Anthropogenic short-lived halogens increase human exposure to mercury contamination due to enhanced mercury oxidation over continents.

Mercury (Hg) is a contaminant of global concern, and an accurate understanding of its atmospheric fate is needed to assess its risks to humans and ecosystem health. Atmospheric oxidation of Hg is key to the deposition of this toxic metal to the Earth's surface. Short-lived halogens (SLHs) can provide halogen radicals to directly oxidize Hg and perturb the budget of other Hg oxidants (e.g., OH and O3). In addition to known ocean emissions of halogens, recent observational evidence has revealed abundant anthropogenic emissions of SLHs over continental areas. However, the impacts of anthropogenic SLHs emissions on the atmospheric fate of Hg and human exposure to Hg contamination remain unknown. Here, we show that the inclusion of anthropogenic SLHs substantially increased local Hg oxidation and, consequently, deposition in/near Hg continental source regions by up to 20%, thereby decreasing Hg export from source regions to clean environments. Our modeling results indicated that the inclusion of anthropogenic SLHs can lead to higher Hg exposure in/near Hg source regions than estimated in previous assessments, e.g., with increases of 8.7% and 7.5% in China and India, respectively, consequently leading to higher Hg-related human health risks. These results highlight the urgent need for policymakers to reduce local Hg and SLHs emissions. We conclude that the substantial impacts of anthropogenic SLHs emissions should be included in model assessments of the Hg budget and associated health risks at local and global scales.

Bioremediation of mercury-polluted soil and water by the plant symbiotic fungus Metarhizium robertsii.

Fungi are central to every terrestrial and many aquatic ecosystems, but the mechanisms underlying fungal tolerance to mercury, a global pollutant, remain unknown. Here, we show that the plant symbiotic fungus Metarhizium robertsii degrades methylmercury and reduces divalent mercury, decreasing mercury accumulation in plants and greatly increasing their growth in contaminated soils. M. robertsii does this by demethylating methylmercury via a methylmercury demethylase (MMD) and using a mercury ion reductase (MIR) to reduce divalent mercury to volatile elemental mercury. M. robertsii can also remove methylmercury and divalent mercury from fresh and sea water even in the absence of added nutrients. Overexpression of MMD and MIR significantly improved the ability of M. robertsii to bioremediate soil and water contaminated with methylmercury and divalent mercury. MIR homologs, and thereby divalent mercury tolerance, are widespread in fungi. In contrast, MMD homologs were patchily distributed among the few plant associates and soil fungi that were also able to demethylate methylmercury. Phylogenetic analysis suggests that fungi could have acquired methylmercury demethylase genes from bacteria via two independent horizontal gene transfer events. Heterologous expression of MMD in fungi that lack MMD homologs enabled them to demethylate methylmercury. Our work reveals the mechanisms underlying mercury tolerance in fungi, and may provide a cheap and environmentally friendly means of cleaning up mercury pollution.

Horizontal gene transfer of the Mer operon is associated with large effects on the transcriptome and increased tolerance to mercury in nitrogen-fixing bacteria.

BACKGROUND: Mercury (Hg) is highly toxic and has the potential to cause severe health problems for humans and foraging animals when transported into edible plant parts. Soil rhizobia that form symbiosis with legumes may possess mechanisms to prevent heavy metal translocation from roots to shoots in plants by exporting metals from nodules or compartmentalizing metal ions inside nodules. Horizontal gene transfer has potential to confer immediate de novo adaptations to stress. We used comparative genomics of high quality de novo assemblies to identify structural differences in the genomes of nitrogen-fixing rhizobia that were isolated from a mercury (Hg) mine site that show high variation in their tolerance to Hg. RESULTS: Our analyses identified multiple structurally conserved merA homologs in the genomes of Sinorhizobium medicae and Rhizobium leguminosarum but only the strains that possessed a Mer operon exhibited 10-fold increased tolerance to Hg. RNAseq analysis revealed nearly all genes in the Mer operon were significantly up-regulated in response to Hg stress in free-living conditions and in nodules. In both free-living and nodule environments, we found the Hg-tolerant strains with a Mer operon exhibited the fewest number of differentially expressed genes (DEGs) in the genome, indicating a rapid and efficient detoxification of Hg from the cells that reduced general stress responses to the Hg-treatment. Expression changes in S. medicae while in bacteroids showed that both rhizobia strain and host-plant tolerance affected the number of DEGs. Aside from Mer operon genes, nif genes which are involved in nitrogenase activity in S. medicae showed significant up-regulation in the most Hg-tolerant strain while inside the most Hg-accumulating host-plant. Transfer of a plasmid containing the Mer operon from the most tolerant strain to low-tolerant strains resulted in an immediate increase in Hg tolerance, indicating that the Mer operon is able to confer hyper tolerance to Hg. CONCLUSIONS: Mer operons have not been previously reported in nitrogen-fixing rhizobia. This study demonstrates a pivotal role of the Mer operon in effective mercury detoxification and hypertolerance in nitrogen-fixing rhizobia. This finding has major implications not only for soil bioremediation, but also host plants growing in mercury contaminated soils.

