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Marine biotoxins distribute widely, have high toxicity, and can be easily accumulated in water or seafood, exposing a serious threat to consumer health. Achieving specific and sensitive detection is the most effective way to prevent emergent issues caused by marine biotoxins; however, the previous detection methods cannot meet the requirements because of ethical or technical drawbacks. Aptamers, a kind of novel recognition element with high affinity and specificity, can be used to fabricate various aptasensors (aptamer-based biosensors) for sensitive and rapid detection. In recent years, an increasing number of aptamers and aptasensors have greatly promoted the development of marine biotoxins detection. In this review, we summarized the recent aptamer-related advances for marine biotoxins detection and discussed their perspectives. Firstly, we summarized the sequences, selection methods, affinity, secondary structures, and the ion conditions of all aptamers to provide a database-like information; secondly, we summarized the reported aptasensors for marine biotoxins, including principles, detection sensitivity, linear detection range, etc.; thirdly, on the basis of the existing reports and our own research experience, we forecast the development prospects of aptamers and aptasensors for marine biotoxins detection. We hope this review not only provides a comprehensive summary of aptamer selection and aptasensor development for marine biotoxins, but also arouses a broad readership amongst academic researchers and industrial chemists.

[D-Leu1]MC-LR and MC-LR, two microcystins differing in one amino acid, constitute a sanitary and environmental problem owing to their frequent and concomitant presence in water bodies of the Americas and their association with human intoxication during recreational exposure to cyanobacterial bloom. Present in reservoirs used for irrigation as well, they can generate problems in the development of crops such as Phaseolus vulgaris, of nutritional and economic interest to the region. Although numerous works address the toxic effects of MC-LR, information on the toxicity of [D-Leu1]MC-LR is limited. Our objective was to study the toxic effects of [D-Leu1]MC-LR and MC-LR (3.5 µg/ml) on P. vulgaris after a single contact at the imbibition stage. Our findings indicate that 10 days post treatment, [D-Leu1]MC-LR generates morphological and physiological alterations more pronounced than those caused by MC-LR. In addition to the alterations produced by [D-Leu1]MC-LR in the development of seedlings and the structure of the leaves, roots and stems, we also found alterations in leaf stomatal density and conductivity, a longer delay in the phototropic response and a decrease in the maximum curvature angles achieved with respect to that observed for MC-LR. Our findings indicate that these alterations are linked to the greater inhibition of phosphatase activity generated by [D-Leu1]MC-LR, rather than to oxidative damage. We observed that 30 days after treatment with MC-LR, plants presented better development and recovery than those treated with [D-Leu1]MC-LR. Further studies are required on [D-Leu1]MC-LR and MC-LR toxicity and their underlying mechanisms of action.

Microcystin-LR (MC-LR) is the most toxic and frequently detected monocyclic heptapeptide hepatotoxin produced by cyanobacteria, which poses a great threat to the natural ecosystem and public health. It is very important to seek environment-friendly and cost-efficient methods to remove MC-LR in water. In this study, the MC-degrading capacities of a novel indigenous bacterial community designated as YFMCD4 and the influence of environmental factors including various temperatures, MC concentrations and pH on the MC-degrading activities were investigated utilizing high-performance liquid chromatography (HPLC). In addition, the MC-degrading mechanism of YFMCD4 was also studied using HPLC coupled with a mass spectrometry equipped with electrospray ionization interface (HPLC-ESI-MS). The data showed MC-LR was completely removed at the maximum rate of 0.5 µg/(mL·h) under the optimal condition by YFMCD4. Two pure bacterial strains Alcaligenes faecalis and Stenotrophomonas acidaminiohila were isolated from YFMCD4 degraded MC-LR at a slower rate. The MC-degrading rates of YFMCD4 were significantly affected by different temperatures, pH and MC-LR concentrations. Two intermediates of a tetrapeptide and Adda appeared in the degradation process. These results illustrate that the novel YFMCD4 is one of the highest effective MC-degrading bacterial community, which can completely remove MC-LR and possesses a significant potential to treat water bodies contaminated by MC-LR.

Microcystin-LR (MC-LR) is an extremely poisonous cyanotoxin that poses a threat to ecosystems and human health. MC-LR has been reported as an enterotoxin. The objective of this study was to determine the effect and the mechanism of subchronic MC-LR toxicity on preexisting diet-induced colorectal damage. C57BL/6J mice were given either a regular diet or a high-fat diet (HFD) for 8 weeks. After 8 weeks of feeding, animals were supplied with vehicle or 120 μg/L MC-LR via drinking water for another 8 weeks, and their colorectal were stained with H&E to detect microstructural alterations. Compared with the CT group, the HFD and MC-LR + HFD-treatment group induced a significant weight gain in the mice. Histopathological findings showed that the HFD- and MC-LR + HFD-treatment groups caused epithelial barrier disruption and infiltration of inflammatory cells. The HFD- and MC-LR + HFD-treatment groups raised the levels of inflammation mediator factors and decreased the expression of tight junction-related factors compared to the CT group. The expression levels of p-Raf/Raf and p-ERK/ERK in the HFD- and MC-LR + HFD-treatment groups were significantly increased compared with the CT group. Additionally, treated with MC-LR + HFD, the colorectal injury was further aggravated compared with the HFD-treatment group. These findings suggest that by stimulating the Raf/ERK signaling pathway, MC-LR may cause colorectal inflammation and barrier disruption. This study suggests that MC-LR treatment may exacerbate the colorectal toxicity caused by an HFD. These findings offer unique insights into the consequences and harmful mechanisms of MC-LR and provide strategies for preventing and treating intestinal disorders.

