Mercury contents and potential exposure risk of rice-containing food products.

Mercury (Hg), especially methylmercury (MeHg), accumulation in rice grain due to rice paddy possessing conditions conducive to Hg methylation has led to human Hg exposure through consumption of rice-based daily meals. In addition to being a food staple, rice is widely used as a raw material to produce a vast variety of processed food products. Little is known about Hg levels in snacking rice-food products and potential Hg exposure from consumption of them, besides previous studies on infant rice cereals. Aiming to provide complementary information for a more complete assessment on Hg exposure risk originated from Hg-containing rice, this study determined total Hg (THg) and MeHg levels in 195 rice-containing and rice-free processed food products covering all major types of snack foods marketed in China and the estimated daily intake (EDI) of dietary Hg from the consumption of these foods. The results clearly showed THg and MeHg contents in rice-containing foods were significantly higher than rice-free products, suggesting the transfer of Hg and MeHg from the rice to the end products, even after manufacturing processes. Moreover, significant positive correlations were observed between THg, MeHg, or MeHg/THg ratio and rice content for samples containing multiple grains as ingredients, further indicating the deciding role of rice for Hg levels in the end food products. Although the EDI of THg and MeHg via rice-based food products were relatively low compared to the reference dose, it should be considered these snacking food products would contribute additive Hg intake outside of the daily regular meals.

Decoding trace element speciation in mushrooms: Analytical techniques, comprehensive data review, and health implications.

This review focuses on trace element speciation in edible mushrooms, providing information on analytical methods, available literature data, and health risk assessment. All steps of analytical procedures were presented, including extraction, separation and quantification. It compiles fragmented literature data on trace element speciation, focusing on arsenic, chromium, selenium, mercury, and antimony. Key findings include non-bioaccumulative chromium, the prevalence of Sb(V), mercury accumulation in contaminated sites, diverse arsenic and selenium speciation. Safe intake limits by agencies like USEPA indicate low risk for Cr(VI) and Sb but significant hazards from mercury and methylmercury, especially in contaminated areas: about 10 % of samples exceed safe limits for inorganic arsenic, and selenium enrichment often surpasses safety thresholds. The review underscores the need for standardized methods, speciation analyses of all toxicologically relevant species, and research on cooking impacts to improve health risk evaluations: establishing safe conditions for mushroom consumption remains a far-fetched goal.

The origin of methyl group in methanogen-mediated mercury methylation: From the Wolfe cycle.

Methylmercury (MeHg) is a bioaccumulating neurotoxin mainly produced by anaerobic microorganisms, with methanogen being one of the important methylators. A critical aspect for understanding the mechanism for microbial mercury (Hg) methylation is the origin of the methyl group. However, the origin of methyl group in methanogen-mediated Hg methylation remains unclear. This study aims to identify the source of methyl group for MeHg synthesis in methanogens. Our study revealed that Hg methylation in Methanospirillum hungatei JF-1 is closely related to methanogenesis process, according to the results of proteomic study and substrate limitation study. Next, we proved that nearly all methyl group in MeHg derives from the Wolfe cycle in this species, rather than the previously demonstrated acetyl-coenzyme A pathway, based on the results of 13C labeling study. We then proposed the Wolfe cycle-dependent Hg methylation mechanism in this species. Further genome analyses and 13C labeling experiments indicated that the involvement of the Wolfe cycle in Hg methylation is probably a universal feature among Hg-methylating methanogens. These findings reveal a unique Hg methylation mechanism in methanogens. Our study broadens the carbon substrates and controlling factors for MeHg synthesis in the environment, which can inform the prediction of MeHg production potential and remediation strategies for MeHg contamination.

The emerging application of LC-based metallomics techniques to unravel the bioinorganic chemistry of toxic metal(loid)s.

