Metabolomic and gut-microbial responses of earthworms exposed to microcystins and nano zero-valent iron in soil.

The earthworm-based vermiremediation facilitated with benign chemicals such as nano zero-valent iron (nZVI) is a promising approach for the remediation of a variety of soil contaminants including cyanotoxins. As the most toxic cyanotoxin, microcystin-LR (MC-LR) enter soil via runoff, irrigated surface water and sewage, and the application of cyanobacterial biofertilizers as part of the sustainable agricultural practice. Earthworms in such remediation systems must sustain the potential risk from both nZVI and MC-LR. In the present study, earthworms (Eisenia fetida) were exposed up to 14 days to MC-LR and nZVI (individually and in mixture), and the toxicity was investigated at both the organismal and metabolic levels, including growth, tissue damage, oxidative stress, metabolic response and gut microbiota. Results showed that co-exposure of MC-LR and nZVI is less potent to earthworms than that of separate exposure. Histological observations in the co-exposure group revealed only minor epidermal brokenness, and KEGG enrichment analysis showed that co-exposure induced earthworms to regulate glutathione biosynthesis for detoxification and reduced adverse effects from MC-LR. The combined use of nZVI promoted the growth and reproduction of soil and earthworm gut bacteria (e.g., Sphingobacterium and Acinetobacter) responsible for the degradation of MC-LR, which might explain the observed antagonism between nZVI and MC-LR in earthworm microcosm. Our study suggests the beneficial use of nZVI to detoxify pollutants in earthworm-based vermiremediation systems where freshwater containing cyanobacterial blooms is frequently used to irrigate soil and supply water for the growth and metabolism of earthworms.

Early pregnancy exposure to Microcystin-LR compromises endometrial decidualization in mice via the PI3K/AKT/FOXO1 signaling pathway.

Previous experimental studies have found that exposure to Microcystin-leucine arginine can impact pregnancy outcomes in female mice. The impact of MC-LR on early pregnancy in mammals is not yet well understood. Both mice and humans need to undergo decidualization to maintain pregnancy. In this study, we tried to evaluate whether MC-LR affects decidualization process in mice. Our research showed that MC-LR decreased maternal weight gain, uterine weight, and implantation site weight. These findings suggested that MC-LR exerted adverse effects on decidualization. In mice, we examined decreased number of polyploid decidual cells, but marked proliferation of mouse endometrial stromal cells the expression levels of prolactin (PRL)and insulin-like growth factor binding protein 1 (IGFBP1) were significantly downregulated in the decidual tissue and primary endometrial stromal cells following MC-LR treatment. Furthermore, further in vitro experiments identified that MC-LR promoted endometrial stromal cell division and cycle transition. Lastly, our study demonstrated that MC-LR impaired decidualization through the PI3K/AKT/FOXO1 pathway. Collectively, these data suggested that exposure to MC-LR impaired decidualization during early pregnancy.

Effects of cyanotoxins on nitrogen transformation in aquaculture systems with microplastics coexposure: Adsorption behavior, bacterial communities and functional genes.

Microcystin-LR (MC-LR) and microplastics (MPs) have attracted increasing attention as important new pollutants in freshwater fishery environments. However, there are few reports on the effects of long-term combined MC-LR and MPs pollution on nitrogen transformation and microbial communities in aquaculture ponds, and the resulting risks have yet to be determined. Therefore, in this study, traditional refractory MPs (polystyrene, PS), biodegradable MPs (polylactic acid, PLA) and MC-LR, which are common in freshwater fishery environments in China, were selected as pollutants to construct a microcosm that simulates freshwater aquaculture ponds. MC-LR coexposure to PS and PLA was tested to reveal the effects of these pollutants on nitrogen transformation and microbial communities in aquaculture ponds, as well as to elucidate the potential risks posed by traditional refractory MPs and biodegradable MPs to freshwater aquaculture ecosystems. The results revealed that the MPs had a relatively high adsorption rate for MC-LR and that PS presented a relatively high adsorption capacity, whereas PLA presented a relatively high desorption capacity. Single or combined MPs and MC-LR pollution disrupted the normal nitrogen cycle in the aquaculture system, causing an overall loss of nitrogen in the water, and denitrification and nitrogen fixation in the water were inhibited to a certain extent through the inhibition of nitrogen cycle-related functional genes, with the PS + MC-LR group having the greatest inhibitory effect. In addition, compared with single-pollutant exposure, combined exposure to MC-LR and MPs had a greater effect on the microbial community composition. Analysis of the integrated biomarker response (IBR) index revealed that the risk of combined exposure to MC-LR and PS was greater than that of single exposure, so this phenomenon merits further attention.

