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.

Dietary intake of methylmercury by 0-5 years children using the duplicate diet method in Japan.

BACKGROUND: The developing brains are sensitive to methylmercury (MeHg). However, the exposure to MeHg in baby foods and toddler meals remains unknown. This study aimed to determine MeHg intake from baby food or toddler meals, and to investigate the relationship with child hair total mercury (THg). METHODS: A total of 3 days of 24-hour dietary diet and hair samples were collected from 260 consenting children aged 0-5 years. We measured the concentrations of THg and MeHg in the diet and THg in the hair. RESULTS: The results of measuring THg were below both the method detection and method quantification limits or either of both in powdered milk (93.8%), 5-6 months (53.3%), and 7-8 months (39.5%). The median daily THg intake was 20.3 (95% confidence interval 0.72-232.5) ng/kgbw. MeHg was not detected in 213 samples with dietary THg concentrations below 1 ng/g. The MeHg concentration with THg concentrations of 1 ng/g or higher was 1.70 (0.87-6.21) ng/g, and MeHg percentage in THg was 90.0%. To estimate MeHg intake, we multiplied the THg concentration by 90.0%, resulting in an estimated MeHg intake of 18.3 (0.65-209.2) ng/kgbw/day. The THg in children's hair was 1.05 (0.31-3.96) ppm, and a weak positive correlation was observed between hair THg and dietary MeHg (r = 0.170). CONCLUSIONS: This study highlights the accurate estimation of MeHg intake in children using a duplicate method. Japanese children consume fish, the MeHg intakes exceeded the reference dose and/or provisional tolerable weekly intake in several children. Further discussion based on epidemiological data is required.

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.

Methylmercury in northern pike (Esox lucius) liver and hepatic mitochondria is linked to lipid peroxidation.

Methylmercury (MeHg) readily bioaccumulates and biomagnifies in aquatic food webs leading to elevated concentrations in fish and may thus induce toxicity. Oxidative stress is a suggested effect of MeHg bioaccumulation in fish. However, studies on how MeHg triggers oxidative stress in wild fish are scarce. The purpose of this study was to link the subcellular distribution of MeHg in the liver of northern pike from the St. Maurice River (Québec, Canada), affected by two run-of-river (RoR) dams, artificial wetlands, forest fires, and logging activity, to lipid peroxidation as an indicator of oxidative stress. We also evaluated the protective effects of the glutathione (GSH) system and selenium (Se), as they are known to alleviate MeHg toxicity. A customized subcellular partitioning protocol was used to separate the liver into metal-sensitive (mitochondria, microsome/lysosome and HDP - heat-denatured proteins) and metal-detoxified fractions (metal-rich granules and HSP - heat-stable proteins). We examined the relation among THg, MeHg, and Se concentration in livers and subcellular fractions, and the hepatic ratio of total GSH (GSHt) to oxidized glutathione (GSSG) on lipid peroxidation levels, using the concentrations of malondialdehyde (MDA), a product of lipid peroxidation. Results showed that hepatic MDA concentration was positively correlated with the combined MeHg and Se concentrations in northern pike liver (r2 = 0.88, p < 0.001) and that MDA concentrations were best predicted by MeHg associated with the mitochondria (r2 = 0.71, p < 0.001). This highlights the need for additional research on the MeHg influence on fish health and the interactions between Hg and Se in northern pike.

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.

Application of diffusive gradient in thin films probes to monitor trace levels of labile methylmercury in freshwaters.

This study aimed to optimize the methods for sampling and analyzing methylmercury (MeHg) concentrated within diffusive gradients in thin films (DGT) and its application to different water bodies. We explored the elution solution for MeHg, comprised of 1.13 mM thiourea and 0.1M HCl, optimizing its volume to 50 mL. In addition, we found that it is necessary to analyze the entire extraction solution after adjusting its pH, to ensure completion of the ethylation reaction. The DGT samplers were deployed in two distinct aquatic environments (i.e., Okjeong Lake and Nakdong River) for up to 6 weeks, and this study demonstrated to predict the time-weighted average concentration with a diffusion coefficient of 7.65 × 10-6 cm2 s-1 for MeHg in the diffusive gel. To assess the diffusive boundary layer (DBL) effects, the DGT samplers with different agarose diffusive gel thickness were deployed. The mass of MeHg accumulated in the DGT resin at a given time decreased with increasing diffusive gel thickness, because of creating longer diffusion pathways within thicker gels. The labile MeHg concentration estimated by the DGT in Okjeong Lake and Nakdong River are found in the range of 61-111 and 55-105 pg L-1, respectively, which were found to be similar to the grab sampling data. Additionally, this study evaluated depth-dependent MeHg in Okjeong Lake. The vertical profile results showed that the concentration of MeHg at the depth of 2.3 and 15.7 m are about 1.5 and 4.6 times of the DGT installed at 0.3 m of the surface layer, respectively, suggesting potential mercury methylation in deep waters. These findings have practical implications for predicting bioavailability, assessing risks, and formulating strategies for water body management and contamination remediation.

