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At least 19 recordsLinked to original sources
PubMed2024

A review focusing on mechanisms and ecological risks of enrichment and propagation of antibiotic resistance genes and mobile genetic elements by microplastic biofilms.

Microplastics (MPs) are emerging ubiquitous pollutants in aquatic environment and have received extensive global attention. In addition to the traditional studies related to the toxicity of MPs and their carrier effects, their unique surface-induced biofilm formation also increases the ecotoxicity potential of MPs from multiple perspectives. In this review, the ecological risks of MPs biofilms were summarized and assessed in detail from several aspects, including the formation and factors affecting the development of MPs biofilms, the selective enrichment and propagation mechanisms of current pollution status of antibiotic resistance genes (ARGs) and mobile genetic elements (MGEs) in MPs biofilms, the dominant bacterial communities in MPs biofilms, as well as the potential risks of ARGs and MGEs transferring from MPs biofilms to aquatic organisms. On this basis, this paper also put forward the inadequacy and prospects of the current research and revealed that the MGEs-mediated ARG propagation on MPs under actual environmental conditions and the ecological risk of the transmission of ARGs and MGEs to aquatic organisms and human beings are hot spots for future research. Relevant research from the perspective of MPs biofilm should be carried out as soon as possible to provide support for the ecological pollution prevention and control of MPs.

Biofilms↗
PubMed2026

Toxicoproteomic analysis reveals arsenic-induced alterations in eye lens proteins of Labeo rohita.

Arsenic occurs extensively in the environment and is classified as a potent carcinogenic substance in humans. Prolonged intake of water contaminated with arsenic results in the development of arsenicosis. In the present study, a toxicoproteomic approach was employed to elucidate arsenic-induced alterations in lens proteins using a fish model. Juveniles of Labeo rohita were exposed to sodium meta-arsenite (NaAsO2) at concentrations of 5, 10, 15, and 20&#xa0;ppm for a period of 10&#xa0;days in triplicate experimental groups. Soluble lens proteins were analyzed using one- and two-dimensional gel electrophoresis, immunoblotting of &#x3b1;A-crystallin and MALDI-TOF mass spectrometry. Cataract development was observed at arsenic concentrations&#x2009;&#x2265;&#x2009;15&#xa0;ppm. Proteomic analyses revealed concentration-dependent alterations in lens protein abundance, including significant reductions in &#x3b2;B1, &#x3b2;B2, and &#x3b2;A2b-crystallin, small heat shock protein and skeletal &#x3b1;-actin (p&#x2009;<&#x2009;0.05). In addition, &#x3b1;A, &#x3b2;A2, and &#x3b2;A2a-crystallin exhibited reduced abundance trends, although these changes were not statistically significant. Two-dimensional immunoblotting revealed 15 distinct &#x3b1;A-crystallin isoforms in control lenses, several of which showed a progressive decrease with increasing arsenic exposure, culminating in complete degradation at 20&#xa0;ppm. These findings demonstrate that arsenic exposure is associated with substantial alterations in lens crystallins and other proteins involved in structural organization and protein homeostasis, coinciding with cataract development at higher exposure concentrations. The identified proteins may serve as potential toxicoproteomic biomarkers of lens damage in aquatic organisms and provide a foundation for future studies investigating the molecular mechanisms of arsenic-induced lens toxicity.

Animals↗
PubMed1979

Toxicity of selenium to developing Xenopus laevis embryos.

Se in the form of sodium selenite is toxic to Xenopus laevis embryos and tadpoles continuously exposed to concentrations above 1 ppm. Concentrations of 2 ppm and above result in severe developmental abnormalities and increased mortality. Uptake and loss of radioactive Se from water are rapid, but depuration is not complete indicating that some Se can remain bound by the organism. The facts that Se is toxic at low levels to Xenopus embryos and tadpoles, can cause developmental abnormalities, and accumulates in tissues suggest that increased release of Se compounds into the environment poses a potential threat to aquatic organisms.

Abnormalities, Drug-Induced↗
PubMed1977

Colonization of the botanical environment by Klebsiella isolates of pathogenic origin.