Optimization of isolation and concentration of the common freshwater cyanobacterial toxins ATX-a, CYN and MC-LR using standard techniques, optimization of cyanobacteria growth.

Some of the most commonly identified freshwater toxins are anatoxin-a (ATX-a), cylindrospermopsin (CYN), and microcystin-LR (MC-LR). The aim of this paper was to compare different methods of extracting and concentrating these cyanotoxins and check the impact of selected physical factors on the accumulation of biomass of Dolichospermum flos-aquae, Microcystis aeruginosa, and Raphidiopsis raciborskii. The effect of different cyanobacteria cultivation conditions on the amount of cyanotoxins synthesized showed no significant changes over time in the average concentration of all tested toxins in the medium compared to the control. Mixing cultures increases the intracellular content of ATX-a. Aerating also positively affects the concentration of MC-LR intracellularly. In order to optimize the solid phase extraction (SPE) process of toxins, the C18 phase or activated carbon was used. In general, higher toxin recoveries were achieved when using the C18 phase. The best result was achieved for ATX-a, 94% recovery with elution using methanol with 0.1% trifluoroacetic acid (TFA). For MC-LR, the best recovery was 59%, and for CYN 22%. The study evaluated the various methods to release cyanotoxins from cyanobacteria showed that: the highest ATX-a concentration (0.60 µg/mg d.w) was obtained using MilliQ water and microwave treatment for 10 to 15 seconds. For MC-LR, the highest extracted amount (6.73 µg/mg d.w) resulted from methanol treatment and boiling at 100°C for 15 minutes. CYN extraction was the most effective by using MilliQ water and alternative freezing/thawing (1.54 µg/mg d.w). In conclusion, changing the optimal parameters of cyanobacterial cultivation, only slightly affects the increase in biomass accumulation and synthesis of cyanobacterial toxins. In the case of ATX, the key is the use of the TFA additive in the SPE process. No single method has been identified as the ideal approach for isolating various intracellular cyanotoxins.

Seasonal Rise in the Contents of Microcystin-LR and Odorous Substances Due to Cyanobacterial Blooms in a Drinking Water Reservoir Supplying Xinyang City, China.

Cyanobacterial blooms have become a serious water pollution problem in many parts of the world, and the monitoring and study of the impacts of biotoxins on human health are of vital importance. In this study, the contents of microcystin-LR, 2-methylisoborneol, and geosmin were measured in water and sediment samples from Nanwan Reservoir, China, by means of bimonthly sampling between February and December 2023. The physicochemical and hydrochemical factors and phytoplankton dynamics in the reservoir were also investigated. The results showed that the overall mean concentration of microcystin-LR (0.729 µg/L) in summer approached the guiding standard (1 µg/L) set by the WHO for drinking water. Furthermore, the content of 2-methylisoborneol (143.5 ng/L) was 14 times higher than the national standard (10 ng/L). The results of laboratory cultures showed that lower light levels and medium temperatures were suitable for the growth of Microcystis and Planktothricoides but higher temperatures promoted the synthesis and release of microcystin-LR and 2-methylisoborneol. In addition, the results of co-cultures showed that the growth of Planktothricoides was inhibited by Microcystis. Our results suggest that cyanobacterial bloom and the presence of the metabolites 2-methylisoborneol and microcystin-LR can decrease the drinking water quality of Nanwan Reservoir.

MC-LR disrupts dopamine synthesis in the substantia nigra of midbrain by enhancing the chaperone-mediated autophagy pathway through direct binding to ERK2.