Degradation of methylmercury into Hg(0) by the oxidation of iron(II) minerals.

Mercury contamination is a global concern, and the degradation and detoxification of methylmercury have gained significant attention due to its neurotoxicity and biomagnification within the food chain. However, the currently known pathways of abiotic demethylation are limited to light-induced photodegradation process and little is known about light-independent abiotic demethylation of methylmercury. In this study, we reported a novel abiotic pathway for the degradation of methylmercury through the oxidation of both mineral structural iron(II) and surface-adsorbed iron(II) in the absence of light. Our findings reveal that methylmercury can be oxidatively degraded by reactive oxygen species, specifically hydroxyl and superoxide radicals, which are generated from the oxidation of iron(II) minerals under dark conditions. Surprisingly, Hg(0) trapping experiments demonstrated that inorganic Hg(II) resulting from the oxidative degradation of methylmercury was rapidly reduced to gaseous Hg(0) by iron(II) minerals. The demethylation of methylmercury, coupled with the generation of Hg(0), suggests a potential natural attenuation process for methylmercury. Our results highlight the underappreciated roles of iron(II) minerals in the abiotic degradation of methylmercury and the release of gaseous Hg(0) into the atmosphere.

Mercury supply limits methylmercury production in paddy soils.

The neurotoxic methylmercury (MeHg) is a product of inorganic mercury (IHg) after microbial transformation. Yet it remains unclear whether microbial activity or IHg supply dominates Hg methylation in paddies, hotspots of MeHg formation. Here, we quantified the response of MeHg production to changes in microbial activity and Hg supply using 63 paddy soils under the common scenario of straw amendment, a globally prevalent agricultural practice. We demonstrate that the IHg supply is the limiting factor for Hg methylation in paddies. This is because IHg supply is generally low in soils and can largely be facilitated (by 336-747 %) by straw amendment. The generally high activities of sulfate-reducing bacteria (SRB) do not limit Hg methylation, even though SRB have been validated as the predominant microbial Hg methylators in paddies in this study. These findings caution against the mobilization of legacy Hg triggered by human activities and climate change, resulting in increased MeHg production and the subsequent flux of this potent neurotoxin to our dining tables.

Understanding mercury accumulation in mosses of two subalpine forests in China.

The role of forest ecosystems in the global mercury (Hg) biogeochemical cycle is widely recognized; however, using litterfall as a surrogate to assess the Hg sink function of forests encounters limitations. We investigated the accumulation characteristics and influencing factors of Hg in mosses from two remote subalpine forests in southwestern China. The results indicated that there was high Hg accumulation in subalpine forest mosses, with average concentrations of 82 ± 49 ng g-1 for total mercury (THg) and 1.3 ± 0.8 ng g-1 for methylmercury (MeHg). We demonstrated that the accumulation capacity of Hg in mosses was significantly dependent on species and substrates (micro-habitats), the mosses on tree trunks exhibited significantly elevated Hg accumulation levels (THg 132 ± 56 ng g-1, MeHg 1.6 ± 0.2 ng g-1) compared to mosses in other substrates. The surface morphologies and biochemical components of leaf (phyllidia), such as cation exchange capacity (CEC), pectin, uronic acid, and metallothionein, play a crucial role in the accumulation of Hg by mosses. These findings provide valuable insights into Hg accumulation in forest mosses. Suggesting that the contribution of mosses Hg accumulation should be considered when assessing atmospheric Hg sinks of forests.

Light-induced degradation of dimethylmercury in different natural waters.