The on-going anthropogenic emission of toxic metal(loid) species into the environment contaminates the food supply and drinking water resources in various parts of the world. Given that inorganic pollutants cannot be degraded, their increased influx into the bloodstream of babies, children and pregnant women is inevitable. Since the ramifications of the ensuing environmental exposure on human health remain poorly defined, fundamentally new insight into their bioinorganic chemistry in organisms is urgently needed. Based on the flow of dietary constituents through organisms, the interaction of toxic metal(loid) species with biomolecules in the bloodstream deserve particular attention as they play an integral role in the mechanisms of their chronic toxicity. Gaining insight into these bioinorganic processes is hampered by the biological complexity of plasma/red blood cells and the low concentrations of the metal(loid) species of interest, but can be overcome by employing LC techniques hyphenated to atomic spectroscopic detectors (i.e. metallomics techniques). This perspective aims to highlight the potential of unconventional hyphenated separation modes to advance our understanding of the bioinorganic chemistry of toxic metal(loid) species in the bloodstream-organ system. Four examples are illustrated. The application of anion-exchange (AEX) and size-exclusion chromatography (SEC) provided new insight into the blood-based bioinorganic mechanisms that direct Cd2+ and MeHg+ to target organs. AEX chromatography also allowed to observe the formation of complexes between Hg2+ and MeHg+ with L-cysteine at pH 7.4, that are implicated in their organ uptake. Lastly, the application of reversed phase (RP) chromatography revealed a possible cytosolic mechanism by which N-acetyl-L-cysteine binds to MeHg+ in the presence of cytosolic glutathione (GSH). New insight into other bioinorganic processes may advance the regulatory framework to better protect public health.

Methylation of mercury and tin by estuarine microbial mats.

After tin and mercury salts were added to estuarine microbial mats increasing amounts of methyltin and methylmercury, respectively, were formed over a 30 to 100 hour time period. Inhibition of the methylation by molybdate, a metabolic inhibitor of sulfate reduction, stimulation by pyruvate addition and lack of methylation by sterilized mats, were evidence that sulfate reducing bacteria within the mats were responsible for the tin and mercury methylation. Methyl mercury was formed from mercuric chloride and mercuric cysteine, but not from mercuric sulfide. We suggest that mercury bound to organic complexes in anoxic sediments is likely methylated by microbial mats. Since estuarine meiofauna and macrofauna fed on microbial mats, the methylmercury and methyltin formed by microbial mats could be an important avenue for the entrance of these compounds into the marine food web.

Intake rates of methylmercury in the Belgian population: Evolution over 40 years.

Methylmercury (MeHg) is one of the most toxic compounds, it bioaccumulates and biomagnifies along the food chain and finally damages human's nervous system. Knowing that the main intake route for MeHg in humans is through fish consumption, intake rates were studied in various countries, but not in Belgium. Based on Hg and MeHg measurements in various fishes, mainly from North Sea catches, in combination with the national food consumption surveys, we could calculate daily Hg and MeHg intake rates for the Belgian population in 1975, 1997 and 2014-2021. These values are then compared with daily intake values reported by other countries and with the acceptable daily intake (ADI) values recommended by international organizations. Daily Hg and MeHg intake rates decreased strongly between 1975 and the 2 later periods: while average intake rates are all below the ADI norms, this is not the case for the 95th percentile rates because they exceed or are very close to the ADI values. Since daily MeHg intake rates correlate well with hair and blood concentrations, these were used as a good proxy of MeHg intoxication and were related to health effects observed in children, adolescents, adults and elderly persons living in Belgium via biomonitoring.

Therapeutic potential of oleanolic acid in modulation of PI3K/Akt/mTOR/STAT-3/GSK-3ß signaling pathways and neuroprotection against methylmercury-induced neurodegeneration.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder that gradually deteriorates motor neurons, leading to demyelination, muscle weakness, and eventually respiratory failure. The disease involves several pathological processes, such as increased glutamate levels, mitochondrial dysfunction, and persistent neuroinflammation, often exacerbated by environmental toxins like mercury. This study explores the therapeutic potential of Olea europaea active phytoconstituents oleanolic acid (OLA) against ALS by targeting the overactivated PI3K/Akt/mTOR/STAT-3/GSK-3ß signalling pathways. Methods involved in-silico studies, in vitro and in vivo experiments in which varying doses of methylmercury 5 mg/kg, p.o. and OLA (100 and 200 mg/kg, i.p.) were administered to rats for 42 days. Behavioural assessments, gross morphological, histopathological, and neurochemical parameters were measured in cerebrospinal fluid (CSF), blood plasma, and brain homogenates (cerebral cortex, hippocampus, striatum, midbrain, cerebellum) along with complete blood count (CBC) analysis. Results revealed OLA's significant neuroprotective properties. OLA effectively modulated targeted pathways, reducing pro-inflammatory cytokines, restoring normal levels of myelin basic protein (MBP) and neurofilament light chain (NEFL), and reducing histopathological changes. Gross pathological studies indicated less tissue damage, while CBC analysis showed improved hematology parameters. Additionally, the combination of OLA and edaravone (10 mg/kg, i.p.) demonstrated enhanced efficacy, improving motor functions and extending survival in ALS model rats. In conclusion, OLA exhibits significant therapeutic potential for ALS, acting as a potent modulator of key pathological signaling pathways. The findings suggest the feasibility of integrating OLA into existing treatment regimens, potentially improving clinical outcomes for ALS patients. However, further research must validate these findings in human clinical trials.