Multistress Interplay: Time and Duration of Ocean Acidification Modulate the Toxicity of Mercury and Other Metals.

The current understanding of multistress interplay assumes stresses occur in perfect synchrony, but this assumption is rarely met in the natural marine ecosystem. To understand the interplay between nonperfectly overlapped stresses in the ocean, we manipulated a multigenerational experiment (F0-F3) to explore how different temporal scenarios of ocean acidification will affect mercury toxicity in a marine copepod Pseudodiaptomus annandalei. We found that the scenario of past acidification aggravated mercury toxicity but current and persistent acidification mitigated its toxicity. We specifically performed a proteomics analysis for the copepods of F3. The results indicated that current and persistent acidification initiated the energy compensation for development and mercury efflux, whereas past acidification lacked the barrier of H+ and had dysfunction in the detoxification and efflux system, providing a mechanistic understanding of mercury toxicity under different acidification scenarios. Furthermore, we conducted a meta-analysis on marine animals, demonstrating that different acidification scenarios could alter the toxicity of several other metals, despite evidence from nonsynchronous scenarios remaining limited. Our study thus demonstrates that time and duration of ocean acidification modulate mercury toxicity in marine copepods and suggests that future studies should move beyond the oversimplified scenario of perfect synchrony in understanding multistress interaction.

Reductions in plasma and urine mercury concentrations following N,N'bis-(2-mercaptoethyl) isophthalamide (NBMI) therapy: a post hoc analysis of data from a randomized human clinical trial.

Environmental mercury exposure possesses a significant risk to many human populations. At present there are no effective treatments for acute mercury toxicity. A new compound, N,N'bis-(2-mercaptoethyl) isophthalamide (NBMI), a lipophilic chelating agent was created to tightly/irreversibly bind mercury. A post hoc dose-dependent analysis of NBMI therapy was undertaken on data from a randomized controlled NBMI human treatment trial on 36 Ecuadorian gold miners with elevated urinary mercury concentrations. Study subjects were randomly assigned to receive 100 milligram (mg) NBMI/day, 300 mg NBMI/day, or placebo for 14 days. For each study subject daily mg NBMI dose/Kilogram (Kg) bodyweight were determined and plasma and urine mercury concentrations (micrograms (µg)/Liter (L)) on study day 1 (pre-NBMI treatment), 15 (after 14 days of NBMI treatment) and 45 (30 days after NBMI treatment) were correlated with NBMI dosing using the linear regression statistic in SAS. Regression revealed significant inverse correlations between increasing per mg NBMI/Kg bodyweight/day and reduced concentrations of urinary and plasma mercury on study day 15 (reduced by in urine = 18-20 µg/L and plasma = 2 µg/L) and study day 30 (reduced by in urine = 15-20 µg/L and plasma = 4 µg/L) and significant correlations between reductions in mercury concentrations in urine and plasma. Significant 30% reductions in urinary mercury concentrations per mg NBMI/Kg bodyweight/day administered for 14 days were observed. This study supports the dose-dependent ability of NBMI therapy to significantly reduce mercury concentrations, particularly in the urine, in an acutely mercury exposed human population. NBMI therapy should be evaluated in other mercury exposed populations.

In vivo chronic exposure to inorganic mercury worsens hypercholesterolemia, oxidative stress and atherosclerosis in the LDL receptor knockout mice.