Photo-induced degradation of dimethylmercury (DMHg) is considered to be an important source for the generation of methylmercury (MMHg). However, studies on DMHg photodegradation are scarce, and it is even debatable about whether DMHg can be degraded in natural waters. Herein, we found that both DMHg and MMHg could be photodegraded in three natural waters collected from the Yellow River Delta, while in pure water only DMHg photodegradation occurred under visible light irradiation. The effects of different environmental factors on DMHg photodegradation were investigated, and the underlying mechanisms were elucidated by density functional theory calculations and a series of control experiments. Our findings revealed that the DMHg degradation rate was higher in the tidal creek water compared to Yellow River, Yan Lake, and purified water. NO3-, NO2-, and DOM could promote the photodegradation with DOM and NO3- showing particularly strong positive effects. Different light sources were employed, and UV light was found to be more effective in DMHg photodegradation. Moreover, MMHg was detected during the photodegradation of DMHg, confirming that the photochemical demethylation of DMHg is a source of MMHg in sunlit water. This work may provide a novel mechanistic insight into the DMHg photodegradation in natural waters and enrich the study of the global biogeochemical cycle of Hg.

Methylmercury induces inflammatory response and autophagy in microglia through the activation of NLRP3 inflammasome.

Methylmercury (MeHg) is a global environmental pollutant with neurotoxicity, which can easily crosses the blood-brain barrier and cause irreversible damage to the human central nervous system (CNS). CNS inflammation and autophagy are known to be involved in the pathology of neurodegenerative diseases. Meanwhile, MeHg has the potential to induce microglia-mediated neuroinflammation as well as autophagy. This study aims to further explore the exact molecular mechanism of MeHg neurotoxicity. We conducted in vitro studies using BV2 microglial cell from the central nervous system of mice. The role of inflammation and autophagy in the damage of BV2 cells induced by MeHg was determined by detecting cell viability, cell morphology and structure, reactive oxygen species (ROS), antioxidant function, inflammatory factors, autophagosomes, inflammation and autophagy-related proteins. We further investigated the relationship between the inflammatory response and autophagy induced by MeHg by inhibiting them separately. The results indicated that MeHg could invade cells, change cell structure, activate NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome and autophagosome, release a large amount of inflammatory factors and trigger the inflammatory response and autophagy. It was also found that MeHg could disrupt the antioxidant function of cells. In addition, the inhibition of NLRP3 inflammasome alleviated both cellular inflammation and autophagy, while inhibition of autophagy increased cellular inflammation. Our current research suggests that MeHg might induce BV2 cytotoxicity through inflammatory response and autophagy, which may be mediated by the NLRP3 inflammasome activated by oxidative stress.

Coastal Mussel (Mytilus spp.) Soft Tissues as Bioindicators of Methylmercury: Exploring the Relationship Between Condition Index and Methylmercury Concentrations.

We investigated total mercury (THg) and methylmercury (MeHg) concentrations in coastal mussels (Mytilus spp.) sampled from the Minas Basin, Bay of Fundy and evaluated the relationship with condition index (CI). THg concentrations were low in sediment (mean THg = 5.15 ± 2.11 ng/g dw; n = 6) and soft tissues (mean THg = 62.3 ± 13.7 ng/g; mean MeHg = 13.2 ± 6.3 ng/g; n = 57). The THg in tissues had no significant relationship with CI (Rs= -0.205, p = 0.126). MeHg in tissues were significantly and negatively correlated with condition index (Rs = -0.361, p = 0.006) indicating that healthier mussels (higher CI) have lower mercury content possibly due to elimination strategies or growth dilution.

Bioconcentration of Inorganic and Methyl Mercury by Algae Revealed Using Dual-Mass Single-Cell ICP-MS with Double Isotope Tracers.

Algae are an entry point for mercury (Hg) into the food web. Bioconcentration of Hg by algae is crucial for its biogeochemical cycling and environmental risk. Herein, considering the cell heterogeneity, we investigated the bioconcentration of coexisting isotope-labeled inorganic (199IHg) and methyl Hg (201MeHg) by six typical freshwater and marine algae using dual-mass single-cell inductively coupled plasma mass spectrometry (scICP-MS). First, a universal pretreatment procedure for the scICP-MS analysis of algae was developed. Using the proposed method, the intra- and interspecies heterogeneities and the kinetics of Hg bioconcentration by algae were revealed at the single-cell level. The heterogeneity in the cellular Hg contents is largely related to cell size. The bioconcentration process reached a dynamic equilibrium involving influx/adsorption and efflux/desorption within hours. Algal density is a key factor affecting the distribution of Hg between algae and ambient water. Cellular Hg contents were negatively correlated with algal density, whereas the volume concentration factors almost remained constant. Accordingly, we developed a model based on single-cell analysis that well describes the density-driven effects of Hg bioconcentration by algae. From a novel single-cell perspective, the findings improve our understanding of algal bioconcentration governed by various biological and environmental factors.

