Methylmercury Exposure Research Articles

Role of calcium overload-mediated disruption of mitochondrial dynamics in offspring neurotoxicity due to methylmercury exposure during pregnancy and lactation.

Methylmercury (MeHg) is a potent neurotoxicant with neurodevelopmental toxicity that is widely ingested into the body through drinking water and food. MeHg crosses the placental barrier and accumulates in the brain of the fetus, affecting the growth and development of the central nervous system. Although it has been demonstrated that MeHg induces neuronal calcium overload in the rat cerebral cortex, the role of calcium overload in MeHg-induced neurodevelopmental toxicity remains unclear. Here, we used ICR-pregnant mice and their resulting offspring and administered the BAPTA-AM calcium antagonist to investigate the molecular mechanisms by which MeHg exposure during gestation and lactation affects neurodevelopment. We found that exposure to MeHg during gestation and lactation resulted in developmental arrest and neurobehavioral dysfunction in the offspring, with calcium overload, disturbed mitochondrial dynamics, and apoptosis. However, the calcium overload inhibitor BAPTA-AM rescued MeHg-induced neurodevelopmental damage, attenuated the onset of calcium overload, reduced mitochondrial kinetic disturbances and apoptosis. Meanwhile, the activation of the CaM/CaMKII/DRP1 signaling pathway induced by calcium overload was inhibited, and the interaction between DRP1 and BAX was attenuated, which alleviated apoptosis to a certain extent. In summary, our study suggests that MeHg-induced calcium overload may induce disturbed mitochondrial dynamics through activation of the CaM/CaMKII/DRP1 signaling pathway, resulting in neuronal apoptosis.

Combined effects of pollution and bacterial infection in Sabella spallanzanii (Gmelin, 1971)

Sabella spallanzanii is a Mediterranean tube-dwelling polychaete living in shallow water. Here we evaluate its ability to respond to individual and combined treatments of methylmercury exposure and Escherichia coli challenge – two typical stressors of the eutrophic environment populated by the animal. Methylmercury is one of the most dangerous and toxic pollutants in marine environments, capable of bioaccumulating and being biomagnified within the food web with consequences for marine organisms. Here, the enzymatic and immune responses of Sabella spallanzanii have been investigated after exposure to methylmercury, along with the combined impacts of E. coli infection. Fan worms were subjected to four different treatments: control conditions (buffer injection); E. coli injection; CH3HgCl exposure combined, or not, with E. coli injection. Electrophoresis was performed to highlight possible alterations in protein patterns, differentially expressed upon bacterial and pollution challenges. Furthermore, enzymatic activities related to immune and physiological responses were assessed in whole body extracts. Our findings reveal the impact of methylmercury on the immunomodulation of S. spallanzanii, particularly in relation to oxidative stress and inflammatory markers. Each treatment led to a modulation of all the tested enzymatic activities, and the combined responses drastically reduced lysozyme activity.

Mercury Levels in Hair of Pregnant Women in Tumbes, Peru: A Cross-Sectional Study.

Mercury, a potent toxin that poses serious risks to human health, particularly for pregnant women and young children, is widely present due to artisanal and small-scale gold mining (ASGM), which impacts water quality. The objective of this study was to evaluate methylmercury exposure among pregnant women in communities downstream from ASGM sites. We characterized hair total mercury (THg) concentrations among 148 pregnant women across 24 communities in the Tumbes region of Peru, downstream from ASGM sites in Ecuador. Using purposeful sampling, we classified communities into three exposure risk zones: Puyango-Tumbes River watershed, Coast, and Zarumilla. The mean THg concentration was 2.08 µg/g ± 1.36, with 45% of participants (67/148) exceeding UNEP/WHO exposure limits (>2.0 µg/g). The median was 1.84 with an interquartile range (IQR) from 1.01 to 2.83. Median THg levels were significantly higher in the Puyango-Tumbes River region (2.72 µg/g; IQR: 1.66-3.55) compared with Zarumilla (1.61 µg/g; IQR: 0.67-2.63; P = 0.001) and to the Coast (1.71 µg/g; IQR: 1.13-2.50; P = 0.01), suggesting that living close to the Puyango-Tumbes River may be associated with a higher mercury exposure risk. After controlling for potential confounders, individuals in the Puyango-Tumbes watershed exhibited a significant 57% higher expected geometric mean of hair THg compared with Zarumilla (95% CI: 0.1-146.2%). These findings underscore the importance of identifying high-risk regional populations and ongoing biomonitoring of the Puyango-Tumbes River watershed.