Heavy metal exposure leads to multiple system dysfunctions. The mechanisms are likely multifactorial and involve inflammation and oxidative stress. The aim of this study was to evaluate markers and risk factors for atherosclerosis in the LDL receptor knockout mouse model chronically exposed to inorganic mercury (Hg) in the drinking water. Results revealed that Hg exposed mice present increased plasma levels of cholesterol, without alterations in glucose. As a major source and target of oxidants, we evaluated mitochondrial function. We found that liver mitochondria from Hg treated mice show worse respiratory control, lower oxidative phosphorylation efficiency and increased H2O2 release. In addition, Hg induced mitochondrial membrane permeability transition. Erythrocytes from Hg treated mice showed a 50% reduction in their ability to take up oxygen, lower levels of reduced glutathione (GSH) and of antioxidant enzymes (SOD, catalase and GPx). The Hg treatment disturbed immune system cells counting and function. While lymphocytes were reduced, monocytes, eosinophils and neutrophils were increased. Peritoneal macrophages from Hg treated mice showed increased phagocytic activity. Hg exposed mice tissues present metal impregnation and parenchymal architecture alterations. In agreement, increased systemic markers of liver and kidney dysfunction were observed. Plasma, liver and kidney oxidative damage indicators (MDA and carbonyl) were increased while GSH and thiol groups were diminished by Hg exposure. Importantly, atherosclerotic lesion size in the aorta root of Hg exposed mice were larger than in controls. In conclusion, in vivo chronic exposure to Hg worsens the hypercholesterolemia, impairs mitochondrial bioenergetics and redox function, alters immune cells profile and function, causes several tissues oxidative damage and accelerates atherosclerosis development.

HgCl2 exposure mediates pyroptosis of HD11 cells and promotes M1 polarization and the release of inflammatory factors through ROS/Nrf2/NLRP3.

Mercury (Hg) is a serious metal environmental pollutant. HgCl2 exposure causes pyroptosis. When macrophages are severely stimulated, they often undergo M1 polarization and release inflammatory factors. However, the mechanisms by which mercuric chloride exposure induces macrophage apoptosis, M1 polarization, and inflammatory factors remain unclear. HD11 cells were exposed to different concentrations of Hg chloride (180, 210 and 240 nM HgCl2). The results showed that mercury chloride exposure up-regulated ROS, C-Nrf2 and its downstream factors (NQO1 and HO-1), and down-regulated N-Nrf2. In addition, the expressions of focal death-related indicators (Caspase-1, NLRP3, GSDMD, etc.), M1 polarization marker CD86 and inflammatory factors (TNF-α, IL-1ß) increased, and the above changes were related to mercury. Oxidative stress inhibitor (NAC) can block ROS/ NrF2-mediated oxidative stress, inhibit mercury-induced pyroptosis and M1 polarization, and effectively reduce the release of inflammatory factors. The addition of Vx-765 to inhibit pyroptosis can effectively alleviate M1 polarization of HD11 cells and reduce the expression of inflammatory factors. HgCl2 mediates pyroptosis of HD11 cells by regulating ROS/Nrf2/NLRP3, promoting M1 polarization and the release of inflammatory factors.

Exposure to a mixture of metal(loid)s and sleep quality in pregnant women during early pregnancy: A cross-sectional study.

Biological characteristics of pregnant women during early pregnancy make them susceptible to both poor sleep quality and metal/metalloid exposure. However, the effects of metal(loid) exposure on sleep quality in pregnant women remain unknown and unexplored. We aimed to examine the relationship between exposure to a mixture of metal(loid)s and pregnant women's sleep quality during early pregnancy. We recruited 493 pregnant women in the first trimester from prenatal clinics in Jinan, Shandong Province, China, and collected their spot urine samples. All urine specimens were assessed for eight metal(loid)s: arsenic (As), cadmium (Cd), iron (Fe), zinc (Zn), molybdenum (Mo), lead (Pb), selenium (Se), and mercury (Hg). We used the Pittsburgh Sleep Quality Index (PSQI) to assess sleep quality. Linear regression, logistic regression, generalized additive models (GAMs), quantile g-computation, and Bayesian kernel machine regression (BKMR) were applied to investigate the relationships between metal(loid) exposure and sleep quality. The results from single metal(loid) models, quantile g-computation models, and BKMR models consistently suggested that Fe was positively related to women's sleep quality. Moreover, in the quantile g-computation models, As was the most critical contributor to the negative effects of the metal(loid) mixture on sleep quality. In addition, we found significant As by Fe interaction for scores of PSQI and habitual sleep efficiency, Pb by Fe interaction for PSQI and sleep latency, and Hg by Fe interaction for PSQI, suggesting the interactive effects of As and Fe, Pb and Fe, Hg and Fe on sleep quality and specific sleep components. Our study provided the first-hand evidence of the effects of metal(loid) exposure on pregnant women's sleep quality. The underlying mechanisms need to be explored in the future.