Microcystins are environmental toxins produced by freshwater cyanobacteria. Microcystin-LR (MC-LR) is one of the most abundant and harmful isomers. MC-LR poses a serious threat to human health. MC-LR could penetrate the blood-brain barrier of mice and accumulate in the substantia nigra (SN) of the midbrain, leading to a reduction in dopamine levels and Parkinson's disease (PD)-like motor dysfunction in mice. The reduction in dopamine levels is a key factor contributing to movement disorders in humans with PD. Dopamine is synthesized in the dopaminergic neurons of the SN by the actions of tyrosine hydroxylase (TH) and dihydroxyphenylalanine decarboxylase (DDC). In this study, we found that MC-LR could enter dopaminergic neurons in the SN and directly bound to extracellular signal-regulated kinase 2 (ERK2), enhancing ERK2 stability. ERK2 further enhanced the transcriptional activity of Heat Shock Protein Family A Member 8 (HSPA8) and promoted the expression of Heat shock cognate 71 kDa protein (HSC70), which in turn amplified the chaperone-mediated autophagy (CMA) pathway and accelerated the degradation of TH and DDC. This affected the dopamine synthesis process, resulting in a significant reduction in dopamine levels. The study is the first to reveal that ERK2 was a direct target of MC-LR, and further enhanced CMA affecting dopamine synthesis, which has important theoretical and practical significance for environmental safety management.

Nicotinamide Alleviates Synergistic Impairment of Intestinal Barrier Caused by MC-LR and NaNO2 Coexposure.

Microcystin-LR (MC-LR) and nitrites from the environment and daily life can be ingested and absorbed by humans via the digestive tract. However, their combined effects on intestinal health remain unclear. Here, the combined impact of MC-LR and sodium nitrite (NaNO2) on the intestines of mice was investigated under actual human exposure conditions. After mice were exposed to MC-LR (10, 100 µg/L) and NaNO2 (30, 300 mg/L) individual and in combination for 6 months, it was found that MC-LR and NaNO2 synergistically decreased intestinal permeability and disrupted intestinal physical, chemical, immune, and microbial barriers. In the coexposure groups, the synergistic impairment to the intestinal barrier was noted with increasing concentrations of MC-LR or NaNO2, but this adverse effect was alleviated by nicotinamide supplementation. This study underscores the potential risks of simultaneous ingestion of MC-LR and nitrite on intestinal health. The protective role of nicotinamide suggests avenues for therapeutic intervention against environmental toxin-induced intestinal impairment.

Astaxanthin Alleviates Hepatic Lipid Metabolic Dysregulation Induced by Microcystin-LR.

Microcystin-LR (MC-LR), frequently generated by cyanobacteria, has been demonstrated to raise the likelihood of liver disease. Few previous studies have explored the potential antagonist against MC-LR. Astaxanthin (ASX) has been shown to possess various beneficial effects in regulating lipid metabolism in the liver. However, whether ASX could alleviate MC-LR-induced hepatic lipid metabolic dysregulation is as yet unclear. In this work, the important roles and mechanisms of ASX in countering MC-LR-induced liver damage and lipid metabolic dysregulation were explored for the first time. The findings revealed that ASX not only prevented weight loss but also enhanced liver health after MC-LR exposure. Moreover, ASX effectively decreased triglyceride, total cholesterol, aspartate transaminase, and alanine aminotransferase contents in mice that were elevated by MC-LR. Histological observation showed that ASX significantly alleviated lipid accumulation and inflammation induced by MC-LR. Mechanically, ASX could significantly diminish the expression of genes responsible for lipid generation (Srebp-1c, Fasn, Cd36, Scd1, Dgat1, and Pparg), which probably reduced lipid accumulation induced by MC-LR. Analogously, MC-LR increased intracellular lipid deposition in THLE-3 cells, while ASX decreased these symptoms by down-regulating the expression of key genes in the lipid synthesis pathway. Our results implied that ASX played a crucial part in lipid synthesis and effectively alleviated MC-LR-induced lipid metabolism dysregulation. ASX might be developed as a novel protectant against hepatic impairment and lipid metabolic dysregulation associated with MC-LR. This study offers new insights for further management of MC-LR-related metabolic diseases.

Microcystin-LR Regulates Interaction between Tumor Cells and Macrophages via the IRE1α/XBP1 Signaling Pathway to Promote the Progression of Colorectal Cancer.