Growth, survival, and pathogenicity of Klebsiella growing in and on environmental foci were examined. Total coliforms present in raw wastes from pulp mills were in excess of 10(5)/ml, and 60 to 80% were Klebsiella. Fecal coliform counts ranged from 10(1) to 10(5)/ml. Klebsiella isolates from industrial effluents and a variety of human and bovine mastitis origins multiplied in pulp waste and commonly exceeded 10(6) cells per ml. Pathogenic isolates also multiplied in dilute aqueous extracts of sawdust to comparable levels. Klebsiella strains from vegetable surfaces and human infections grew rapidly on the surfaces of potatoes and lettuce and exceeded 10(3) organisms per g of surface peel and leaf after a 24h incubation at room temperature. After 7 weeks on potatoes stored at 5 degrees C, some 10 to 30% of the day 1 Klebsiella counts were recoverable. Three Klebsiella isolates of pathogenic origin were passed 45 times through sterile pulp effluent (270 generations), and mean lethal dose levels in mice were periodically monitored. In two instances, a significant decrease in virulence was noted after 15 to 26 passes (90 to 156 generations). The third culture, of bovine mastitis origin, retained its original mean lethal dose value. Botanical milieu provided suitable habitats for the multiplication and colonization of Klebsiella isolates of disease origins in the same manner as indigenous isolates. Aquatic environments polluted with botanical material served as potential reservoirs for perpetuating the growth and spread of opportunistic Klebsiella pathogens that may ultimately colonize animals, humans, and aquatic organisms.

Animals↗
PubMed2026

Characterization and functional insights of histone deacetylases in bivalves: implications for temperature and immune response in Chlamys nobilis.

Histone deacetylases serve as pivotal epigenetic regulators that modulate chromatin remodeling and gene transcription, playing critical roles in immune defense and environmental stress responses in aquatic organisms. However, the evolutionary characteristics and functional roles of the HDAC family in bivalves remain poorly understood. In this study, genome-wide identification of the HDAC family across 30 bivalve species yielded 558 HDAC genes. Phylogenetic reconstruction categorized these genes into four conserved groups and revealed a unique, bivalve-specific SIRT8 clade. Using the noble scallop Chlamys nobilis as a representative model, expression profiling revealed distinct expression patterns among CnHDAC members. Class I and most Class III members were predominantly expressed in the gonads, while Class II members were enriched in immune-related tissues, implying their potential involvement in bivalve immunity. Upon temperature stress, CnHDAC1/2, CnHDAC11-1, CnHDAC11-2, CnSIRT2-1, CnSIRT4, CnSIRT6, and CnSIRT8-3 were significantly induced, highlighting their critical roles in temperature adaptation. Upon Vibrio exposure, CnHDAC1/2, CnHDAC8, CnSIRT4, and CnSIRT6 were upregulated, while CnHDAC4/5/7/9, CnHDAC6/10, CnSIRT2-2, CnSIRT5, CnSIRT7, and CnSIRT8-3 were downregulated, suggesting a coordinated epigenetic regulatory mechanism underlying host immune defense. In conclusion, this study systematically elucidates the evolutionary landscape of the HDAC family and underscores its potential involvement in environmental resilience and host immunity, providing a theoretical basis for the breeding of disease-resistant and stress-tolerant aquaculture bivalves.

Animals↗
PubMed2026

Plasticity of hepatic metabolism in Arctic char (Salvelinus alpinus) in response to cyclic hypoxia.