Iron nanoparticles in combination with other conventional Fe sources remediate mercury toxicity-affected plants and soils by nutrient accumulation in bamboo species.

The issue of mercury (Hg) toxicity has recently been identified as a significant environmental concern, with the potential to impede plant growth in forested and agricultural areas. Conversely, recent reports have indicated that Fe, may play a role in alleviating HM toxicity in plants. Therefore, this study's objective is to examine the potential of iron nanoparticles (Fe NPs) and various sources of Fe, particularly iron sulfate (Fe SO4 or Fe S) and iron-ethylene diamine tetra acetic acid (Fe - EDTA or Fe C), either individually or in combination, to mitigate the toxic effects of Hg on Pleioblastus pygmaeus. Involved mechanisms in the reduction of Hg toxicity in one-year bamboo species by Fe NPs, and by various Fe sources were introduced by a controlled greenhouse experiment. While 80 mg/L Hg significantly reduced plant growth and biomass (shoot dry weight (36%), root dry weight (31%), and shoot length (31%) and plant tolerance (34%) in comparison with control treatments, 60 mg/L Fe NPs and conventional sources of Fe increased proline accumulation (32%), antioxidant metabolism (21%), polyamines (114%), photosynthetic pigments (59%), as well as root dry weight (25%), and shoot dry weight (22%), and shoot length (22%). Fe NPs, Fe S, and Fe C in plant systems substantially enhanced tolerance to Hg toxicity (23%). This improvement was attributed to increased leaf-relative water content (39%), enhanced nutrient availability (50%), improved antioxidant capacity (34%), and reduced Hg translocation (6%) and accumulation (31%) in plant organs. Applying Fe NPs alone or in conjunction with a mixture of Fe C and Fe S can most efficiently improve bamboo plants' tolerance to Hg toxicity. The highest efficiency in increasing biochemical and physiological indexes under Hg, was related to the treatments of Fe NPs as well as Fe NPs + FeS + FeC. Thus, Fe NPs and other Fe sources might be effective options to remove toxicity from plants and soil. The future perspective may help establish mechanisms to regulate environmental toxicity and human health progressions.

Exploring the association between two groups of metals with potentially opposing renal effects and renal function in middle-aged and older adults: Evidence from an explainable machine learning method.

BACKGROUND: Machine learning models have promising applications in capturing the complex relationship between mixtures of exposures and outcomes. OBJECTIVE: Our study aimed at introducing an explainable machine learning (EML) model to assess the association between metal mixtures with potentially opposing renal effects and renal function in middle-aged and older adults. METHODS: This study extracted data from two cycle years of the National Health and Nutrition Examination Survey (NHANES). Participants aged 45 years or older with complete data on six metals (lead, cadmium, manganese, mercury, and selenium) and related covariates were enrolled. The EML model was developed by the optimized machine learning model together with Shapley Additive exPlanations (SHAP) to assess the chronic kidney disease (CKD) risk with metal mixtures. The results from EML were further compared in detail with multiple logistic regression (MLR) and Bayesian kernel machine regression (BKMR). RESULTS: After adjusting for included covariates, MLR pointed out the lead and arsenic were generally positively associated with CKD, but manganese had a negative association. In the BKMR analysis, each metal was found to have a non-linear association with the risk of CKD, and interactions can exist between metals, especially for arsenic and lead. The EML ranked the feature importance: lead, manganese, arsenic and selenium were close behind in importance after gender, age or BMI for participants with CKD. Strong interactions between mercury and lead, manganese and cadmium and arsenic and manganese were identified by partial dependence plot (PDP) of SHAP and bivariate exposure-response effect plots of BKMR. The EML model determined the "trigger point" at which the risk of CKD abruptly changed. CONCLUSION: Co-exposure to metals with different nephrotoxicity could have different joint association with renal function, and EML can be a powerful method for studying complex exposure mixtures.

