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

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

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

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

Mercury supply limits methylmercury production in paddy soils.

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

Soil Geobacteraceae are the key predictors of neurotoxic methylmercury bioaccumulation in rice.

Contamination of rice by the potent neurotoxin methylmercury (MeHg) originates from microbe-mediated Hg methylation in soils. However, the high diversity of Hg methylating microorganisms in soils hinders the prediction of MeHg formation and challenges the mitigation of MeHg bioaccumulation via regulating soil microbiomes. Here we explored the roles of various cropland microbial communities in MeHg formation in the potentials leading to MeHg accumulation in rice and reveal that Geobacteraceae are the key predictors of MeHg bioaccumulation in paddy soil systems. We characterized Hg methylating microorganisms from 67 cropland ecosystems across 3,600 latitudinal kilometres. The simulations of a rice-paddy biogeochemical model show that MeHg accumulation in rice is 1.3-1.7-fold more sensitive to changes in the relative abundance of Geobacteraceae compared to Hg input, which is recognized as the primary parameter in controlling MeHg exposure. These findings open up a window to predict MeHg formation and accumulation in human food webs, enabling more efficient mitigation of risks to human health through regulations of key soil microbiomes.

The mystery of methylmercury-perturbed calcium homeostasis: AMPK-DRP1-dependent mitochondrial fission initiates ER-mitochondria contact formation.

Methylmercury (MeHg), as a global environmental pollutant, is of concern globally due to its neurodevelopmental toxicity. Mitochondria-associated membranes (MAMs) are highly dynamic sites of endoplasmic reticulum (ER)-haemocyte contact. MAMs are closely associated with the pathophysiology of neurological disorders due to their role in the transfer of calcium ions (Ca2+) between mitochondria and the ER. However, the molecular mechanisms that control these interactions in MeHg-induced neurotoxicity have not yet been characterized. In the current study, MeHg caused increases in the levels of both cytosolic and mitochondrial Ca2+ in PC12 cells and promoted MAMs formation in both in vivo and in vitro experiments. Of note, MeHg perturbed mitochondrial dynamics, promoting a shift toward a fission phenotype, and this was supported by the dysregulation of fission regulators. Interestingly, the MeHg-induced promotion of MAMs formation and increase in Ca2+ levels were effectively attenuated by the inhibition of mitochondrial fission using Mdivi-1, a DRP1 inhibitor. Furthermore, MeHg triggered the AMPK pathway, and most of the aforementioned changes were significantly rescued by Compound C. Mechanistic investigations revealed a reciprocal relationship between AMPK- and Ca2+-mediated mitochondrial fission. The specific inhibitor of Ca2+ uniporter, ruthenium-red (RuR), effectively abolished the feedback regulation of mitochondrial dynamics and MAMs formation mediated by AMPK in response to MeHg-induced Ca2+ overload. This study reveals a novel role of AMPK-DRP1-mediated mitochondrial fragmentation in the coupling of ER-mitochondrial calcium microdomains in MeHg-induced neurotoxicity. The findings provide valuable insights for the development of strategies to regulate mitochondrial imbalances in neurological diseases.

New Insights into MeHg Accumulation in Rice (Oryza sativa L.): Evidence from Cysteine.

The intake of methylmercury (MeHg)-contaminated rice poses immense health risks to rice consumers. However, the mechanisms of MeHg accumulation in rice plants are not entirely understood. The knowledge that the MeHg-Cysteine complex was dominant in polished rice proposed a hypothesis of co-transportation of MeHg and cysteine inside rice plants. This study was therefore designed to explore the MeHg accumulation processes in rice plants by investigating biogeochemical associations between MeHg and amino acids. Rice plants and underlying soils were collected from different Hg-contaminated sites in the Wanshan Hg mining area. The concentrations of both MeHg and cysteine in polished rice were higher than those in other rice tissues. A significant positive correlation between MeHg and cysteine in rice plants was found, especially in polished rice, indicating a close geochemical association between cysteine and MeHg. The translocation factor (TF) of cysteine showed behavior similar to that of the TF of MeHg, demonstrating that these two chemical species might share a similar transportation mechanism in rice plants. The accumulation of MeHg in rice plants may vary due to differences in the molar ratios of MeHg to cysteine and the presence of specific amino acid transporters. Our results suggest that cysteine plays a vital role in MeHg accumulation and transportation inside rice plants.

Sea anemones, methylmercury, and bacterial infection: A closer look at multiple stressors.