Multiple effects of carbon, sulfur and iron on microbial mercury methylation in black-odorous sediments.

Black-odorous sediments provide ideal conditions for microbial mercury methylation. However, the multiple effects of carbon, sulfur, and iron on the microbial methylmercury of mercury in black-odorous sediments remains unclear. In this study, we conducted mercury methylation experiments using sediments collected from organically contaminated water bodies, as well as black-odorous sediments simulated in the laboratory. The results showed that black-odorous sediments exhibit a high capacity for mercury methylation. By simulating the blackening and odorization process in sediments, it was confirmed that dissolved oxygen, organic matter and sulfide were the primary factors triggering the black-odorous phenomenon in sediments. Regarding the influence of key factors in sediments on methylmercury formation, the batch tests demonstrated that high concentrations of organics additions (above 200 mg/L) may reduce bacterial activity and weaken mercury methylation in sediments. Under five different iron-sulfur ratios, the concentrations of methylmercury in the black-odorous sediments showed an increasing trend, the ratio of 5.0 Fe/S exhibited the highest MeHg accumulation. The iron-sulfur ratio in the sediment had a significant effect on the mercury methylation process, which was mainly due to the competition between Fe2+ and Hg2+ for sulfide sites and the adsorption/coprecipitation of Hg2+ by FeS. These findings offer a potential avenue for further understanding and controlling mercury methylation, contributing to the mitigation of the potential threat of mercury pollution to the environment and human health.

Environmental pollution challenges public health surveillance: the case of mercury exposure and intoxication in Brazil.

Pollution, causing millions of deaths annually, disproportionally affects low- and middle-income countries (LMICs). Mercury ranks among the three main chemicals of major public health concern, and even low levels can cause cardiovascular and nervous outcomes, with children and indigenous populations being especially vulnerable. Nearly 80% of all emissions in South America originate from the Amazon. Brazil, the fifth-largest contributor to global mercury emissions, exemplifies the challenges faced by LMICs in effectively monitoring and addressing mercury exposure/intoxication. Despite having powerful tools such as SINAN (a digital platform for compulsory disease reporting), and Community Health Agents, data reveals significant underreporting, especially in the Amazon. Furthermore, SINAN has important delays in its update: for instance, 196 cases of Munduruku Indigenous people in 2019 have only been included in 2023. In this Personal View, we outline insightful recommendations to enhance public health surveillance and implement enduring, effective strategies to monitor, report and address mercury exposure/intoxication, focusing on the Brazilian Amazon. Although these recommendations are tailored to the challenges of this country, they hold potential for adaptation by other Amazonian countries facing similar issues (high mercury emissions and the presence of vulnerable populations, among others).

Impact of geochemistry and microbes on the methylmercury production in mangrove sediments.

Unraveling the geochemical and microbial controls on methylmercury (MeHg) dynamics in mangrove sediments is important, as MeHg can potentially pose risks to marine biota and people that rely on these ecosystems. While the important role of sulfate-reducing bacteria in MeHg formation has been examined in this ecologically important habitat, the contribution of non-Hg methylating communities on MeHg production remains particularly unclear. Here, we collected sediment samples from 13 mangrove forests in south China and examined the geochemical parameters and microbial communities related to the Hg methylation. MeHg concentrations were significantly correlated to the OM-related parameters such as organic carbon content, total nitrogen, and dissolved organic carbon concentrations, suggesting the importance of OM in the MeHg production. Sulfate-reducing bacteria were the major Hg-methylators in mangrove sediments. Desulfobacteraceae and Desulfobulbaceae dominated the Hg-methylating microbes. Classification random forest analysis detected strong co-occurrence between Hg methylators and putative non-Hg methylators, thus suggesting that both types of microorganisms contribute to the MeHg dynamics in the sediments. Our study provides an overview of MeHg contamination in south China and advances our understanding of Hg methylation in mangrove ecosystems.