Molecular crosstalk and putative mechanisms underlying mitochondrial quality control: The hidden link with methylmercury-induced cognitive impairment.

Methylmercury (MeHg) is a neurotoxin associated with foetal neurodevelopmental and adult cognitive deficits. Neurons are highly dependent on the tricarboxylic acid cycle and oxidative phosphorylation to produce ATP and meet their high energy demands. Therefore, mitochondrial quality control (MQC) is critical for neuronal homeostasis. While existing studies have generated a wealth of data on the toxicity of MeHg, the complex cascades and molecular pathways governing the mitochondrial network remain to be elucidated. Here, 0.6, 1.2 and 2.4 mg/kg body weight of MeHg were administered intragastrically to pregnant Sprague Dawley rats to model maternal MeHg exposure. The results of the in vivo study revealed that MeHg-treated rats tended to perform more directionless repetitive strategies in the Morris Water Maze and fewer target-orientation strategies than control offspring. Moreover, pathological injury and synaptic toxicity were observed in the hippocampus. Transmission electron microscopy (TEM) demonstrated that the autophagosomes encapsulated damaged mitochondria, while showing a typical mitochondrial fission phenotype, which was supported by the activation of PINK1-dependent key regulators of mitophagy. Moreover, there was upregulation of DRP1 and FIS1. Additionally, MeHg compensation promoted mitochondrial biogenesis, as evidenced by the activation of the mitochondrial PGC1-α-NRF1-TFAM signalling pathway. Notably, SIRT3/AMPK was activated by MeHg, and the expression and activity of p-AMPK, p-LKB1 and SIRT3 were consistently coordinated. Collectively, these findings provide new insights into the potential molecular mechanisms regulating MeHg-induced cognitive deficits through SIRT3/AMPK MQC network coordination.

Methylmercury exposure of the sponge O. lobularis induces strong tissue and cell defects.

Mediterranean marine biota suffers from various anthropogenic threats. Among them, pollutants such as mercury (Hg) represent important environmental issues that are exacerbated by bioaccumulation and bioamplification along food webs via its organic form, monomethylmercury (MMHg). To date, very little is known regarding the impact of mercury on Porifera and the few available studies have been exclusively focused on Demospongiae. This work studies the effect of MMHgCl at different biological levels of Oscarella lobularis (Porifera, Homoscleromorpha). Bioaccumulation assays show that MMHgCl significantly accumulated in sponge tissues after a 96-h exposure to 0.1 µg L-1. Toxicity assays (LC5096h) show a sensibility that depends on life-stage (adult vs bud). Additionally, we show that the exposure to 1 µg L-1 MMHgCl negatively impacts the epithelial integrity and the regeneration process in buds, as shown by the loss of cell-cell contacts and the alteration of osculum morphogenesis. For the first time in a sponge, a whole set of genes classically involved in metal detoxification and in antioxidant response were identified. Significant changes in catalase, superoxide dismutase and nuclear factor (erythroid-derived 2)-like 2 expressions in exposed juveniles were measured. Such an integrative approach from the physiological to the molecular scales on a non-model organism expands our knowledge concerning sensitivity and toxicity mechanisms induced by MMHg in Porifera, raising new questions regarding the possible defences used by marine sponges.

Role of low-proportion, hydrophobic dissolved organic matter components in inhibiting methylmercury uptake by phytoplankton.

Uptake of methylmercury (MeHg), a potent neurotoxin, by phytoplankton is a major concern due to its role as the primary pathway for MeHg entry into aquatic food webs, thereby posing a significant risk to human health. While it is widely believed that the MeHg uptake by plankton is negatively correlated with the concentrations of dissolved organic matter (DOM) in the water, ongoing debates continue regarding the specific components of DOM that exerts the dominant influence on this process. In this study, we employed a widely-used resin fractionation approach to separate and classify DOM derived from algae (AOM) and natural rivers (NOM) into distinct components: strongly hydrophobic, weakly hydrophobic, and hydrophilic fractions. We conduct a comparative analysis of different DOM components using a combination of spectroscopy and mass spectrometry techniques, aiming to identify their impact on MeHg uptake by Microcystis elabens, a prevalent alga in freshwater environments. We found that the hydrophobic components had exhibited more pronounced spectral characteristics associated with the protein structures while protein-like compounds between hydrophobic and hydrophilic components displayed significant variations in both distributions and the values of m/z (mass-to-charge ratio) of the molecules. Regardless of DOM sources, the low-proportion hydrophobic components usually dominated inhibition of MeHg uptake by Microcystis elabens. Results inferred from the correlation analysis suggest that the uptake of MeHg by the phytoplankton was most strongly and negatively correlated with the presence of protein-like components. Our findings underscore the importance of considering the diverse impacts of different DOM fractions on inhibition of phytoplankton MeHg uptake. This information should be considered in future assessments and modeling endeavors aimed at understanding and predicting risks associated with aquatic Hg contamination.