Neurological risks arising from the bioaccumulation of heavy metal contaminants: A focus on mercury.

This study investigated the concentrations of heavy metals in the water sources of the upstream region of the Huangpu River, the Yangtze River Estuary, and various areas in Shanghai, as well as the heavy metal concentrations in the blood of Shanghai residents. It aimed to analyze the heavy metal elements absorbed by the human body and the resulting pathological effects. The results revealed that surface water primarily contains five heavy metals: copper (Cu), lead (Pb), zinc (Zn), arsenic (As), and mercury (Hg), while water sediments primarily contain seven heavy metals: Cu, cadmium (Cd), Pb, chromium (Cr), Zn, As, and Hg. The main heavy metals present in the human body are Pb, Hg, As, and Cd. By reviewing previous articles, it was found that heavy metal concentrations in human blood are higher than those in surface water, suggesting uncertainties in the heavy metal content of surface water and its tendency to settle at the bottom. Furthermore, a comparison of heavy metal content in sediments revealed that Hg is the most readily absorbed heavy metal by the human body and is also a toxic environmental pollutant. Within the cell, Hg is highly toxic to mitochondria and may cause oxidative stress and neurodegenerative disease. This study concludes that water sediments serve as the major source of pollution in the human body and pose significant health risks, thereby necessitating the implementation of effective preventive measures.

Selenium and zinc alleviate hepatotoxicity induced by heavy metal mixture (cadmium, mercury, lead and arsenic) via attenuation of inflammo-oxidant pathways.

Heavy metals (HM) are believed to be injurious to humans. Man is exposed to them on daily basis unknowingly, with no acceptable protocol to manage its deleterious effects. These metals occur as mixture of chemicals with varying concentrations in our atmosphere. There are growing calls for the use of essential metals in mitigating the injurious effects induced by heavy metals exposure to man; therefore, the aim of this study was to evaluate the protective effects of essential metals (Zinc and Selenium) in a mixture of heavy metal toxicity. In this study, except for negative controls, all other groups were treated with lead (PbCl2 , 20 mg kg-1 ); cadmium (CdCl2 , 1.61 mg kg-1 ); mercury (HgCl2 , 0.40 mg kg-1 ), and arsenic (NaAsO3, 10 mg kg-1 ) that were formed in distilled water. Pb, Cd, As, and Hg were administered as mixtures to 35, 6 weeks old rats weighing between 80 to 100 g for 60 days. Group I served as normal control without treatment, group II positive control received HM mixture, while groups III to V received HMM with Zn, Se, and Zn + Se respectively. Animal and liver weights, HM accumulation in the liver, food intake (FI), water intake (WI), liver function test, malondialdehyde (MDA), and inflammatory/transcription factor/apoptosis markers were checked. Also, antioxidant enzymes, and histological studies were carried out. Metal mixture accumulated in the liver and caused toxicities which were ameliorated by Zn and Se administration. HM caused significant decrease in FI, WI and distorted the level of liver enzymes, lipid peroxidation, inflammatory markers, antioxidants and architecture of the liver. Co administration with Zn or Se or both reversed the distortions. This study lays credence to the evolving research on the public health implications of low dose metal mixtures and the possible ameliorative properties of Zn and Se.

Fish and Seafood Safety: Human Exposure to Toxic Metals from the Aquatic Environment and Fish in Central Asia.

Toxic metals that are released into aquatic environments from natural and anthropogenic sources are absorbed by aquatic organisms and may threaten the health of both aquatic organisms and humans. Despite this, there have been limited studies on the metal concentrations in fish and humans in Central Asia. This study summarizes the presence of the toxic metals arsenic (As), mercury (Hg), cadmium (Cd), and lead (Pb) in aquatic bodies, fish, and seafood products and conducts a risk assessment. While certain areas show a notable increase in fish and seafood consumption, the overall intake in Central Asia remains below recommended levels. However, in regions with high fish consumption, there is a potential for elevated exposure to toxic metals, especially Hg. The risk of exposure to toxic metals in fish and seafood in Central Asia emerges as a significant concern. Comprehensive monitoring, regulation, and remediation efforts are imperative to ensure the safety of water sources and food consumption in the region. Public awareness campaigns and the establishment of dietary guidelines play a crucial role in minimizing the health risks associated with consumption.