Microcystin-LR (MC-LR), a cyanobacterial toxin, is a potent carcinogen implicated in colorectal cancer (CRC) progression. However, its impact on the tumor microenvironment (TME) during CRC development remains poorly understood. This study investigates the interaction between tumor cells and macrophages mediated by MC-LR within the TME and its influence on CRC progression. CRC mice exposed to MC-LR demonstrated a significant transformation from adenoma to adenocarcinoma. The infiltration of macrophages increased, and the IRE1α/XBP1 pathway was activated in CRC cells after MC-LR exposure, influencing macrophage M2 polarization under co-culture conditions. Additionally, hexokinase 2 (HK2), a downstream target of the IRE1α/XBP1 pathway, was identified, regulating glycolysis and lactate production. The MC-LR-induced IRE1α/XBP1/HK2 axis enhanced lactate production in CRC cells, promoting M2 macrophage polarization. Furthermore, co-culturing MC-LR-exposed CRC cells with macrophages, along with the IRE1α/XBP1 pathway inhibitor 4µ8C and the hexokinase inhibitor 2-DG, suppressed M2 macrophage-induced CRC cell migration, clonogenicity, and M2 macrophage polarization. This study elucidates the mechanism by which MC-LR-mediated interactions through the IRE1α/XBP1 pathway promote CRC progression, highlighting potential therapeutic targets.

Microcystin-LR activates serine/threonine kinases and alters the phosphoproteome in human HepaRG cells.

Microcystin-LR (MCLR) exposure has been associated with development of hepatocellular carcinoma (HCC). Many of the carcinogenic mechanisms for MCLR have been attributed to the induction of cell survival and proliferation through altered protein phosphorylation pathways by inhibition of protein phosphatases 1 (PP1) and PP2A. The current study determined MCLR effects on the phosphoproteome in human HepaRG cells. Differentiated HepaRG cells were treated with either vehicle or MCLR followed by phosphoproteomic analysis and Western blotting of MAPK-activated proteins. MCLR decreased cell viability at 24 h at doses as low as 0.03 µM. MCLR also caused a dose-dependent increase in phosphorylation of signaling and stress kinases. The number of decreased phosphosites by 0.1 µM MCLR was similar between the 2 h (212) and 24 h (154) timepoints. In contrast, a greater number of phosphosites were increased at 24 h (567) versus the 2 h timepoint (136), indicating the hyperphosphorylation state caused by MCLR-mediated inhibition of PPs is time-dependent. A kinase perturbation analysis predicted that MCLR exposure at both 2 h and 24 h increased the function of aurora kinase B (AURKB), checkpoint kinase 1 (CHEK1), and serum and glucocorticoid-regulated kinase 1 (SGK1). STRING database analysis of the phosphosites altered by MCLR exposure revealed pathways associated with cell proliferation and survival, including ribosomal protein S6 kinase (RSK), and vascular endothelial growth factor receptor (VEGFR2)-mediated vascular permeability. In addition, several cancer-related KEGG pathways were enriched at both 2 h and 24 h timepoints, and multiple cancer-related disease-gene associations were identified at the 24 h timepoint. Many of the kinases and pathways described above play crucial roles in the development of HCC by affecting processes such as invasion and metastasis. Overall, our data indicate that MCLR-mediated changes in protein phosphorylation involve biological pathways related to carcinogenesis that may contribute to the development of HCC.

Potential (co-)contamination of dairy milk with AFM1 and MC-LR and their synergistic interaction in inducing mitochondrial dysfunction in HepG2 cells.

Several toxic metabolites, such as aflatoxin M1 (AFM1), are known to contaminate dairy milk. However, as mentioned in an external EFSA report, there is a knowledge gap regarding the carry-over of certain emerging toxins such as microcystin-LR (MC-LR). Therefore, this work aimed to develop an LC-MS/MS method for MC-LR quantification in dairy milk. Also, the method included AFM1 as a common fungal metabolite and applied to analyze 113 dairy milk samples collected directly after the end of the summer peak. Both toxins were below their LODs, keeping the question on MC-LR carry-over still unanswered. Moreover, an in silico analysis, using a 3D molecular modeling was performed, pointing to a possible interaction between MC-LR and milk proteins, especially ß-lactoglobulin. Since AFM1 and MC-LR are hepatotoxic, their interaction in inducing mitochondrial dysfunction in HepG2 cells was investigated at low (subcytotoxic) concentrations. Live cell imaging-based assays showed an inhibition in cell viability, without involvement of caspase-3/7, and a hyperpolarization in the mitochondrial membrane potential after the exposure to a mixture of 100 ng mL-1 AFM1 and 1000 ng mL-1 MC-LR for 48h. Extracellular flux analysis revealed inhibitions of several key parameters of mitochondrial function (basal respiration, ATP-linked respiration, and spare respiratory capacity).

S-scheme carbon doped-TiO2/ZnIn2S4 heterojunction for enhanced photocatalytic degradation of microcystin-LR and hydrogen evolution.

