderate ecological risk, except the PA habitat in the YR wetland, showing moderate to high risk. Soil organic matter significantly influenced THg and MeHg distribution, while MeHg% correlated well with soil salinity and pH. These findings highlight the importance of organic-rich coastal wetland soils in THg and MeHg accumulation, with the soil properties influencing net MeHg production. Furthermore, SA habitat generally exhibited higher MeHg%, suggesting its invasion elevates the ecological risk of MeHg in coastal wetlands. ENVIRONMENTAL IMPLICATION: Mercury (Hg), a global pollutant, poses great risks to wildlife and humans. Since industrialization, anthropogenic Hg release surpassed natural sources. Long-term exposure leads to biomagnification of Hg. This study assessed Hg and methylmercury pollution and risks in soils of five China's coastal wetlands dominated by Phragmites australis and Spartina alterniflora. Environmental factors (total carbon, total organic carbon, total nitrogen, salinity, pH) were analyzed to reveal key variables influencing Hg pollution and methylation. Essential for quantifying Hg pollution in coastal wetlands, the findings provide a scientific basis for effective wetland conservation policies and addressing environmental health in these regions.

Study of mercury bioavailability using isotope dilution and BCR sequential extraction in the sediment of Yellow Sea and East China Sea, China.

Mercury (Hg) emitted from East Asian has increased the risk of Hg in China Marginal Seas for decades. However, the speciation of Hg (especially the bioavailable Hg) in these regions remains unclear. To address this problem, we analyzed total Hg (THg) and methylmercury (MeHg) in the sediment and porewater of Yellow sea (YS) and East China Sea (ECS) and determined the speciation of Hg using both improved BCR sequential extraction and isotope dilution (ID) techniques. Nearshore areas of YS and ECS exhibited higher THg levels in sediments and porewater, suggesting the significant contribution of terrestrial inputs. The spatial distribution of MeHg showed similar trends with THg, but the sites with higher MeHg concentrations did not align with those of THg. The improved BCR sequential extraction method showed the residual fraction dominated Hg content (∼44 %) in both systems, with a minor bioavailable carbonate fraction (1 %). The Spearman correlation analysis indicates that Eh and pH are the two factors significantly affected Hg bioavailability in the sediment. The bioavailability of Hg (estimated by the BCR method) showed a significant positive correlation with MeHg levels in the sediment (R²=0.47, P < 0.05), suggesting that BCR can be used to estimate the potential of Hg methylation in the sediment. However, the extent of bioavailable Hg in BCR and ID method were 1.15 ± 0.38 % and 29.5 ± 14.8 %, respectively, implying that Hg bioavailability may be underestimated by BCR techniques compared to ID methods (T-test, P < 0.01).

Uncovering the Role of Methylmercury on DNA Lesions at Cytotoxic Concentrations in Glutathione-Depleted Cells: Insights from Experimental and Computational Studies.

Organomercurials (RHg+), especially methylmercury (MeHg+) and ethylmercury (EtHg+), are considered to be more neurotoxic than the inorganic counterpart (Hg2+). They cause massive DNA damage in cells, especially in neurons, where cellular glutathione (GSH) levels are significantly low. However, the mechanism by which RHg+ exerts massive DNA damage at cytotoxic concentrations in brain cells remains obscure. In this study, we investigated the effect of RHg+ on the structural and electronic properties of nucleosides and its effects on DNA damage. The direct interaction of RHg+ with the nucleoside significantly weakens N-glycosidic bonds, decreases the C-H bond energy of sugar moieties, and increases the electrophilicity of the C8-center of purine bases. As a consequence, RHg+-conjugated DNA molecules are extremely labile and highly sensitive to any nucleophiles/radicals present in GSH-depleted cells and, thus, undergo enhanced oxidative and unusual alkylative DNA damage. We also report a functional model of organomercurial lyase, which showed excellent cytoprotective effect against RHg+-induced cytotoxicity; this reverses the activity of glutathione reductase inhibited by MeHgCl and ceases oxidative and alkylating DNA damage. This intriguing finding provides new mechanistic insight into the mode of action of organomercurials in GSH-depleted cells and their adverse effects on individuals with neurodegenerative disorders associated with oxidative stress.

Methylmercury cycling in the Bohai Sea and Yellow Sea: Reasons for the low system efficiency of methylmercury production.

Coastal seas contribute the majority of human methylmercury (MeHg) exposure via marine fisheries. The terrestrial area surrounding the Bohai Sea and Yellow Sea (BS and YS) is one of the mercury (Hg) emission "hot spots" in the world, resulting in high concentrations of Hg in BS and YS seawater in comparison to other marine systems. However, comparable or even lower Hg levels were detected in seafood from the BS and YS than other coastal regions around the word, suggesting a low system bioaccumulation of Hg. Reasoning a low system efficiency of MeHg production (represented by MeHg/THg (total Hg) in seawater) may be present in these two systems, seven cruises were conducted in the BS and YS to test this hypothesis. MeHg/THg ratios in BS and YS seawater were found to be lower than that in most coastal systems, indicating that the system efficiency of MeHg production is relatively lower in the BS and YS. The low system efficiency of MeHg production reduces the risk of Hg in the BS and YS with high Hg discharge intensity. By measuring in situ production and degradation of MeHg using double stable isotope addition method, and MeHg discharge flux from various sources and its exchange at various interfaces, the budgets of MeHg in the BS and YS were estimated. The results indicate that in situ methylation and demethylation are the major source and sink of MeHg in the BS and YS. By comparing the potential controlling processes and environmental parameters for MeHg/THg in the BS and YS with the other coastal seas, estuaries and bays, lower transport efficiency of inorganic Hg from water column to the sediment, slower methylation of Hg, and rapid demethylation of MeHg were identified to be major reasons for the low system efficiency of MeHg production in the BS and YS. This study highlights the necessity of monitoring the system efficiency of MeHg production, associated processes, and controlling parameters to evaluate the efficiency of reducing Hg emissions in China as well as the other countries.