Impact of developmental methylmercury exposure on avian embryonic development, hatchling growth, and survival.

Methylmercury (MeHg) is a globally ubiquitous and persistent environmental toxicant that negatively affects animal behavior, health, and reproduction. In birds, MeHg is transferred from female to egg, contaminating embryos during sensitive stages of early embryonic development and growth. This toxic exposure in the prenatal environment not only induces mortality but also possible lasting impacts on physiology, health, and survival, even once hatched. The purpose of our study was to further elucidate the negative effects of MeHg exposure during avian embryonic development and explore how such exposure can impact offspring development, growth, and survival, both in ovo and posthatch. To assess this, we experimentally dosed fertile mallard and wood duck eggs with MeHg II chloride and reared developing embryos and ducklings to various endpoints. We found that embryos not only readily accumulated MeHg throughout incubation, but they also displayed varying dose-dependent disparities in body mass and morphometrics, with control individuals being larger during early and late embryonic stages of development (p < 0.05). Furthermore, hatched offspring exposed to MeHg exhibited increasingly slower growth rates between 7 to 10 and 10 to 15 days posthatch (p < 0.05), and were found to have lower survival probabilities both under controlled laboratory conditions (p < 0.005), and in the natural environment (p < 0.05). Our findings on the detrimental effects of MeHg on avian embryos and hatchlings emphasize the need for more proactive means of environmental protection and remediation to protect vulnerable avian populations and the ecosystems they inhabit.

As, Cd, Hg, and Pb Biological Concentrations and Anthropometry in Slovak Adolescents.

Anthropometry provides a non-invasive technique for evaluating growth and obesity and serves as an indicator of health status. This cross-sectional study aims to investigate the association of internal arsenic (As), cadmium (Cd), total mercury (THg), methylmercury (MeHg), and lead (Pb) exposure with anthropometric parameters, including obesity, in adolescents. Participants (N = 320) were children aged 10-14 years (mean 11.8 years) from eastern Slovakia, at an early stage of adolescence characterized by growth acceleration. Metal concentrations in blood and urine were measured by ICP-MS (for As, Cd, and Pb), GC/ICP-MS (for MeHg) and amalgamation technique AAS (for THg). Median concentrations of the studied elements in whole blood (Cd: 0.16, Pb: 10.6, THg: 0.25, MeHg: 0.11µg/L) and urine (Cd: 0.25, Pb: 0.73, As: 3.38µg/g creatinine) were relatively low in our study group. The results showed that blood Cd and Pb concentrations were inversely associated with several anthropometric parameters (body weight, BMI, body fat percentage, chest circumference, and waist circumference) in both boys and girls. Conversely, blood THg concentration was positively associated with these parameters in boys. A positive relationship was also observed between blood MeHg concentration and height in boys, while negative associations between blood Cd and Pb concentrations and height were significant only in girls. No associations were found between metal concentrations (As, Cd, Pb) in urine and parameters of physical growth or obesity. This study demonstrates that even low-level exposure to Cd, Pb, and Hg can influence growth and obesity indicators in adolescents, with distinct sex-specific patterns, highlighting the need for ongoing monitoring and protection against environmental metal exposure.

Seafood Toxicant Exposure During Pregnancy, Lactation, and Childhood and Child Outcomes: A Scoping Review.