Specimens of the Mediterranean sea anemone Anemonia viridis were exposed to methylmercury (MeHg) and bacterial infection to study their immune responses to a well-known toxic pollutant. Anemones were housed in laboratory conditions and divided into five experimental groups: 1. control (no microinjection); 2. filtered seawater + buffer injection; 3. filtered seawater + Escherichia coli injection; 4. MeHg + buffer injection; 5. MeHg + E. coli injection. Data showed an increase in antioxidant enzyme production compared to the constitutive condition, while methylmercury inhibited lysozyme production. The buffer inoculation had no statistically significant effects on the animals. In addition, electrophoretic and protease analyses revealed differences in the type of proteins produced, as well as a modulation of proteases depending on the treatment. The study demonstrated the immunomodulatory effect of the organic pollutant on A. viridis, validating its use as a model organism for marine coastal biomonitoring programmes and multiple stress studies.

Genomic and transcriptomic characterization of methylmercury detoxification in a deep ocean Alteromonas mediterranea ISS312.

Methylmercury (MeHg) is one of the most worrisome pollutants in marine systems. MeHg detoxification is mediated by merB and merA genes, responsible for the demethylation of MeHg and the reduction of inorganic mercury, respectively. Little is known about the biological capacity to detoxify this compound in marine environments, and even less the bacterial transcriptional changes during MeHg detoxification. This study provides the genomic and transcriptomic characterization of the deep ocean bacteria Alteromonas mediterranea ISS312 with capacity for MeHg degradation. Its genome sequence revealed four mer operons containing three merA gene and two merB gene copies, that could be horizontally transferred among distant related genomes by mobile genetic elements. The transcriptomic profiling in the presence of 5 µM MeHg showed that merA and merB genes are within the most expressed genes, although not all mer genes were equally transcribed. Besides, we aimed to identify functional orthologous genes that displayed expression profiles highly similar or identical to those genes within the mer operons, which could indicate they are under the same regulatory controls. We found contrasting expression profiles for each mer operon that were positively correlated with a wide array of functions mostly related to amino acid metabolism, but also to flagellar assembly or two component systems. Also, this study highlights that all merAB genes of the four operons were globally distributed across oceans layers with higher transcriptional activity in the mesopelagic deeper waters. Our study provides new insights about the transcriptional patterns related to the capacity of marine bacteria to detoxify MeHg, with important implications for the understanding of this process in marine ecosystems.

Wildfire burn severity and stream chemistry influence aquatic invertebrate and riparian avian mercury exposure in forested ecosystems.

Terrestrial soils in forested landscapes represent some of the largest mercury (Hg) reserves globally. Wildfire can alter the storage and distribution of terrestrial-bound Hg via reemission to the atmosphere or mobilization in watersheds where it may become available for methylation and uptake into food webs. Using data associated with the 2007 Moonlight and Antelope Fires in California, we examined the long-term direct effects of wildfire burn severity on the distribution and magnitude of Hg concentrations in riparian food webs. Additionally, we quantified the cross-ecosystem transfer of Hg from aquatic invertebrate to riparian bird communities; and assessed the influence of biogeochemical, landscape variables, and ecological factors on Hg concentrations in aquatic and terrestrial food webs. Benthic macroinvertebrate methylmercury (MeHg) and riparian bird blood total mercury (THg) concentrations varied by 710- and 760-fold, respectively, and Hg concentrations were highest in predators. We found inconsistent relationships between Hg concentrations across and within taxa and guilds in response to stream chemical parameters and burn severity. Macroinvertebrate scraper MeHg concentrations were influenced by dissolved organic carbon (DOC); however, that relationship was moderated by burn severity (as burn severity increased the effect of DOC declined). Omnivorous bird Hg concentrations declined with increasing burn severity. Overall, taxa more linked to in situ energetic pathways may be more responsive to the biogeochemical processes that influence MeHg cycling. Remarkably, 8 years post-fire, we still observed evidence of burn severity influencing Hg concentrations within riparian food webs, illustrating its overarching role in altering the storage and redistribution of Hg and influencing biogeochemical processes.

[The Role of Supersulfide in Methylmercury Detoxification].