4-[(E)-2-(1-Pyrenyl)Vinyl]Pyridine Complexes: How to Modulate the Toxicity of Heavy Metal Ions to Target Microbial Infections.

Pyrene derivatives are regularly proposed for use in biochemistry as dyes due to their photochemical characteristics. Their antibacterial properties are, however, much less well understood. New complexes based on 4-[(E)-2-(1-pyrenyl)vinyl]pyridine (PyPe) have been synthesized with metal ions that are known to possess antimicrobial properties, such as zinc(II), cadmium(II), and mercury(II). The metal ion salts, free ligand, combinations thereof, and the coordination compounds themselves were tested for their antibacterial properties through microdilution assays. We found that the ligand is able to modulate the antibacterial properties of transition metal ions, depending on the complex stability, the distance between the ligand and the metal ions, and the metal ions themselves. The coordination by the ligand weakened the antibacterial properties of heavy metal ions (Cd(II), Hg(II), Bi(III)), allowing the bacteria to survive higher concentrations thereof. Mixing the ligand and the metal ion salts without forming the complex beforehand enhanced the antibacterial properties of the cations. Being non-cytotoxic itself, the ligand therefore balances the biological consequences of heavy metal ions between toxicity and therapeutic weapons, depending on its use as a coordinating ligand or simple adjuvant.

Mercury pollution risks of agricultural soils and crops in mercury mining areas in Guizhou Province, China: effects of large mercury slag piles.

The historical large mercury slag piles still contain high concentrations of mercury and their impact on the surrounding environment has rarely been reported. In this study, three different agricultural areas [the area with untreated piles (PUT), the area with treated piles (PT), and the background area with no piles (NP)] were selected to investigate mercury slag piles pollution in the Tongren mercury mining area. The mercury concentrations of agricultural soils ranged from 0.42 to 155.00 mg/kg, determined by atomic fluorescence spectrometry of 146 soil samples; and mercury concentrations in local crops (rice, maize, pepper, eggplant, tomato and bean) all exceeded the Chinese food safety limits. Soil and crop pollution trends in the three areas were consistent as PUT > PT > NP, indicating that mercury slag piles have exacerbated pollution. Mercury in the slag piles was adsorbed by multiple pathways of transport into soils with high organic matter, which made the ecological risk of agricultural soils appear extremely high. The total hazard quotients for residents from ingesting mercury in these crops were unacceptable in all areas, and children were more likely to be harmed than adults. Compared to the PT area, treatment of slag piles in the PUT area may decrease mercury concentrations in paddy fields and dry fields by 46.02% and 70.36%; further decreasing health risks for adults and children by 47.06% and 79.90%. This study provided a scientific basis for the necessity of treating large slag piles in mercury mining areas.

Should ebselen be considered for the treatment of mercury intoxication? A minireview.

Mercury is a ubiquitous environmental contaminant and can be found in inorganic (Hg0, Hg+ and Hg2+) and organic forms (chiefly CH3Hg+ or MeHg+). The main route of human, mammals and bird exposure occurs via predatory fish ingestion. Occupational exposure to Hg0 (and Hg2+) can also occur; furthermore, in gold mining areas the exposure to inorganic Hg can also be high. The toxicity of electrophilic forms of Hg (E+Hg) is mediated by disruption of thiol (-SH)- or selenol (-SeH)-containing proteins. The therapeutic approaches to treat methylmercury (MeHg+), Hg0 and Hg2+ are limited. Here we discuss the potential use of ebselen as a potential therapeutic agent to lower the body burden of Hg in man. Ebselen is a safe drug for humans and has been tested in clinical trials (for instance, brain ischemia, noise-induce hearing loss, diabetes complications, bipolar disorders) at doses varying from 400 to 3600 mg per day. Two clinical trials with ebselen in moderate and severe COVID are also approved. Ebselen can be metabolized to an intermediate with -SeH (selenol) functional group, which has a greater affinity to electrophilic Hg (E+Hg) forms than the available thiol-containing therapeutic agents. Accordingly, as observed in vitro and rodent models in vivo, Ebselen exhibited protective effects against MeHg+, indicating its potential as a therapeutic agent to treat MeHg+ overexposure. The combined use of ebselen with thiol-containing molecules (e.g. N-acetylcysteine and enaramide)) is also commented, because they can have synergistic protective effects against MeHg+.