Determining dietary recommendations for seafood consumed during pregnancy, lactation, and childhood requires consideration of the known nutritional benefits and potential harm due to toxicant exposure as they relate to child outcomes. This study aimed to describe the scope of the evidence associated with seafood-related toxicant exposure and child outcomes and to identify toxicant-outcome pairs that may have sufficient evidence to conduct a systematic review. We included studies examining seafood toxicant exposure during pregnancy, lactation, and childhood, and child outcomes. In total, 81 studies were included: 69 studies on exposure during pregnancy and lactation and 14 on exposure during childhood. The number of studies varied by toxicant and exposure population (maternal; child): mercury (n = 49; 7), methylmercury (n = 13; 3), polychlorinated biphenyls (PCBs; n = 11; 1), selenium (n = 11; 1), lead (n = 9; 3), perfluoroalkyl and polyfluoroalkyl substances (n = 8; 2), dichlorodiphenyltrichloroethane (n = 5; 1), arsenic (n = 4; 4), cadmium (n = 4; 4), zinc (n = 3; 2), polybrominated diphenyl ethers (n = 3; 1), dioxin-like compounds (n = 3; 0), iron (n = 2; 1), and magnesium (n = 1; 1). No studies examined polybrominated biphenyls, polycyclic aromatic hydrocarbons, iodine, aldrin, dieldrin, chlordane, chlorpyrifos, or microplastic exposures. Outcomes also varied by exposure population (maternal;child): neurodevelopment (n = 35; 9), child exposure biomarkers (n = 22; 4), growth (n = 17; 1), other adverse events (n = 4; 0), cardiometabolic (n = 3; 2), chronic disease indicators (n = 2; 0), and immune-related (n = 1; 2). Twelve maternal toxicant-outcome pairs had ≥3 studies, including mercury, methylmercury, lead, PCBs, perfluoroalkyl and polyfluoroalkyl substances, and arsenic as exposures and neurodevelopment, child exposure biomarkers, growth, and cardiometabolic as outcomes. For child exposure, only mercury and neurodevelopment had ≥3 studies. In conclusion, this scoping review shows relevant evidence for 14 of the 22 toxicants. Only 12 maternal and 1 child toxicant-outcome pairs, the majority of which examined maternal (methyl)mercury exposure, had ≥3 studies, our cutoff for consideration for systematic review. This scoping review indicates a paucity of research examining seafood toxicants beyond mercury and exposure during childhood. Systematic reviews are required to evaluate the associations for each toxicant-outcome pairs. The protocol was registered at Open Science Framework (https://doi.org/10.17605/OSF.IO/FQZTA).

A Meta-Analysis of Mercury Biomagnification in Freshwater Predatory Invertebrates: Community Diversity and Dietary Exposure Drive Variability.

Accurate estimates of methylmercury (MeHg) exposure are valuable to actionably assess risk and protect wildlife and human health. MeHg trophic transfer is a critical driver of risk: MeHg is generally biomagnified by a factor of 8.3 ± 7.5 from one trophic level to the next, averaged across freshwater communities (mean ± standard deviation). This variability can produce disparate risks even where basal MeHg concentrations are similar. Taxonomy may be one driver of this variability: physiologically diverse groups, like vertebrates and invertebrates, may assimilate MeHg differently. To determine whether taxonomy affects trophic transfer efficiency, we conducted a meta-analysis characterizing predatory invertebrate MeHg biomagnification. Our analyses estimated that freshwater predatory invertebrates biomagnify MeHg by factors of 2.1 ± 0.2 to 4.3 ± 0.3, with a 98.9 ± 0.4% posterior probability that factors are below 5 (mean ± standard error). When vertebrates or primary producers were included, a site's trophic magnification factor was 18.6 ± 6.2 to 54.1 ± 7.7% higher than estimates for invertebrates alone. Biomagnification was inversely correlated to prey MeHg concentration and varied among systematic and functional groups. These data suggest that predatory invertebrates biomagnify MeHg less efficiently than vertebrates and that a community's diversity and structure determine its biomagnification efficiency. Incorporating organismal variation in trophic transfer estimates may improve the assessment, communication, and management of MeHg risk.

Methylmercury Concentrations More Strongly Associated With Trait Variation Than Food Web Position in Plethodontid Salamanders.