Early life exposure to mercury and relationships with telomere length and mitochondrial DNA content in European children.

BACKGROUND: Telomere length (TL) and mitochondrial function expressed as mitochondrial DNA copy number (mtDNAcn) are biomarkers of aging and oxidative stress and inflammation, respectively. Methylmercury (MeHg), a common pollutant in fish, induces oxidative stress. We hypothesized that elevated oxidative stress from exposure to MeHg decreases mtDNAcn and shortens TL. METHODS: Study participants are 6-11-year-old children from the HELIX multi-center birth cohort study, comprising six European countries. Prenatal and postnatal total mercury (THg) concentrations were measured in blood samples, TL and mtDNAcn were determined in child DNA. Covariates and confounders were obtained by questionnaires. Robust regression models were run, considering sociodemographic and lifestyle covariates, as well as fish consumption. Sex, ethnicity, and fish consumption interaction models were also run. RESULTS: We found longer TL with higher pre- and postnatal THg blood concentrations, even at low-level THg exposure according to the RfD proposed by the US EPA. The prenatal association showed a significant linear relationship with a 3.46 % increase in TL for each unit increased THg. The postnatal association followed an inverted U-shaped marginal non-linear relationship with 1.38 % an increase in TL for each unit increased THg until reaching a cut-point at 0.96 µg/L blood THg, from which TL attrition was observed. Higher pre- and postnatal blood THg concentrations were consistently related to longer TL among cohorts and no modification effect of fish consumption nor children's sex was observed. No association between THg exposure and mtDNAcn was found. DISCUSSION: We found evidence that THg is associated with TL but the associations seem to be time- and concentration-dependent. Further studies are needed to clarify the mechanism behind the telomere changes of THg and related health effects.

Comparative study of susceptibility to methylmercury cytotoxicity in cell types composing rat peripheral nerves: a higher susceptibility of dorsal root ganglion neurons.

Methylmercury is an environmental polluting organometallic compound that exhibits neurotoxicity, as observed in Minamata disease patients. Methylmercury damages peripheral nerves in Minamata patients, causing more damage to sensory nerves than motor nerves. Peripheral nerves are composed of three cell types: dorsal root ganglion (DRG) cells, anterior horn cells (AHCs), and Schwann cells. In this study, we compared cultured these three cell types derived from the rat for susceptibility to methylmercury cytotoxicity, intracellular accumulation of mercury, expression of L-type amino acid transporter 1 (LAT1), which transports methylmercury into cells, and expression of multidrug resistance-associated protein 2 (MRP2), which transports methylmercury-glutathione conjugates into the extracellular space. Of the cells examined, we found that DRG cells were the most susceptible to methylmercury with markedly higher intracellular accumulation of mercury. The constitutive level of LAT1 was higher and that of MRP2 lower in DRG cells compared with those in AHC and Schwann cells. Additionally, decreased cell viability caused by methylmercury was significantly reduced by either the LAT1 inhibitor, JPH203, or siRNA-mediated knockdown of LAT1. On the other hand, an MRP2 inhibitor, MK571, significantly intensified the decrease in the cell viability caused by methylmercury. Our results provide a cellular basis for sensory neve predominant injury in the peripheral nerves of Minamata disease patients.

Field-aged rice hull biochar stimulated the methylation of mercury and altered the microbial community in a paddy soil under controlled redox condition changes.

Mercury (Hg) contaminated paddy soils are hot spots for methylmercury (MeHg) which can enter the food chain via rice plants causing high risks for human health. Biochar can immobilize Hg and reduce plant uptake of MeHg. However, the effects of biochar on the microbial community and Hg (de)methylation under dynamic redox conditions in paddy soils are unclear. Therefore, we determined the microbial community in an Hg contaminated paddy soil non-treated and treated with rice hull biochar under controlled redox conditions (< 0 mV to 600 mV) using a biogeochemical microcosm system. Hg methylation exceeded demethylation in the biochar-treated soil. The aromatic hydrocarbon degraders Phenylobacterium and Novosphingobium provided electron donors stimulating Hg methylation. MeHg demethylation exceeded methylation in the non-treated soil and was associated with lower available organic matter. Actinobacteria were involved in MeHg demethylation and interlinked with nitrifying bacteria and nitrogen-fixing genus Hyphomicrobium. Microbial assemblages seem more important than single species in Hg transformation. For future directions, the demethylation potential of Hyphomicrobium assemblages and other nitrogen-fixing bacteria should be elucidated. Additionally, different organic matter inputs on paddy soils under constant and dynamic redox conditions could unravel the relationship between Hg (de)methylation, microbial carbon utilization and nitrogen cycling.