Predictive modeling of methylmercury in rice (Oryza sativa L.) and species-sensitivity-distribution-based derivation of the threshold of soil mercury in karst mountain areas.

The bioavailable mercury (Hg) in the soil is highly active and can affect the formulation of methyl-Hg (MeHg) in soil and its accumulation in rice. Herein, we predicted the concentration of MeHg in rice using bioavailable Hg extracted from soils; additionally, we determined the threshold value of soil Hg in karst mountain areas based on species sensitivity distribution. The bioavailable Hg was extracted using calcium chloride, hydrochloric acid (HCl), diethylenetriaminepentaacetic acid mixture, ammonium acetate, and thioglycolic acid. Results showed that HCl is the best extractant, and the prediction model demonstrated good predictability of the MeHg concentration in rice based on the HCl-extractable Hg, pH, and soil organic matter (SOM) data. Compared with the actual MeHg concentration in rice, approximately 99% of the predicted values (n = 103) were within the 95% prediction range, indicating the good performance of the rice MeHg prediction model based on soil pH, SOM, and bioavailable Hg in karst mountain areas. Based on this MeHg prediction model, the safety threshold of soil Hg was calculated to be 0.0936 mg/kg, which is much lower than the soil pollution risk screening value of agricultural land (0.5 mg/kg), suggesting that a stricter standard should be applied regarding soil Hg in karst mountain areas. This study presents the threshold of soil Hg pollution for rice safety in karst mountain areas, and future studies should target this threshold range.

Effects of nanomolar methylmercury on developing human neural stem cells and zebrafish Embryo.

Exposure to mercury and its organic form methylmercury (MeHg), is of great concern for the developing nervous system. Despite available literature on MeHg neurotoxicity, there is still uncertainty about its mechanisms of action and the doses that trigger developmental effects. Our study combines two alternative methodologies, the human neural stem cells (NSC) and the zebrafish (ZF) embryo, to address the neurotoxic effects of early exposure to nanomolar concentrations of MeHg. Our results show linear or nonmonotonic (hormetic) responses depending on studied parameters. In ZF, we observed a hormetic response in locomotion and larval rotation, but a concentration-dependent response for sensory organ size and habituation. We also observed a possible delayed response as MeHg had greater effects on larval activity at 5 days than at 24 h. In NSC cells, some parameters show a clear dose dependence, such as increased apoptosis and differentiation to glial cells or decreased neuronal precursors; while others show a hormetic response: neuronal differentiation or cell proliferation. This study shows that the ZF model was more susceptible than NSC to MeHg neurotoxicity. The combination of different models has improved the understanding of the underlying mechanisms of toxicity and possible compensatory mechanisms at the cellular and organismal level.

Warming inhibits HgII methylation but stimulates methylmercury demethylation in paddy soils.

Inorganic mercury (HgII) can be transformed into neurotoxic methylmercury (MeHg) by microorganisms in paddy soils, and the subsequent accumulation in rice grains poses an exposure risk for human health. Warming as an important manifestation of climate change, changes the composition and structure of microbial communities, and regulates the biogeochemical cycles of Hg in natural environments. However, the response of specific HgII methylation/demethylation to the changes in microbial communities caused by warming remain unclear. Here, nationwide sampling of rice paddy soils and a temperature-adjusted incubation experiment coupled with isotope labeling technique (202HgII and Me198Hg) were conducted to investigate the effects of temperature on HgII methylation, MeHg demethylation, and microbial mechanisms in paddy soils along Hg gradients. We showed that increasing temperature significantly inhibited HgII methylation but promoted MeHg demethylation. The reduction in the relative abundance of Hg-methylating microorganisms and increase in the relative abundance of MeHg-demethylating microorganisms are the likely reasons. Consequently, the net Hg methylation production potential in rice paddy soils was largely inhibited under the increasing temperature. Collectively, our findings offer insights into the decrease in net MeHg production potential associated with increasing temperature and highlight the need for further evaluation of climate change for its potential effect on Hg transformation in Hg-sensitive ecosystems.