Salamanders serve as bioindicators of mercury (Hg) in both terrestrial and aquatic habitats and are an important link in the food web between low-trophic prey and higher-trophic predators. We investigated the drivers of methylmercury (MeHg) exposure in three common plethodontid salamander species in New York State, USA, including comparisons among regions, habitat types (terrestrial and semiaquatic), and color morphs of Plethodon cinereus (striped and unstriped). Nonlethal tail samples were collected from one terrestrial species (P. cinereus) and two semiaquatic species (Eurycea bislineata and Desmognathus spp.) in the Adirondack Mountains (ADK) and the Finger Lakes National Forest (FLNF) regions. Samples were analyzed for MeHg and stable isotopes, including δ15N and δ13C which are proxies of trophic position and diet, respectively. Despite elevated biota Hg concentrations typically found in the ADK, salamander MeHg concentrations did not differ by region in the terrestrial species and one of the semiaquatic species. In addition, diet and trophic level did not explain MeHg exposure in salamanders. Semiaquatic salamanders exhibited higher MeHg concentrations than terrestrial salamanders in the FLNF only. Within species, only snout-vent length predicted MeHg concentrations in E. bislineata with few other variables significant as predictors of MeHg concentrations in path models. Among P. cinereus individuals in the FLNF, the striped morph had greater MeHg concentrations than the unstriped morph, and food web tracers were not different between morphs. Overall, New York State salamander Hg concentrations were elevated compared to other locations where these species are present. The present study establishes baseline Hg data in salamanders for future assessments of changes in Hg bioavailability to forests of New York State. Environ Toxicol Chem 2024;43:2045-2057. © 2024 SETAC.

Epigenetic alternations in the SYP and DLG4 genes due to low-level methylmercury exposure during neuronal differentiation in vitro.

Methylmercury (MeHg) is an environmental toxin known to damage the central nervous system. When pregnant women ingest seafood, which may contain accumulated MeHg, fetal development may be affected. The embryonic period, a time of major epigenetic change, is susceptible to epigenetic disruptions due to chemical exposure. Therefore, understanding the molecular mechanism underlying MeHg's effects on neuronal development requires consideration of epigenetic factors. In this study, we investigated epigenetic modifications in the synaptophysin (SYP) and discs large MAGUK scaffold protein 4 (DLG4) genes. LUHMES cells were exposed to 1 nM MeHg for 6 days during days 2-8 of neural differentiation. MeHg exposure significantly reduced the number of spikes observed on day 16 of differentiation. Both mRNA and protein expression levels of SYP and DLG4 were significantly decreased by MeHg exposure. Additionally, MeHg treatment reduced acetyl histone H3 levels associated with transcriptional activity in the SYP gene while increasing histone H3 lysine 27 tri-methylation (H3K27me3) levels related to transcriptional repression. Conversely, regarding the DLG4 gene, MeHg exposure increased H3K27me3 levels. Differential changes in DNA methylation (high and low methylation states) were observed in the SYP and DLG4 genes due to MeHg exposure depending on CpG site position. In conclusion, this study suggests that epigenetic changes, particularly histone modifications, contribute to decreased MeHg exposure-induced SYP and DLG4 expression during neuronal differentiation.

Mercury Exposure Assessment from the First Harmonised Total Diet Study in Portugal

The aim of this study was to estimate the Portuguese population’s baseline exposure to methyl and inorganic mercury by a harmonised total diet study (TDS) methodology and the risk of exceeding the Tolerable Weekly Intake (TWI). TDS food samples representative of the whole diet of the population were prepared as consumed, and analysed for total mercury. European Food Safety Authority’s (EFSA) conservative approach was used to estimate methylmercury and inorganic mercury and exposure was estimated using Monte Carlo Risk Assessment (MCRA) software. Mean, median and P95 exposure of the overall population (18 to 74 years old) to methylmercury and to inorganic mercury were 1.25, 0.01 and 5.45 µg/kg bw/week, and 0.37, 0.15 and 1.27 µg/kg bw/week, respectively. The percentage of individuals exceeding TWI was 27.6 for methylmercury and 3.5 for inorganic mercury. Regarding childbearing age women (18 to 45 years old), methylmercury mean exposure was 1.13 µg/kg bw/week with 25% of women exceeding the TWI. Cod and hake were the main contributors to mercury intake.