Methylmercury is a ubiquitous neurotoxic substance present in the environment, and health concerns, especially through the consumption of seafood, remain. Glutathione (GSH)-mediated detoxification and the excretion of methylmercury are known metabolic detoxification pathways. We have also discovered a mechanism by which endogenous super-sulfides convert methylmercury to nontoxic metabolites such as bis-methylmercury sulfide. However, these metabolites are present in very small quantities, and the significance of the detoxification of methylmercury by super-sulfides is not well understood. Methylmercury binds to thiol groups in vivo but can also react with highly reactive selenols (selenocysteine residues). Such covalent bonds (S-mercuration and Se-mercuration) are broken by nucleophilic substitution reactions with other thiol and selenols, however, the contribution of super-sulfides to this substitution reaction is not well understood. Interestingly, a recent study suggested that selenoprotein P, the major selenium transport protein in plasma, binds to methylmercury, however, Se-mercuration was not determined. In this review, we introduce these series of reactions and discuss their involvement with super-sulfides in methylmercury toxicity.

Methylmercury-induced brain neuronal death in CHOP-knockout mice.

Apoptosis is one of the hallmarks of MeHg-induced neuronal cell death; however, its molecular mechanism remains unclear. We previously reported that MeHg exposure induces neuron-specific ER stress in the mouse brain. Excessive ER stress contributes to apoptosis, and CHOP induction is considered to be one of the major mechanisms. CHOP is also increased by MeHg exposure in the mouse brain, suggesting that it correlates with increased apoptosis. In this study, to clarify whether CHOP mediates MeHg-induced apoptosis, we examined the effect of CHOP deletion on MeHg exposure in CHOP-knockout mice. Our data showed that CHOP deletion had no effect on MeHg exposure-induced weight loss or hindlimb impairment in mice, nor did it increase apoptosis or inhibit neuronal cell loss. Hence, CHOP plays little role in MeHg toxicity, and other apoptotic pathways coupled with ER stress may be involved in MeHg-induced cell death.

Algae decomposition released dissolved organic matter subfractions on dark abiotic mercury methylation.

To understand the mechanism of dark abiotic mercury (Hg) methylation by algae-derived dissolved organic matter (DOM) and effectively manage the environmental risks of mercury methylation in aquaculture areas, we investigated the influence of subfractions of DOM released from algae (Ulothrix sp.) decomposition on mercury methylation. The results showed that the hydrophobic basic component (HOB) in DOM exhibited the most substantial promotion effect on Hg methylation. The methylmercury (MeHg) production in the HOB treatment increased significantly, while the production rate of MeHg (%MeHg represented the concentration ratio of MeHg to THg) in the six subfractions treated solutions decreased significantly with the increase of Hg concentration. The change of the %MeHg was more evident at low Hg concentration, indicating the limited number of binding sites and methyl donors on DOM. As a consequence, Hg(Ⅱ) in the solution could not be converted into MeHg in equal proportion. Furthermore, the production of MeHg in solution was significantly reduced by the decomposed algae DOM, and its concentration was in the range of 0.017-0.085 ng·L-1 (significantly lower than undecomposed algal). The difference between the decomposed and the non-decomposed algae DOM reached a significant level (P < 0.05). When the DOM decayed for 20 and 30 days, the Hg methylation ability of DOM was weakened most obviously. During the decomposition process, considerable variations were observed among the subfractions, with HOB consistently playing a dominant role in Hg methylation. At the same time, the hydrophilic acid component exhibited a significant inhibitory effect on Hg methylation. Generally, the main components (e.g. HOB and HIA (hydrophilic acid component)) of DOM affecting mercury methylation were found in our study, which provided a better understanding of algae-derived DOM subfractions on the Hg methylation, in an attempt to prevent and control water pollution in aquaculture areas.

Single and combined effects of increased temperature and methylmercury on different stages of the marine rotifer Brachionus plicatilis.

Rapid, anthropogenic activity-induced global warming is a severe problem that not only raises water temperatures but also shifts aquatic environments by increasing the bioavailability of heavy metals (HMs), with potentially complicated effects on aquatic organisms, including small aquatic invertebrates. For this paper, we investigated the combined effects of temperature (23 and 28 °C) and methylmercury (MeHg) by measuring physiological changes, bioaccumulation, oxidative stress, antioxidants, and the mitogen-activated protein kinase signaling pathway in the marine rotifer Brachionus plicatilis. High temperature and MeHg adversely affected the survival rate, lifespan, and population of rotifers, and bioaccumulation, oxidative stress, and biochemical reactions depended on the developmental stage, with neonates showing higher susceptibility than adults. These findings demonstrate that increased temperature enhances potentially toxic effects from MeHg, and susceptibility differs with the developmental stage. This study provides a comprehensive understanding of the combined effects of elevated temperature and MeHg on rotifers. ENVIRONMENTAL IMPLICATION: Methylmercury (MeHg) is a widespread and harmful heavy metal that can induce lethal effects on aquatic organisms in even trace amounts. The toxicity of metals can vary depending on various environmental conditions. In particular, rising temperatures are considered a major factor affecting bioavailability and toxicity by changing the sensitivity of organisms. However, there are few studies on the combinational effects of high temperatures and MeHg on aquatic animals, especially invertebrates. Our research would contribute to understanding the actual responses of aquatic organisms to complex aquatic environments.