The emergence of cyclic hypoxia puts aquatic organisms' homeostasis under significant strain. Energetic metabolism as well as protein synthesis and folding are particularly altered during hypoxia, while reoxygenation imposes an oxidative challenge. Currently, little is known about how hypoxia-sensitive organisms respond to large oxygen fluctuations. Our previous work on Arctic char revealed that this salmonid, despite being strongly affected by acute hypoxia and reoxygenation (H/R), can successfully reestablish homeostasis, notably through adjustments to hepatic mitochondrial metabolism. However, the mechanisms underlying this acclimation remain poorly understood. We hypothesized that Arctic char remodel their hepatic proteome to optimize energy metabolism, reorganize oxygen-demanding pathways, and maintain cellular homeostasis during repeated H/R cycles. By exposing Arctic char to two or fifteen days of diel cyclic hypoxia, we confirmed this species' limited capacity to respond to acute H/R. Nevertheless, after fifteen cycles, fish adjusted their energetic metabolism through coordinated regulation of carbohydrate and lipid pathways and upregulation of amino acid metabolism. Mitochondrial metabolism was strongly reorganized, particularly at the ubiquinone-Complex III interaction level, alongside adjustments in proline utilization and protein processing. Moreover, protein processing and folding pathways were stimulated in both mitochondria and the endoplasmic reticulum. However, chronic cyclic hypoxia may still promote non-mitochondrial ROS production, DNA replication stress, and impaired immune function. This study highlights how a hypoxia-sensitive fish progressively reorganizes its metabolism and oxygen-demanding pathways to establish a phenotype adapted to chronic cyclic hypoxia, while also revealing the physiological costs associated with this acclimation.

Animals↗
PubMed2026

Effects of acute hypoxia followed by reoxygenation on intestinal histomorphology, oxidative stress and hypoxia signaling biomarkers, and microbiota in pikeperch (Sander lucioperca).

In aquatic environments, natural and anthropogenic factors commonly reduce dissolved oxygen (DO) and trigger hypoxia, which threatens the health and survival of aquatic organisms. As an important economic fish species in China, pikeperch (Sander lucioperca) is extremely sensitive to hypoxia. However, there are relatively few reports on how hypoxia and reoxygenation affect its intestinal physiology and microbial community. Three treatment groups were set for pikeperch: normoxia (DO&#xa0;=&#xa0;8.5&#xa0;&#xb1;&#xa0;0.5&#xa0;mg/L), 48&#xa0;h hypoxia (DO&#xa0;=&#xa0;2.5&#xa0;&#xb1;&#xa0;0.1&#xa0;mg/L), and reoxygenation (48&#xa0;h hypoxia followed by 6&#xa0;h reoxygenation at normal DO), to evaluate alterations in intestinal histopathology, tight junction gene expression, oxidative stress, hypoxia signaling molecules and intestinal microbiota composition. The results showed that hypoxia significantly decreased muscularis thickness by approximately 32.5% and reduced the expression of tight junction genes (Occludin, Claudin2, and ZO-2). Moreover, hypoxia significantly increased oxidative stress index levels (GSH-Px, CAT, and MDA), markedly upregulated the expression of Bax, Caspase3, and HIF-1&#x3b1;, while significantly downregulating the expression of Bcl-2, Egln1, and Egln2. Notably, reoxygenation elicited partial compensatory effects against these hypoxia-induced changes. 16S rRNA sequencing analysis revealed that hypoxic stress altered the intestinal microbial community composition of pikeperch and increased its diversity. In the hypoxia group, the abundance of the phylum Bacillota, along with the genera Halomonas and Acinetobacter, was significantly elevated, whereas in the reoxygenation group, the genus Lactobacillus increased approximately 180-fold. The results indicated that hypoxia caused intestinal oxidative damage, cell apoptosis, and intestinal microbiota dysbiosis in pikeperch, while short-term reoxygenation achieved partial recovery from these hypoxia-triggered intestinal injuries. The present research provides valuable references for in-depth exploration of the molecular mechanisms behind the response of pikeperch to acute hypoxia and reoxygenation stress, while also offering a novel perspective to understand the mechanism by which hypoxia impacts intestinal health in fish.

Animals↗
PubMed2025

Integrating RNA sequencing with deep learning-based metabolic toxicity prediction: A new perspective on screening prioritized liquid crystal monomers.