A follow-up geospatial analysis and probabilistic human health risk assessment of methylmercury in fish in Eeyou Istchee (Québec, Canada)

The Cree Peoples of the Eeyou Istchee territory (northern Québec, Canada) rely on fish as a part of their traditional and contemporary diet. Fish is a culturally significant food and a source of nutrients, but it is also the main pathway of methylmercury (MeHg) exposure for humans. Significant hydroelectric developments in this territory are responsible for increasing the concentrations of MeHg found in fish and thus increase the human exposure to this neurotoxic compound. As this is an ongoing issue, our study assessed the current MeHg fish-tissue concentrations in Eeyou Istchee and the spatial distribution of MeHg hot spots using Geographic Information Systems (GIS) to compare our results to those found in previous studies from the same region. We also performed a probabilistic hazard assessment of the exposure to MeHg from fish consumption. The GIS models indicated significant clustering of increased MeHg fish-tissue concentrations around hydroelectric reservoirs and showed higher MeHg fish-tissue concentrations around newer hydroelectric reservoirs, but a decrease in older reservoirs. Similar to past studies, we found that fish consumption continues to pose an MeHg exposure hazard for men who consume large piscivore species (i.e., lake trout, walleye, and pike), while for women, lake trout and walleye consumption constitute a hazard (any size), and pike should be consumed with caution. The hazard of exposure was mainly associated with intake rate in all cases. Lastly, we recommend monitoring MeHg fish-tissue concentrations in this region, as the MeHg tissue concentrations remain elevated, and updated consumption guidelines where and when necessitated.

Trends and drivers of global dietary methylmercury exposure during 1995–2020

Trends and drivers of global dietary methylmercury exposure during 1995–2020

Methylmercury exposure and risk of wintering migratory birds in the Poyang Lake basin, China

Mercury (Hg), especially methylmercury (MeHg), is a pervasive contaminant that poses significant risks to birds occupying high trophic levels. However, we have little knowledge about the mercury exposure and its risks for birds in Poyang Lake basin, China. Therefore, during 2020-2021, we investigated MeHg concentrations in breast feathers of wintering migratory birds (n=430 from 43 species belonging to 9 orders) in Poyang Lake Nanji Wetland and Jiangxi Nanfengmian National Nature Reserve, China. MeHg concentrations in breast feathers varied greatly by species, foraging guilds and taxonomic orders, among which the highest concentration was detected in great egret (8849±5975ngg-1 dw). Comparing with studies worldwide, high MeHg concentrations in feathers of Ardeidae from Pelecaniformes were found in this area. Moreover, herons migrating between northern and southern China had lower MeHg concentration than residents in southern China related to habitat Hg. Considering the applicability and sensitivity of the equations for the transformation of MeHg concentrations in feathers to blood-equivalent total Hg (THg) values, method CJ that the equation based on songbirds was used for the transformation of the songbirds and the equation based on seabirds for the others performed better than other three for risk assessment of bird Hg in this study. 23.1% of birds from Poyang Lake were at risk of Hg exposure based on the method CJ. Carnivorous birds from Pelecaniformes had the highest risk levels, with 37.2% categorized as no risk (≤200ngg-1 ww), 48.9% as low risk (200-1000ngg-1 ww), 11.1% as moderate risk (1000-3000ngg-1 ww), 1.1% as high risk (3000-4000ngg-1 ww), and 1.7% as severe risk (>4000ngg-1 ww). These risks suggest long-term monitoring and further advanced studies about freshwater waterbirds Hg exposure is necessary.

A novel approach to assessing the joint effects of mercury and fish consumption on neurodevelopment in the New Bedford Cohort.