A hidden demethylation pathway removes mercury from rice plants and mitigates mercury flux to food chains.

Dietary exposure to methylmercury (MeHg) causes irreversible damage to human cognition and is mitigated by photolysis and microbial demethylation of MeHg. Rice (Oryza sativa L.) has been identified as a major dietary source of MeHg. However, it remains unknown what drives the process within plants for MeHg to make its way from soils to rice and the subsequent human dietary exposure to Hg. Here we report a hidden pathway of MeHg demethylation independent of light and microorganisms in rice plants. This natural pathway is driven by reactive oxygen species generated in vivo, rapidly transforming MeHg to inorganic Hg and then eliminating Hg from plants as gaseous Hg°. MeHg concentrations in rice grains would increase by 2.4- to 4.7-fold without this pathway, which equates to intelligence quotient losses of 0.01-0.51 points per newborn in major rice-consuming countries, corresponding to annual economic losses of US$30.7-84.2 billion globally. This discovered pathway effectively removes Hg from human food webs, playing an important role in exposure mitigation and global Hg cycling.

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+.

Gut microbiome play a crucial role in geographical and interspecies variations in mercury accumulation by fish.

Mercury (Hg) contamination in fish has raised global concerns for decades. The Hg biotransformation can be manipulated by gut microbiome and it is found to have a substantial impact on the speciation and final fate of Hg in fish. However, the contribution of intestinal microbiota in geographical and interspecies variations in fish Hg levels has not been thoroughly understood. The present study compared the Hg levels in wild marine fish captured from two distinct regions in South China sea. We observed a quite "ironic" phenomenon that MeHg levels in carnivorous fish from a region with minimal human impacts (Xisha Islands, 92 ± 7.2 ng g-1 FW) were much higher than those from a region with severe human impacts (Daya Bay, 19 ± 0.41 ng g-1 FW). Furthermore, the results showed that gut microbiome determined Hg biotransformation and played a crucial role in the variances in fish Hg levels across different geographical locations and species. The intestinal methylators, rather than demethylators, were more significant in affecting Hg biotransformation in fish. The carnivorous species in Xisha Islands exhibited a higher abundance of intestinal methylators, leading to higher MeHg accumulation. Besides, the gut microbiome could be shaped in response to the elevated Hg levels in these fish, which may benefit their adaptation to Hg toxicity and overall health preservation. However, anthropogenic activities (particularly overfishing) in Daya Bay have severely affected the fish population, disrupting the reciprocal relationships between fish and intestinal microbiota and rendering them more susceptible to pathogenic microbes. Overall, this study provided a comprehensive understanding of the role of gut microbiome in Hg bioaccumulation in fish and offered valuable insights into the co-evolutionary dynamics between fish and gut microbiome in the presence of Hg exposure.

Foraging behavior and sea ice-dependent factors affecting the bioaccumulation of mercury in Antarctic coastal waters.

To elucidate the potential risks of the toxic pollutant mercury (Hg) in polar waters, the study of accumulated Hg in fish is compelling for understanding the cycling and fate of Hg on a regional scale in Antarctica. Herein, the Hg isotopic compositions of Antarctic cod Notothenia coriiceps were assessed in skeletal muscle, liver, and heart tissues to distinguish the differences in Hg accumulation in isolated coastal environments of the eastern (Chinese Zhongshan Station, ZSS) and the antipode western Antarctica (Chinese Great Wall Station, GWS), which are separated by over 4000 km. Differences in odd mass-independent isotope fractionation (odd-MIF) and mass-dependent fractionation (MDF) across fish tissues were reflection of the specific accumulation of methylmercury (MeHg) and inorganic Hg (iHg) with different isotopic fingerprints. Internal metabolism including hepatic detoxification and processes related to heart may also contribute to MDF. Regional heterogeneity in iHg end-members further provided evidence that bioaccumulated Hg origins can be largely influenced by polar water circumstances and foraging behavior. Sea ice was hypothesized to play critical roles in both the release of Hg with negative odd-MIF derived from photoreduction of Hg2+ on its surface and the impediment of photochemical transformation of Hg in water layers. Overall, the multitissue isotopic compositions in local fish species and prime drivers of the heterogeneous Hg cycling and bioaccumulation patterns presented here enable a comprehensive understanding of Hg biogeochemical cycling in polar coastal waters.