Nearly 99&#x202f;% of liquid crystal monomers (LCMs) toxicological data remains gaps, especially to aquatic organisms. Herein, this study proposes a rapid and high-throughput screening method for identifying priority LCMs in natural water. Using six fluorinated LCMs (LCMsF) with significant enrichment characteristics in zebrafish as examples, RNA sequencing revealed that LCMsF-induced metabolic disturbances are predominant, including 28 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway abnormalities attributed to 498 differentially expressed genes. Notably, the intricate sequencing process resulted in the inability to rapid identify additional 857 LCMsF that may induce metabolic disturbances. To address this, LCMsT-MTP, a predictive deep learning model based on RNA sequencing, was developed. This model integrates a comprehensive representation of LCMsF structures and metabolic toxicity target sequences. LCMsT-MTP improves upon traditional methods that are limited to single targets and mechanisms by facilitating the simultaneous identification of 21 metabolic toxicities induced by LCMsF. In addition, the LCMsT-MTP model was further applied to non-fluorinated LCMs (LCMsNone F) that satisfy the applicability domains test. Accordingly, a metabolic toxicity priority list of LCMs was proposed, with &#x223c;95&#x202f;% of LCMs classified as high or medium risk. Priority list validation by molecular dynamics confirmed that the interactions of LCMsF/LCMsNone F and metabolic toxicity targets in representative KEGG pathways were distinct.

Animals↗
PubMed2026

Identification and characterization of a wet adhesive protein extracted from Dreissena bugensis, the freshwater quagga mussel.

Mechanisms of wet adhesion have evolved in several aquatic organisms over millions of years. Yet, the repertoire of synthetic biocompatible wet adhesive materials is still limited. The byssus is a well-studied proteinaceous bioadhesive structure utilized by several bivalves to support sessile lifestyles in turbulent conditions. The quagga mussel (Dreissena bugensis) is a freshwater byssate and a notorious invasive species in the Great Lakes region. To identify adhesive proteins in the quagga mussel byssus, we utilized quantitative proteomics and found several proteins enriched at the byssus-substrate interface. Among the identified proteins was the Dbfp7 protein family. Dbfp7 is a small, polymorphic, and mostly disordered protein that lacks significant amounts of 3,4-dihydroxyphenylalanine (DOPA), a modified amino acid found in several marine mussel byssal proteins. Atomic force microscopy nanomechanical mapping of Dbfp7 films demonstrates that this protein exhibits adhesive ability in aqueous conditions. While DOPA is critical for marine mussel adhesion, interfacial electrochemistry of freshwater adhesive plaques suggests that freshwater byssates circumvent catechol-based adhesion. The functional characterization of Dbfp7 as a freshwater mussel adhesive protein advances the understanding of fundamental requirements for biocompatible wet adhesion, a crucial step for the development of bioinspired wet adhesive materials, such as improved medical adhesives.

Animals↗
PubMed1979

Measurement of the aquatic toxicity of volatile nitrosamines.

The acute toxicity of N-nitrosodimethylamine (DMN) and N-nitrosodiethylamine (DEN) was determined for three groups of aquatic organisms: algae, invertebrates, and fish. Toxicity of DMN and DEN to algae was assessed as a repression in the growth rate of either Selenastrum capricornutum or Anabaena flos-aquae in static bioassay tests. DMN and DEN concentrations of 1-10 ppm depressed algal growth in all cases. Invertebrate toxicity was determined in 96-h static bioassay tests with Dugesia dorotocephala and Gammarus limnaeus. The data indicated that these organisms are not highly susceptible to nitrosamine toxicity. The 96-h LC50s for D. dorotocephala were 1365 and 1490 ppm for DMN and DEN, respectively. Similar studies with G. limnaeus indicated LC50s of 330 and 500 ppm for DMN and DEN, respectively. Fish toxicity was also determined in 96-h statis bioassays with the fathead minnow (Pimephales promelas). Acute toxicities were calculated as LC50s of 940 and 775 ppm for DMN and DEN, respectively. Algae were calculated as LC50s of 940 and 775 ppm for DMN and DEN, respectively. Algae were quite sensitive to relative low levels of volatile nitrosamines, but higher organisms (invertebrates and fish) were relatively insensitive.

Animals↗
PubMed2026

Harnessing probiotics to combat nonylphenol toxicity: a multiomics approach of gut microbiome remodelling in Silurus meridionalis.