Resource quality can have conflicting effects on host–parasite interactions; for example, higher resource quality might increase host investment in immune function, or conversely, might permit greater parasite reproduction. Thus, anticipating the impact of changing resource quality on host–parasite interactions is challenging, especially because we often lack a mechanistic understanding of how resource quality influences host physiology and fitness to alter infection outcomes. We investigated whether there are generalizations in how resource quality affects multiple host clones' interactions with different parasites. We used the Daphnia freshwater zooplankton model system to experimentally investigate how a resource quality gradient from high‐quality green algae to poor‐quality cyanobacteria diets influences host fitness, physiology, and infection by two parasites: a bacterium, Pasteuria ramosa, and a fungus, Metschnikowia bicuspidata. We ran a separate experiment for each parasite using a factorial design with four diets, two Daphnia dentifera host clones, and parasite‐inoculated and ‐uninoculated treatments (16 treatments per experiment). Diet strongly influenced infection by the fungus but not the bacterium. These relationships between diet and infection cannot be explained by changes in feeding rate (and, therefore, parasite exposure). Instead, the impact of diet on fungal infection was associated with impacts of diet on the earliest stage of infection: hosts that fed on poor quality diets had very few attacking spores in their guts. Diet did not significantly influence host immune responses. Diet influenced spore production differently for the two parasites, with reduced resource quality limiting the number of fungal spores and the size (but not number) of bacterial spores. Diet, host clone, and infection all affected host fitness. Interestingly, diet influenced the impact of the bacterium, a parasitic castrator that induces gigantism; for one clone, infected hosts fed high‐quality diets still produced a substantial number of offspring, whereas resource limitation hindered gigantism. Finally, there were often costs of resisting infection, though these generally were not affected by diet. Overall, we show that resource quality differentially impacts the exposure, infection, and proliferation processes for different parasites and host clones, which highlights the need to use multi‐genotype and multi‐parasite studies to better understand these complex interactions.

Freshwater harmful algal blooms (HABs) are increasing in number and severity worldwide. These HABs are chiefly composed of one or more species of cyanobacteria, also known as blue-green algae, such as Microcystis and Anabaena. Numerous HAB cyanobacterial species produce toxins (e.g., microcystin and anatoxin—collectively referred to as HAB toxins) that disrupt ecosystems, impact water and air quality, and deter recreation because they are harmful to both human and animal health. Exposure to these toxins can occur through ingestion, inhalation, or skin contact. Acute health effects of HAB toxins have been well documented and include symptoms such as nausea, vomiting, abdominal pain and diarrhea, headache, fever, and skin rashes. While these adverse effects typically increase with amount, duration, and frequency of exposure, susceptibility to HAB toxins may also be increased by the presence of comorbidities. The emerging science on potential long-term or chronic effects of HAB toxins with a particular emphasis on microcystins, especially in vulnerable populations such as those with pre-existing liver or gastrointestinal disease, is summarized herein. This review suggests additional research is needed to define at-risk populations who may be helped by preventative measures. Furthermore, studies are required to develop a mechanistic understanding of chronic, low-dose exposure to HAB toxins so that appropriate preventative, diagnostic, and therapeutic strategies can be created in a targeted fashion.

The integration of graphene materials into electrochemical biosensing platforms has gained significant interest in recent years. Bulk quantities of graphene can be synthesized by oxidation of graphite to graphite oxide and subsequent exfoliation to graphene oxide (GO). However, the size of the resultant GO sheets changes from the parent graphite yielding a polydispersed solution of sizes ranging from a few nanometers to tens of micrometers. Here, we investigate the direct effect of GO sheets sizes on biosensor performance. We separated different GO sheets sizes, and we characterized them via atomic force, scanning electron, Raman and X-ray photoelectron spectroscopies and solid state nuclear magnetic resonance (NMR). As proof of concept, the sensing performance of these GO samples was probed using a well-known ssDNA aptasensor against microcystin-LR toxin and an immunosensor against β-lactoglobulin. The resulting aptasensors and immunosensors are fabricated by using covalent attachment and physical adsorption. We found that the aptasensors fabricated using physical adsorption, the binding signal variation was dramatically increased with increasing the GO sheet size. In contrast, for the aptasensor fabricated using covalent immobilization, the binding signal variation decreased with increasing GO sheet size. However, for the β-lactoglobulin immunosensors, the optimum signals were observed at intermediate GO sheet size. GO sheet size could enhance or inhibit the sensitivity of the graphene-based electrochemical sensors. Our results demonstrate that controlling the size of GO sheets may have a profound impact in specific biosensing applications.