Differential response of Hg-methylating and MeHg-demethylating microbiomes to dissolved organic matter components in eutrophic lake water.

Methylmercury (MeHg) production in aquatic ecosystems is a global concern because of its neurotoxic effect. Dissolved organic matter (DOM) plays a crucial role in biogeochemical cycling of Hg. However, owing to its complex composition, the effects of DOM on net MeHg production have not been fully understood. Here, the Hg isotope tracer technique combined with different DOM treatments was employed to explore the influences of DOM with divergent compositions on Hg methylation/demethylation and its microbial mechanisms in eutrophic lake waters. Our results showed that algae-derived DOM treatments enhanced MeHg concentrations by 1.42-1.53 times compared with terrestrial-derived DOM. Algae-derived DOM had largely increased the methylation rate constants by approximately 1-2 orders of magnitude compared to terrestrial-derived DOM, but its effects on demethylation rate constants were less pronounced, resulting in the enhancement of net MeHg formation. The abundance of hgcA and merB genes suggested that Hg-methylating and MeHg-demethylating microbiomes responded differently to DOM treatments. Specific DOM components (e.g., aromatic proteins and soluble microbial byproducts) were positively correlated with both methylation rate constants and the abundance of Hg-methylating microbiomes. Our results highlight that the DOM composition influences the Hg methylation and MeHg demethylation differently and should be incorporated into future Hg risk assessments in aquatic ecosystems.

Mercury species induce metabolic reprogramming in freshwater diatom Cyclotella meneghiniana.

Mercury is a hazardous pollutant of global concern. While advances have been made in identifying the detrimental effects caused by Hg species in phytoplankton, knowledge gaps remain regarding the metabolomic perturbations induced by inorganic mercury (Hg(II)) and monomethylmercury (MeHg) in these organisms. Diatoms represent a major phytoplankton group essential in various global biogeochemical cycles. The current study combined targeted metabolomics, bioaccumulation, and physiological response assays to investigate metabolic perturbations in diatom Cyclotella meneghiniana exposed for 2 h to nanomolar concentrations of Hg(II) and MeHg. Our findings highlight that such exposures induce reprogramming of the metabolism of amino acids, nucleotides, fatty acids, carboxylic acids and antioxidants. These alterations were primarily mercury-species dependent. MeHg exposure induced more pronounced reprogramming of the metabolism of diatoms than Hg(II), which led to less pronounced effects on ROS generation, membrane permeability and chlorophyll concentrations. Hg(II) treatments presented distinct physiological responses, with more robust metabolic perturbations at higher exposures. The present study provides first-time insights into the main metabolic alterations in diatom C. meneghiniana during short-term exposure to Hg species, deepening our understanding of the molecular basis of these perturbations.

Changes in transcriptome regulations of a marine rotifer Brachionus plicatilis under methylmercury stress.

Mercury (Hg), a heavy metal pollutant worldwide, can be transformed into methylmercury (MeHg) by various aquatic microorganisms in water, thus accumulating along the aquatic food chain and posing a particular challenge to human health. Zooplankton plays a crucial role in aquatic ecosystems and serves as a major component of the food chain. To evaluate the effects of MeHg on the rotifer Brachionus plicatilis and reveal the underlying mechanism of these effects, we exposed B. plicatilis to MeHg by either direct immersion or by feeding with MeHg-poisoned Chlorella pyrenoidesa, respectively, and conducted a transcriptomic analysis. The results showed that B. plicatilis directly exposed to MeHg by immersion showed significant enrichment of the glutathione metabolism pathway for detoxification of MeHg. In addition, the exposure to MeHg by feeding induced a significant enrichment of lysosome and notch signaling pathways of rotifers, supporting the hypothesis that MeHg can induce autophagy dysfunction in cells and disturb the nervous system of rotifers. In two different routes of MeHg exposure, the pathway of cytochrome P450 in rotifers showed significant enrichment for resisting MeHg toxicity. Our results suggest further studies on the potential mechanism and biological responses of MeHg toxicity in other links of the aquatic food chain.