BACKGROUND: As a ubiquitous environmental endocrine disruptor, nonylphenol (NP) threatens aquatic organisms, driving the need for sustainable mitigation strategies. While probiotics represent promising eco-friendly supplements, their molecular mechanisms against NP toxicity remain unclear. In this study, S. meridionalis received 7-week of probiotic (Bacillus subtilis and Lactobacillus acidophilus) pretreatment followed by 15 days of NP exposure. Integrated metagenomics, transcriptomics, and metabolomics analyses, with Reverse transcription quantitative real-time PCR (RT&#x2012;qPCR) and Enzyme-linked immunosorbent assay (ELISA) validation, were performed to elucidate microbial, genetic and metabolic responses. Growth performance, including the specific growth rate (SGR) and weight gain rate (WGR), was concurrently assessed. RESULTS: NP exposure significantly suppressed WGR and SGR, and induced gut microbiota dysbiosis alongside and lipid metabolism disorders in S. meridionalis. Probiotic pretreatment effectively reversed these toxic effects and restored the inhibited WGR and SGR. Multiomics integration revealed that the protective effects of probiotics were mediated by a coherent "microbe-host" co-metabolism network across 3 progressive layers: (1) Microbial Remodelling: in which beneficial taxa (e.g., Bacteroides eggerthii and Cetobacterium sp.) were enriched, and the functional capacity for short-chain fatty acid (SCFA) synthesis and ethanolamine metabolism was enhanced; (2) Host Gene Regulation: in which key lipid metabolism genes (ek1, cept1, ept1, mogat2, and abcg2a) were upregulated, and lipase activity was restored; and (3) Metabolic Pathway Activation and Physiological Repair: in which the activity of the NP-suppressed Kennedy pathway was reactivated, thereby promoting phosphatidylethanolamine (PE) and phosphatidylcholine (PC) synthesis and ultimately restoring gut barrier function. These results were further were corroborated by RT&#x2012;qPCR and ELISA. CONCLUSION: This study systematically elucidated that probiotics alleviated NP toxicity by remodelling a "microbiota-host Kennedy pathway gene-metabolite (PE and PC)-growth performance" regulatory network. The key mechanism is the beneficial microbiota activating the host Kennedy pathway and restoring gut phospholipid homeostasis and barrier function. These findings provide a theoretical basis for developing targeted, lipid metabolism focused probiotic feed additives for use in sustainable aquaculture.

Probiotics↗
PubMed2025

Multi-Omics Platforms Reveal Synergistic Intestinal Toxicity in Tilapia from Acute Co-Exposure to Polystyrene Microplastics, Sulfamethoxazole, and BDE153.

Polystyrene microplastic (MP) and its co-existing contaminants may exert different toxic effects on its surrounding aquatic organisms. In order to detect the intestinal harmful responses, tilapia were subjected to exposure with 75 nm of MPs, 100 ng&#xb7;L-1 of sulfamethoxazole (SMZ), 5 ng&#xb7;L-1 of BDE153, and combinations thereof over periods of 2, 4, and 8 days. Enzymatic assays, transcriptomics, proteomics, and metabolomics were employed to evaluate intestinal histopathological effects. Results showed that significant reductions were observed in ATP, ROS, SOD, EROD, lipid metabolism-related enzymes, pro-inflammatory cytokines (TNF&#x3b1; and IL-1&#x3b2;), and apoptosis marker caspase 3 across all groups at day 8. Histological evaluation revealed diminished goblet cell density, with distinct vacuole formation in the BDE153+MPs group. KEGG pathway analysis highlighted disruptions in endocytosis, MAPK signaling, phagosome formation, and actin cytoskeleton regulation. Proteomic findings indicated notable enrichment in endocytosis (decreased sorting nexin-2; increased Si:dkey-13a21.4), MAPK/PPAR signaling, protein processing in the endoplasmic reticulum (Sec61 subunit gamma), and cytoskeletal modulation (reduced fibronectin; elevated activation peptide fragment 1), with or without SMZ and BDE153. Metabolomic profiling showed significant alterations in ABC transporters, aminoacyl-tRNA biosynthesis, protein digestion and absorption, and linoleic acid metabolism. In summary, these findings suggest that BDE153 and MPs synergistically exacerbate intestinal damage and gene/protein expression over time, while SMZ appears to exert an antagonistic, mitigating effect.

Animals↗