Development of a sensor to detect methylmercury toxicity.

Methylmercury (MeHg) is a well-known neurotoxicant that induces various cellular functions depending on cellular- and developmental-specific vulnerabilities. MeHg has a high affinity for selenol and thiol groups, thus impairing the antioxidant system. Such affinity characteristics of MeHg led us to develop sensor vectors to assess MeHg toxicity. In this study, MeHg-mediated defects in selenocysteine (Sec) incorporation were demonstrated using thioredoxin reductase 1 cDNA fused with the hemagglutinin tag sequence at the C-terminus. Taking advantage of such MeHg-mediated defects in Sec incorporation, a cDNA encoding luciferase with a Sec substituted for cysteine-491 was constructed. This construct showed MeHg-induced decreases in signaling in a dose-dependent manner. To directly detect truncated luciferase under MeHg exposure, we further constructed a new sensor vector fused with a target for proteasomal degradation. However, this construct was inadequate because of the low rate of Sec insertion, even in the absence of MeHg. Finally, a Krab transcriptional suppressor fused with Sec was constructed and assessed to demonstrate MeHg-dependent increases in signal intensity. We confirmed that the vector responded specifically and in a dose-dependent manner to MeHg in cultured cerebellar granule cells. This vector is expected to allow monitoring of MeHg-specific toxicity via spatial and temporal imaging.

L-cysteine mediated rapid separation of Hg2+ and MeHg+ by anion-exchange HPLC.

Owing to the on-going emission of Hg into the global environment, new insight into their bioinorganic chemistry in mammals is urgently required to better understand their adverse health effects and analytical methods to quantify Hg2+ and MeHg+ in environmental samples are needed. Analytical separations can help to address both of these needs. While Hg2+ and MeHg+ have been most frequently separated by cation and reversed-phase (RP) HPLC, we here report on using anion-exchange (AEX) HPLC in conjunction with a flame atomic absorption spectrometer (FAAS) to observe the retention behavior of these mercury species in the pH range 5.0-8.0 using mobile phases comprised of 10 mM l-cysteine (Cys) in 100 mM phosphate buffer. The results obtained for pH 5.0 served as a starting point to develop a rapid HPLC separation for these mercurials. The addition of 5-20 % methanol (MeOH) to this mobile phase revealed that MeOH did not appreciably change the retention of Hg2+, but significantly reduced the retention of MeHg+. A 15 % MeOH-containing mobile phase offered the best compromise between achieving a rapid baseline separation in <400 s at affordable costs. To assess the suitability and robustness of the developed AEX-HPLC separation method for the analysis of environmental samples an inductively coupled plasma atomic emission spectrometer (ICP-AES) was employed as the mercury-specific detector. The developed AEX-HPLC-ICP-AES method allowed to achieve detection limits of 1.5 ppm for Hg2+ and 2.9 ppm for MeHg+ and was successfully applied to analyze wastewater that had been spiked with Hg2+ and MeHg+.

Quinolone antibiotics stimulate bacterial mercury methylation by Geobacter metallireducens GS-15.

Bacterial mercury (Hg) methylation is critical for bioremediating Hg pollution, but the impact of emerging antibiotics on this process has rarely been reported. This study innovatively investigated the interactions between Hg-methylating bacteria of Geobacter metallireducens GS-15 and two quinolone antibiotics: lomefloxacin (LOM) and ciprofloxacin (CIP) at 5 µg/L. Short-term LOM exposure increased methylmercury (MeHg) yield by 36 % compared to antibiotic-free conditions, caused by hormesis to alter bioactivities of single GS-15 cells. Long-term CIP exposure led to more antibiotic resistance and mercury tolerance in GS-15 cells, doubling MeHg productivity and significantly increasing expression of Hg methylation (hgcA by 95 folds) and antibiotic resistance (gyrA by 54 folds) genes, while mercury resistance gene merA only increased by 2.5 folds than without selective pressure. These results suggest quinolone antibiotics at environmentally contaminated concentrations stimulate bacterial Hg methylation to form highly toxic MeHg, raising considerable concern for the Hg-antibiotic complex in contaminated environments.

Methylmercury chloride inhibits meiotic maturation of mouse oocytes in vitro by disrupting the cytoskeleton.