Photocatalytic degradation of pollutants coupled with hydrogen (H2) evolution has emerged as a promising solution for environmental and energy crises. However, the fast recombination of photoexcited electrons and holes limits photocatalytic activities. Herein, an S-scheme heterojunction carbon doped-TiO2/ZnIn2S4 (C-TiO2/ZnIn2S4) was designed by substituting oxygen sites within C-TiO2 by ZnIn2S4. Under visible light irradiation, the optimal C-TiO2/ZnIn2S4 exhibits a higher degradation efficiency (88.6%) of microcystin-LR (MC-LR), compared to pristine C-TiO2 (72.9%) and ZnIn2S4 (66.8%). Furthermore, the H2 yield of the C-TiO2/ZnIn2S4 reaches 1526.9 µmol g-1 h-1, which is 3.83 times and 2.87 times that of the C-TiO2 and ZnIn2S4, respectively. Experimental and theoretical investigations reveal that an internal electric field (IEF) informed in the C-TiO2/ZnIn2S4 heterojunction, accelerates the separation of photogenerated charge pairs, thereby enhancing photocatalytic efficiency of MC-LR degradation and H2 production. This work highlights a new perspective on the development of high-performance photocatalysts for wastewater treatment and H2 generation.

Probiotics Alleviate Microcystin-LR-Induced Developmental Toxicity in Zebrafish Larvae.

Microcystin-LR (MCLR) poses a significant threat to aquatic ecosystems and public health. This study investigated the protective effects of the probiotic Lactobacillus rhamnosus against MCLR-induced developmental toxicity in zebrafish larvae. Zebrafish larvae were exposed to various concentrations of MCLR (0, 0.9, 1.8, and 3.6 mg/L) with or without L. rhamnosus from 72 to 168 h post-fertilization (hpf). Probiotic supplementation significantly improved survival, hatching, and growth rates and reduced malformation rates in MCLR-exposed larvae. L. rhamnosus alleviated MCLR-induced oxidative stress by reducing reactive oxygen species (ROS) levels and enhancing glutathione (GSH) content and catalase (CAT) activity. Probiotics also mitigated MCLR-induced lipid metabolism disorders by regulating key metabolites (triglycerides, cholesterol, bile acids, and free fatty acids) and gene expression (ppara, pparb, srebp1, and nr1h4). Moreover, 16S rRNA sequencing revealed that L. rhamnosus modulated the gut microbiome structure and diversity in MCLR-exposed larvae, promoting beneficial genera like Shewanella and Enterobacter and inhibiting potential pathogens like Vibrio. Significant correlations were found between gut microbiota composition and host antioxidant and lipid metabolism parameters. These findings suggest that L. rhamnosus exerts protective effects against MCLR toxicity in zebrafish larvae by alleviating oxidative stress, regulating lipid metabolism, and modulating the gut microbiome, providing insights into probiotic-based strategies for mitigating MCLR toxicity in aquatic organisms.

Exposure to microcystin-LR promotes the progression of colitis-associated colorectal cancer by inducing barrier disruption and gut microbiota dysbiosis.

Microcystins (MCs) are secondary metabolites generated by cyanobacterial blooms, among which microcystin-LR (MC-LR) stands out as the most widely distributed variant in aquatic environments. However, the effects of MC-LR on the colorectum and its role in promoting colorectal tumor progression remain unclear. Therefore, this study aims to scrutinize the impact of MC-LR on a mice model of colitis-associated colorectal cancer and elucidate the potential underlying molecular mechanisms. In this study, we used AOM/DSS mice and orally administered MC-LR at doses of 40 µg/kg or 200 µg/kg. Exposure to MC-LR increased tumor burden, promoted tumor growth, shortened colon size, and decreased goblet cell numbers and tight junction protein levels in intestinal tissues. Additionally, exposure to MC-LR induced alterations in the structure of gut microbiota in the mouse colon, characterized by an increase in the relative abundance of Escherichia_coli and Shigella_sonnei, and a decline in the relative abundance of Akkermansia_muciniphila. Transcriptomic analysis revealed that MC-LR exposure activated the IL-17 signaling pathway in mouse colorectal tissues and participated in inflammation regulation and immune response. Immunofluorescence results demonstrated an increase in T-helper 17 (Th17) cell levels in mouse colorectal tumors following MC-LR exposure. The results from RT-qPCR revealed that MC-LR induced the upregulation of IL-6, IL-1ß, IL-10, IL-17A, TNF-α, CXCL1, CXCL2, CXCL5 and CCL20. The novelty of this study lies in its comprehensive approach to understanding the mechanisms by which MC-LR may contribute to CRC progression, offering new perspectives and valuable reference points for establishing guidance standards regarding MC-LR in drinking water. Our findings suggest that even at guideline value, MC-LR can have profound effects on susceptible mice, emphasizing the need for a reevaluation of guideline value and a deeper understanding of the role of environmental toxins in cancer progression.