Understanding health risks from methylmercury (MeHg) exposure is complicated by its link to fish consumption, which may confound or modify toxicities. One solution is to include fish intake and a biomarker of MeHg exposure in the same analytical model, but resulting estimates do not reflect the independent impact of accumulated MeHg or fish exposure. In fish-eating populations, this can be addressed by separating MeHg exposure into fish intake and average mercury content of the consumed fish. We assessed the joint association of prenatal MeHg exposure (maternal hair mercury level) and fish intake (among fish-eating mothers) with neurodevelopment in 361 children aged 8 years from the New Bedford Cohort (New Bedford, Massachusetts; born in 1993-1998). Neurodevelopmental assessments used standardized tests of IQ, language, memory, and attention. Covariate-adjusted regression assessed the association of maternal fish consumption, stratified by tertile of estimated average fish mercury level, with neurodevelopment. Associations between maternal fish intake and child outcomes were generally beneficial for those in the lowest average fish mercury tertile but detrimental in the highest average fish mercury tertile, where, for example, each serving of fish was associated with 1.3 fewer correct responses (95% CI, -2.2 to -0.4) on the Boston Naming Test. Standard analyses showed no outcome associations with hair mercury level or fish intake. This article is part of a Special Collection on Environmental Epidemiology.

Reduction of Glyoxalase 1 Expression Links Fetal Methylmercury Exposure to Autism Spectrum Disorder Pathogenesis.

Glyoxalase 1 (Glo1) is an essential enzyme to detoxify methylglyoxal (MGO), a cytotoxic byproduct of glycolysis. Accumulating studies have shown an important role of Glo1 in regulating cortical development and neurogenesis, potentially contributing to the pathogenesis of autism spectrum disorder (ASD) when impaired. We have previously shown that prenatal exposure to non-apoptotic low-dose methylmercury (MeHg), an environmental pollutant, induces premature cortical neurogenesis and ASD-like behaviors in a rodent model. In this study, we aimed to determine the underlying molecular mechanisms that mediate prenatal MeHg-induced premature neuronal differentiation and abnormal neurodevelopment. Using single-cell RNA sequencing (scRNA-seq) and real-time quantitative PCR (RT-qPCR), we found that prenatal MeHg exposure at a non-apoptotic dose significantly reduced Glo1 gene expression in embryonic cultured radial glia precursors (RGPs). In cultured RGPs, the knockdown of Glo1 expression increased neuronal production at the expense of the cultured RGPs population, while overexpression of Glo1 restored MeHg-induced neuronal differentiation back to normal levels. Furthermore, we found that co-treatment with both MeHg and multiple MGO scavengers or a CREB inhibitor (iCREB) mitigated MeHg-induced premature neuronal differentiation, reinforcing the role of Glo1 and CREB in mediating MeHg-induced neuronal differentiation. Our findings demonstrate a direct link between MeHg exposure and expression of an ASD risk gene Glo1 in cortical development, supporting the important role of gene-environment interaction in contributing to the etiology of neural developmental disorders, such as ASD.

Narrowing regional dietary disparities can help reduce methylmercury exposure in China

Narrowing regional dietary disparities can help reduce methylmercury exposure in China

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.

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 (600ppm) 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.

Methylmercury exposure at dosage conditions that do not affect growth can impair memory in adolescent mice.

The online version contains supplementary material available at 10.1007/s43188-024-00239-y.

Quercetin prevents methylmercury-induced mitochondrial dysfunction in the cerebral cortex of mice

Methylmercury (MeHg) exposure can cause nerve damage and mitochondrial dysfunction. Mitochondrial dysfunction is mainly mediated by mitochondrial biogenesis and mitochondrial dynamics disorders. Quercetin (QE) plays an important role in activating silencing information regulator 2 related enzyme 1 (SIRT1), and SIRT1 activates peroxisome-proliferator-activated receptor-γ co-activator 1α (PGC-1α), which can regulate mitochondrial biogenesis and mitochondrial dynamics. The main purpose of this study was to explore the alleviating effects of QE on MeHg-induced nerve damage and mitochondrial dysfunction. The results showed that QE could reduce the excessive production of reactive oxygen species (ROS) and the loss of membrane potential induced by MeHg. Meanwhile, QE activated SIRT1 activity and SIRT1/PGC-1α signaling pathway, improved mitochondrial biogenesis and fusion and reduced mitochondrial fission. In summary, we hypothesized that QE prevents MeHg-induced mitochondrial dysfunction by activating SIRT1/PGC-1α signaling pathway.