Methylmercury chloride (MMC) is a persistent heavy metal contaminant that can bioaccumulate in humans via the food chain, exerting detrimental effects on health. Nevertheless, the specific influence of MMC on oocyte meiotic maturation has yet to be elucidated. This research demonstrated that MMC exposure during the in vitro cultivation of mouse oocytes did not influence germinal vesicle breakdown but markedly decreased oocyte maturation rates. Subsequent analysis indicated that MMC exposure resulted in aberrant spindle morphology and disorganized chromosome alignment, alongside continuous activation of the spindle assembly checkpoint (SAC). However, MMC exposure didn't alter the localization pattern of microtubule-organizing center-associated proteins. MMC exposure considerably diminished the acetylation level of α-tubulin, signifying reduced microtubule stability. Additionally, MMC exposure disrupted the dynamic alterations of F-actin. MMC exposure didn't affect mitochondrial localization, mitochondrial membrane potential, adenosine triphosphate content or the concentrations of reactive oxygen species. Nonetheless, MMC exposure triggered DNA damage and modified histone modification levels. Consequently, the defects in oocyte maturation induced by MMC exposure can be attributed to impaired cytoskeleton dynamics and DNA damage. This study offers the first comprehensive elucidation of the negative impacts of MMC on oocyte maturation, highlighting the potential reproductive health risks associated with MMC exposure.

Exploring mercury detoxification in fish: The role of selenium from tuna byproduct diets for sustainable aquaculture.

Exposure to mercury (Hg) through fish consumption poses significant environmental and public health risks, given its status as one of the top ten hazardous chemicals. Aquaculture is expanding, driving a surge in demand for sustainable aquafeeds. Tuna byproducts, which are rich in protein, offer potential for aquafeed production, yet their use is challenged by the high content of heavy metals, particularly Hg. However, these byproducts also contain elevated levels of selenium (Se), which may counteract Hg adverse effects. This study examines the fate of dietary Hg and Se in an aquaculture model fish. Biomolecular speciation analyses through hyphenated analytical approaches were conducted on the water-soluble protein fraction of key organs of juvenile rainbow trout (Oncorhynchus mykiss) exposed to various combinations of Hg and Se species, including diets containing tuna byproducts, over a six-month period. The findings shed light on the dynamics of Hg and Se compounds in fish revealing potential Hg detoxification mechanisms through complexation with Hg-biomolecules, such as cysteine, glutathione, and metallothionein. Furthermore, the trophic transfer of selenoneine is demonstrated, revealing novel opportunities for sustainable aquafeed production. Understanding the interactions between Hg and Se in aquaculture systems is crucial for optimizing feed formulations and mitigating environmental risks. This research contributes to the broader goal of advancing sustainable practices in aquaculture while addressing food security challenges.

Total mercury and methylmercury in lake water in years before and after removal of mercury-polluted pulp fiber sediment.

There is an elevated presence of mercury (Hg) in the biosphere because of anthropogenic activities. The resulting damage to ecosystems and human health increases dramatically when microorganisms produce highly toxic methylmercury (MeHg). Total Hg (THg), MeHg and ancillary water chemistry were measured in two connected lakes, separated by a short stream stretch, before (1996, 1998 and 2003) and after (2007, 2009 and 2010) the removal of Hg-polluted pulp fiber sediment. Over the study period, there was a decrease in sulfate in the surface water of both lakes, presumably because of declining atmospheric sulfate deposition. Together, the reductions in OM, sulfate, and Hg, resulted in decreased MeHg concentrations as well as decreased MeHg:THg ratios in the bottom water overlying the sediment. There was also a reduction in zooplankton MeHg and fish total Hg in both lakes. Multiple regressions, using the bottom water data before and after remediation from both lakes, indicated that both the yearly maximum MeHg concentration [MeHgmax] and MeHgmax:THg correlated positively with the simultaneously measured sulfate deficit (a proxy for microbial sulfate reduction) and inorganic Hg concentration (IHg = THg - MeHg). This may suggest that the removal of Hg and the decreased sulfate reduction not only led to a decrease in available Hg substrate for methylation but also disfavored the Hg methylation process. As opposed to sulfate deficit, other measurements reflecting heterotrophic microbial activity such as inorganic carbon (IC), ammonium (NH4+), and iron (Fe) did not show significant correlations with MeHg or MeHg:THg when the data from both lakes were combined.

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.

[Responses to "A Review of the Book 'Minamata Disease and the Responsibility of Medical Authorities'"].