Microcystins (MCs), toxins generated by cyanobacteria, feature microcystin-LR (MC-LR) as one of the most prevalent and toxic variants in aquatic environments. MC-LR not only causes environmental problems but also presents a substantial risk to human health. This study aimed to investigate the impact of MC-LR on APC[sup.min/+] mice, considered as an ideal animal model for intestinal tumors. We administered 40 µg/kg MC-LR to mice by gavage for 8 weeks, followed by histopathological examination, microbial diversity and metabolomics analysis. The mice exposed to MC-LR exhibited a significant promotion in colorectal cancer progression and impaired intestinal barrier function in the APC[sup.min/+] mice compared with the control. Gut microbial dysbiosis was observed in the MC-LR-exposed mice, manifesting a notable alteration in the structure of the gut microbiota. This included the enrichment of Marvinbryantia , Gordonibacter and Family_XIII_AD3011_group and reductions in Faecalibaculum and Lachnoclostridium . Metabolomics analysis revealed increased bile acid (BA) metabolites in the intestinal contents of the mice exposed to MC-LR, particularly taurocholic acid (TCA), alpha-muricholic acid (α-MCA), 3-dehydrocholic acid (3-DHCA), 7-ketodeoxycholic acid (7-KDCA) and 12-ketodeoxycholic acid (12-KDCA). Moreover, we found that Marvinbryantia and Family_XIII_AD3011_group showed the strongest positive correlation with taurocholic acid (TCA) in the mice exposed to MC-LR. These findings provide new insights into the roles and mechanisms of MC-LR in susceptible populations, providing a basis for guiding values of MC-LR in drinking water.

This paper presents recent development and applications of thermal lens microscopy (TLM) and beam deflection spectrometry (BDS) for the analysis of water samples and sea ice. Coupling of TLM detection to a microfluidic system for flow injection analysis (μFIA) enables the detection of microcystin-LR in waters with a four samples/min throughput (in triplicate injections) and provides an LOD of 0.08 µg/L which is 12-times lower than the MCL for microcystin-LR in water. μFIA-TLM was also applied for the determination of total Fe and Fe(II) in 3 µL samples of synthetic cloudwater. The LODs were found to be 100 nM for Fe(II) and 70 nM for total Fe. The application of µFIA-TLM for the determination of ammonium in water resulted in an LOD of 2.3 µM for injection of a 5 µL sample and TLM detection in a 100 µm deep microfluidic channel. For the determination of iron species in sea ice, the BDS was coupled to a diffusive gradient in the thin film technique (DGT). The 2D distribution of Fe(II) and total Fe on DGT gels provided by the BDS (LOD of 50 nM) reflected the distribution of Fe species in sea ice put in contact with DGT gels.

Environmental toxins represent a growing public health concern. Microcystin‐LR (MC‐LR), a potent cyanobacterial toxin found in freshwater ecosystems, has been linked to multisystem toxicity. However, its impact on renal pathology ‐ particularly through regulated cell death ‐ remains poorly characterized. This study investigates the molecular basis of MC‐LR‐induced nephrotoxicity in murine models, focusing on ferroptosis and epigenetic regulation. Using both acute and chronic MC‐LR exposure paradigms, marked kidney fibrosis and ferroptosis are observed, evidenced by lipid peroxidation, mitochondrial damage, and collagen deposition. Mechanistically, MC‐LR suppressed transcription of glutathione peroxidase 4 (GPX4) in tubular epithelial cells. This downregulation is associated with promoter hypermethylation, increased expression of DNA methyltransferases DNMT1 and DNMT3a, and enhanced recruitment of the transcriptional repressor E2F4 and co‐repressor NCoR. Notably, MC‐LR directly bound DNMT1 and DNMT3a, stabilizing their protein levels by blocking proteasomal degradation. Pharmacological inhibition of DNA methyltransferases (SGI‐1027) or ferroptosis (ferrostatin‐1) significantly ameliorated renal injury. These findings uncover a previously unrecognized epigenetic mechanism by which MC‐LR drives ferroptosis and kidney damage. Targeting the DNMT‐GPX4 axis may offer therapeutic opportunities for mitigating toxin‐induced organ injury and protecting public health against environmental biohazards. MC‐LR stabilizes DNMT1/3a by blocking their ubiquitin‐mediated degradation, leading to Gpx4 promoter hypermethylation and E2F4/NCoR‐associated transcriptional repression, which drives renal tubular ferroptosis in mice. Pharmacological inhibition of DNA methylation (SGI‐1027) or ferroptosis (Fer‐1) disrupts this DNMT‐GPX4 axis, thereby alleviating MC‐LR‐induced ferroptosis and nephrotoxicity.