Assessment of heavy metals and environmental stress conditions on the production potential of polyunsaturated fatty acids (PUFAs) in indigenous microalgae isolated from the Gulf of Mannar coastal waters.

The present study evaluated the effects of heavy metals, viz., lead, mercury, and cadmium, on growth, chlorophyll a, b, c, carotenoids, and PUFA content of marine microalgae Chlorella sp. and Cylindrotheca fusiformis. At 96-h exposure, the IC50 values for Hg2+, Pb2+, and Cd2+ were 0.85 mg/L, 2.4 mg/L, and 5.3 mg/L respectively, in Chlorella sp. In C. fusiformis, IC50 values for Hg2+, Pb2+, and Cd2+ were 0.5 mg/L, 1.2 mg/L, and 3 mg/L respectively. The pigment contents of both microalgae were significantly affected upon heavy metal exposure. In Chlorella sp. and C. fusiformis, the exposed concentrations of Hg2+ averagely decreased the PUFA content by 76.34% and 78.68%, respectively. Similarly, Pb2+-exposed concentrations resulted in 54.50% and 82.64% average reductions in PUFA content of Chlorella sp. and C. fusiformis, respectively. Cd2+-exposed concentrations showed 32.58% and 40.54% average reduction in PUFA content of Chlorella sp. and C. fusiformis, respectively. Among the environmental stress conditions, the dark treatment has increased total PUFA content by 6.63% in Chlorella sp. and 3.92% in C. fusiformis. It was observed that the 50% nitrogen starvation (two-stage) significantly improved the PUFA production from 26.47 ± 6.55% to 40.92 ± 10.74% in Chlorella sp. and from 11.23 ± 5.01 to 32.8 ± 14.17% in C. fusiformis. The toxicity for both microalgae was followed in the order Hg2+ > Pb2+ > Cd2+. Among the two species, Chlorella sp. has shown a high tolerance to heavy metals and can be effectively utilized in PUFA production.

Mercury poisoning in a bodybuilder.

A 64-year-old man had progressive unsteadiness over several years, with tingling in his feet. He was a longstanding bodybuilding enthusiast. Clinical assessment and neurophysiology confirmed a cerebellar ataxia and axonal peripheral neuropathy. His serum mercury concentration was significantly raised. We diagnosed chronic mercury toxicity secondary to excessive tuna consumption. We advised him to stop eating tuna and prescribed dimercaptosuccinic acid, after which his serum mercury concentrations subsequently fell. This case report highlights the importance of considering dietary and nutritional causes of neurological disease. We also discuss the mechanisms, diagnosis and treatment of mercury toxicity.

Polymorphic Loci of Xenobiotic Biotransformation Genes in Accumulated Mercury Pollution Liquidators and in Workers with Chronic Mercury Vapors Exposure.

The allele and genotype frequencies of the polymorphic loci CYP1A1 (rs1048943), GSTP1 (rs1695 and rs1138272), GSTM1, and GSTT1 genes were studied in 517 men: in 389 accumulated mercury pollution liquidators (207 firefighters of the Ministry of the Russian Federation for Civil Defence, Emergencies and Elimination of Consequences of Natural Disasters and 182 employees of the Federal Environmental Operator) and 128 former workers (82 patients in the delayed period of chronic mercury intoxication and 46 individuals contacted with mercury and had no chronic mercury intoxication). We found differences in the frequencies of AA and AG genotypes in groups of former workers (χ2=6.96, p=0.008) for the polymorphic locus rs1048943, while the AG-CYP1A1 genotype was characterized by a 5.5-fold decrease in the odds ratio for the development of chronic mercury intoxication (OR=0.18, p=0.0041). An unfavorable combination of genotypes of the studied polymorphic loci increases the risk of undesirable health effects.