Drs. Futatsuka, Eto, and Uchino expressed their opinions in the Journal of the Japanese Society for Hygiene in the form of a review of my book, "Minamata Disease and the Responsibility of Medicine." (The reviewers translated it as "Responsibility of Medical Authorities," but for my purposes in writing this book, I believe it should be translated as "Responsibility of Medicine.") The nine major comments of the three reviewers described in this book review were reviewed from the basic perspective of toxicology, epidemiology, and neuroscience. This book review is fraught with either medical, logical, or ethical problems in all the nine points as follows: (1) the inadequate way in which exposure and health hazards are considered from the toxicological perspective, (2) problems in interpreting epidemiological information, (3) the failure to consider recent achievements in methylmercury toxicosis studies, (4) presenting the reviewers' own theories without regard to the content of my book while calling it a "book review," (5) presenting and criticizing what Takaoka does not claim as if he does, and (6) making claims that are inconsistent with the three reviewers' own views. The problems with this book review will become even clearer when you read "Minamata Disease and the Responsibility of Medicine" itself.

Assessment of mercury methylation and methylmercury demethylation potentials in water and sediments along the Wabigoon River system.

Monomethylmercury (MMHg) plays a crucial role in the accumulation of mercury (Hg) within aquatic food chains. Since ambient levels of methylmercury are governed by the balance of simultaneous methylation and demethylation processes, determining in situ methylation and demethylation rates is critically important to understand the dynamics of methylmercury in the environment. This is especially important in the Wabigoon River system in Ontario, Canada, which is severely contaminated with Hg by a chlor-alkali facility operating in the 1960s, and still exhibits some of the highest recorded fish mercury concentrations in Canada. This work used a simultaneous addition of isotope enriched Hg and MMHg tracers to ascertain Hg methylation and MMHg demethylation potentials. At the locations investigated for this study, the most favourable conditions for Hg methylation were found at the Hydroelectric dam, being able to transform 4.2 % and 4.4 % of added Hg in water and sediments per day, respectively, to MMHg. This could correspond to 1.9 ng/L and 29 ng/g of new MMHg being produced from current ambient Hg. Clay Lake, which is considered a sink for mercury and exhibiting a seasonal anoxic environment at its bottom waters, also demonstrated significant MMHg generation, being able to produce 2.7 ng/L and 13 ng/g of MMHg per day, respectively. Demethylation rates in sediments of riverbed and wetland locations showed an average half-life for methylmercury of 2.1 days, indicating a rapid turnover of MMHg in the Wabigoon River. However, significantly lower demethylation rates were also measured near the inflow of Clay Lake, where it took up to 144 days for MMHg to decrease by 50 %. Generally, most of the investigated locations downstream of the pollution source displayed the potential to generate methylmercury, which could be distributed throughout the Wabigoon River system and therefore require attention with respect to future remediation activities.

Dietary protein affects tissue accumulation of mercury and induces hepatic Phase I and Phase II enzyme expression after co-exposure with methylmercury in mice.

Methylmercury (MeHg) is a ubiquitous environmental contaminant, well known for its neurotoxic effects. MeHg can interact with several nutrients in the diet and affect nutrient metabolism, however the interaction between MeHg and dietary proteins has not been thoroughly investigated. Male BALB/c mice were fed diets based on either casein, cod or chicken as protein sources, which were or were not spiked with MeHg (3.5 mg Hg kg-1). Following 13 weeks of dietary exposure to MeHg, the animals accumulated mercury in a varying degree depending on the diet, where the levels of mercury were highest in the mice fed casein and MeHg, lower in mice fed cod and MeHg, and lowest in mice fed chicken and MeHg in all tissues assessed. Assessment of gut microbiota revealed differences in microbiota composition based on the different protein sources. However, the introduction of MeHg eliminated this difference. Proteomic profiling of liver tissue uncovered the influence of the dietary protein sources on a range of enzymes related to Phase I and Phase II detoxification mechanisms, suggesting an impact of the diet on MeHg metabolism and excretion. Also, enzymes linked to pathways including methionine and glycine betaine cycling, which in turn impact the production of glutathione, an important MeHg conjugation molecule, were up-regulated in mice fed chicken as dietary protein. Our findings indicate that dietary proteins can affect expression of hepatic enzymes that potentially influence MeHg metabolism and excretion, highlighting the relevance of considering the dietary composition in risk assessment of MeHg through dietary exposure.