Microcystin-LR prenatal exposure induces coronary heart disease through macrophage polarization imbalance mediated by trophoblast-derived extracellular vesicles.

Microcystin-leucine arginine (MC-LR) has been reported to exhibit placental toxicity, leading to potential adverse pregnancy outcomes. Placental abnormalities often coincide with congenital heart defects (CHD). However, the extent to which MC-LR-induced placental abnormalities contribute to CHD and the cellular mechanisms underlying this association remain unknown. In this study, we observed abnormal polarization of placental macrophages in pregnant mice exposed to MC-LR during pregnancy, and the embryos developed cardiac developmental defects that persisted into adulthood. Trophoblast-derived extracellular vesicles (T-EVs) increase in number during pregnancy and act as a critical signal in macrophage polarization. However, MC-LR significantly affected the miRNA expression profile of T-EVs. Upon internalization into macrophages, T-EV-derived miR-377-3p specifically targets the 3'UTR region of NR6A1 to inhibit gene expression. Silencing of transcription suppressor NR6A1 leads to abnormal activation of the downstream mTOR/S6K1/SREBP pathway, inducing metabolic reprogramming and ultimately leading to M1 polarization of macrophages. This study elucidated the placental mechanism underlying MC-LR-induced CHD for the first time, providing insights into the environmental risks associated with CHD.

Suspended particulate matter-biofilm aggregates benefit microcystin removal in turbulent water but trigger toxicity toward Daphnia magna.

Suspended particulate matter (SPM) and biofilm are critical in removing contaminants in aquatic environments, but the environmental behavior and ecological toxicity of SPM-biofilm aggregates modulated by turbulence intensities are largely unknown. This study determined the removal pathways of microcystin-LR (MC-LR) by SPM and its biofilm under different turbulence intensities (2.25 × 10-3, 1.01 × 10-2, and 1.80 × 10-2 m2/s3). Then, we evaluated the toxicity of SPM-biofilm aggregates to Daphnia magna. The results revealed that SPM contributed to the adsorption of MC-LR, and the removal of MC-LR can be accelerated with biofilm formation on SPM, with 95.66 % to 97.45 % reduction in MC-LR concentration under the studied turbulence intensities. Higher turbulence intensity triggered more frequent contact of SPM and MC-LR, formed compact but smaller clusters of SPM-biofilm aggregates, and enhanced the abundance of mlrA and mlrB; thus benefiting the adsorption, biosorption, and biodegradation of MC-LR. Furthermore, the SPM-biofilm aggregates formed in turbulent water triggered oxidative stress to Daphnia magna, while a weak lethal toxic effect was identified under moderate turbulence intensity. The results indicate that the toxicity of SPM-biofilm aggregates fail to display a linear relationship with turbulence intensity. These findings offer new perspectives on understanding the environmental behavior and ecological outcomes of SPM and its biofilms in turbulent aquatic environments.

Impact of butylparaben on growth dynamics and microcystin-LR production in Microcystis aeruginosa.

The presence of butylparaben (BP), a prevalent pharmaceutical and personal care product, in surface waters has raised concerns regarding its impact on aquatic ecosystems. Despite its frequent detection, the toxicity of BP to the cyanobacterium Microcystis aeruginosa remains poorly understood. This study investigates the influence of BP on the growth and physiological responses of M. aeruginosa. Results indicate that low concentrations of BP (below 2.5 mg/L) have negligible effects on M. aeruginosa growth, whereas higher concentrations (5 mg/L and 10 mg/L) lead to significant growth inhibition. This inhibition is attributed to the severe disruption of photosynthesis, evidenced by decreased Fv/Fm values and chlorophyll a content. BP exposure also triggers the production of reactive oxygen species (ROS), resulting in elevated activity of antioxidant enzymes. Excessive ROS generation stimulates the production of microcystin-LR (MC-LR). Furthermore, lipid peroxidation and cell membrane damage indicate that high BP concentrations cause cell membrane rupture, facilitating the release of MC-LR into the environment. Transcriptome analysis reveals that BP disrupts energy metabolic processes, particularly affecting genes associated with photosynthesis, carbon fixation, electron transport, glycolysis, and the tricarboxylic acid cycle. These findings underscore the profound physiological impact of BP on M. aeruginosa and highlight its role in stimulating the production and release of MC-LR, thereby amplifying environmental risks in aquatic systems.

Simultaneous inactivation of Microcystis aeruginosa and degradation of microcystin-LR in water by activation of periodate with sunlight.

Harmful algal blooms pose tremendous threats to ecological safety and human health. In this study, simulated solar light (SSL) irradiation was used to activate periodate (PI) for the inactivation of Microcystis aeruginosa and degradation of microcystin-LR (MC-LR). We found that PI-SSL system could effectively inactivate 5 × 106 cells·mL-1 algal cells below the limit of detection within 180 min. ·OH and iodine (IO3· and IO4·) radicals generated in PI-SSL system could rupture cell membranes, releasing intracellular substances including MC-LR into the reaction system. However, the released MC-LR could be degraded into non-toxic small molecules via hydroxylation and ring cleavage processes in PI-SSL system, reducing their environmental risks. High algae inactivation performance of PI-SSL system in solution with a wide pH range (3-9), with the coexisting anions (Cl-, NO3- and SO42-) and the copresence of natural organic matters (humic acid and fulvic acid), real water (lake water and river water), as well as in continuous-flow reactor (14 h) were also achieved. In addition, under natural sunlight irradiation, effective algae inactivation could also be achieved in an enlarged reactor (1 L). Overall, our study showed that PI-SSL system could avoid the inference by the background substances and could be employed as a feasible technique to treat algal bloom water.

Metabolomics reveals the lipid metabolism disorder in Pelophylax nigromaculatus exposed to environmentally relevant levels of microcystin-LR.

Cyanobacterial blooms have emerged as a significant environmental issue worldwide in recent decades. However, the toxic effects of microcystin-LR (MC-LR) on aquatic organisms, such as frogs, have remained poorly understood. In this study, frogs (Pelophylax nigromaculatus) were exposed to environmentally relevant concentrations of MC-LR (0, 1, and 10 µg/L) for 21 days. Subsequently, we assessed the impact of MC-LR on the histomorphology of the frogs' livers and conducted a global MS-based nontarget metabolomics analysis, followed by the determination of substances involved in lipid metabolism. Results showed that MC-LR significantly induced histological alterations in the frogs' hepatopancreas. Over 200 differentially expressed metabolites were identified, primarily enriched in lipid metabolism. Biochemical analysis further confirmed that MC-LR exposure led to a disorder in lipid metabolism in the frogs. This study laid the groundwork for a mechanistic understanding of MC-LR toxicity in frogs and potentially other aquatic organisms.

The effects of nanoplastics and microcystin-LR coexposure on Aristichthys nobilis at the early developmental stages.

Nanoplastics (NPs) and microcystin-LR (MC-LR) are two common and harmful pollutants in water environments, especially at aquafarm where are full of plastic products and algae. It is of great significance to study the toxic effects and mechanisms of the NPs and/or MC-LR on fish at the early stage. In this study, the embryo and larvae of a filtering-feeding fish, Aristichthys nobilis, were used as the research objects. The results showed that the survival and hatching rates of the embryo were not significantly affected by the environmental concentration exposure of these two pollutants. Scanning electron microscopy (SEM) observation displayed that NPs adhered to the surface of the embryo membrane. Transcriptomic and bioinformatic analyses revealed that the NPs exposure activated neuromuscular junction development and skeletal muscle fiber in larvae, and affected C5-Branched dibasic acid metabolism. The metabolic and biosynthetic processes of zeaxanthin, xanthophyll, tetraterpenoid, and carotenoid were suppressed after the MC-LR exposure, which was harmful to the retinol metabolism of fish. Excessive production of superoxide dismutase (SOD) was detected under the MC-LR exposure. The MC-LR and NPs coexposure triggered primary immunodeficiency and adaptive immune response, leading to the possibility of reduced fitness of A.nobilis during the development. Collectively, our results indicate that environmental concentration NPs and MC-LR coexposure could cause toxic damage and enhance sick risk in A.nobilis, providing new insights into the risk of NPs and MC-LR on filtering-feeding fish.