Flusilazole is a triazole-based fungicide that persists in various environments because of its high stability and solubility, raising concerns about its developmental and ecological impacts. Although numerous studies have reported flusilazole-induced toxicity, the specific effects and mechanisms of flusilazole-induced hepatotoxicity during development remain unclear. In this study, we examined the in vivo and in vitro toxicities in Danio rerio (zebrafish) and zebrafish-derived liver (ZFL) cells. Morphological changes in the liver and alterations in liver regeneration were evaluated using fabp10a:dsRed and fabp10a:CFP-NTR transgenic models. Flusilazole exposure was shown to deteriorate hepatic structure and regenerative capacity, with potential long-term consequences for aquatic organisms. Moreover, in ZFL cells, flusilazole treatment induced oxidative stress, mitochondrial malfunction, and disruption of calcium and iron homeostasis, leading to the induction of apoptosis and ferroptosis. Transcriptomic analysis supported these findings. Additionally, disturbances in ERK and Akt signaling indicated interference with pathways central to cell survival, growth, and tissue repair. Together, these findings establish that flusilazole exerts developmental hepatotoxic effects and highlight its potential hazards to ecosystems.

Di-ethylhexyl phthalate (DEHP) is an endocrine disruptor with established neurotoxic as well as potential neurodegenerative effects. The myelin sheath plays a crucial role in maintaining the health of the nervous system, whereas demyelination contributes to the onset of brain diseases. This study investigated the effect of DEHP on the neurological development with special reference to endoplasmic reticulum (ER) stress, inflammation, and concurrently with demyelination and cellular apoptotic development in zebrafish larvae. Results indicated that DEHP exposure can lead to demyelination through ER stress and inflammation, as evident from the decreased expression of myelin basic protein (Mbp) in both the brain and spinal cord of zebrafish larvae analyzed through immunofluorescent assay. The mRNA expression of axon marker nfl significantly increased, while tuba1a was decreased with DEHP exposure. Western blotting analysis revealed that ER stress markers such as phosphorylated inositol-requiring enzyme 1 alpha (p-Ire1α), activating transcription factor 4 (Atf4), binding immunoglobulin protein (Bip), phosphorylated e-IF2 alpha (p-eIF2α), CCAAT/enhancer-binding protein homologous protein (Chop), and inflammatory markers (nuclear factor kappa B subunit p65; Nf-κb p65), ionized calcium-binding adaptor molecule 1 (Iba1), and glial fibrillary acid protein (Gfap), were significantly upregulated on exposure to DEHP. Scototaxis, a behavioral assay, showed an altered anxiety-like behaviour in DEHP-treated larvae. Oxidative stress markers, such as superoxide dismutase (SOD), catalase, and monoamine oxidase (MAO) were also elevated. Apoptotic cells were observed in DEHP-treated zebrafish larvae in acridine orange staining. Overall, the DEHP exposure to zebrafish larvae caused myelin sheath degeneration and axonal dysfunction due to the generation of ER stress and inflammation.

The phenotype of action potentials (AP) in mammalian dorsal root ganglion (DRG) neurons is biphasic and thereby distinct from those in the CNS and spinal cord. The sensation of pain by DRG and its prevention may occur via many types of channels, receptors, and neurotransmitters; these are at least Cav, Kv, Nav, and TRP. The Cav, Kv, and Nav channels are prevailingly involved in the excitability of DRG neurons, while the TRP family enables the mechanosensitivity. The latter are the main family of channels, and thereby the list is extensive because of the presence of many distinct α subunits among them. Also, all major receptor channels are described in DRG, but purinergic ones could be considered important because of sensitization to ATP as a neurotransmitter. This work presents a comparative and detailed synthesis of the electrophysiological properties of intact DRG and isolated neurons, with an emphasis on the K channels involved in action potential generation.

Astaxanthin (AST) as a natural carotenoid exhibits potent antioxidant and anti-inflammatory capacities. This work investigated AST's protective effects against microcystin-LR (MC-LR) toxicity to zebrafish embryos. When the zebrafish embryos were exposed to a sublethal, environmentally relevant concentration of MC-LR (10 μg/L, approximately half of the LC value), AST (100 μg/L) could significantly reduce MC-LR-induced mortality by 39.8% and deformity rates by 60.0%. Furthermore, AST decreased ROS and MDA levels by 11.0% and 14.5%, respectively, and enhanced the activities of superoxide dismutase (SOD, 4.4-fold), catalase (CAT, 1.2-fold), and glutathione reductase (GR, 1.6-fold). It also ameliorated MC-LR-induced inflammatory responses, as evidenced by a 49.1% reduction in neutral red staining, a 42.0% to 42.9% improvement in host resistance, and a significant down-regulation of major cytokines (IL-1β, IL-6, IL-8, TNF-α) by 0.4 to 0.6-fold. Analysis of the transcriptome revealed that AST can inhibit the C-type lectin receptor signaling pathway and others to counteract the inflammatory and oxidative stress induced by MC-LR. Our findings confirm that AST neutralizes the toxicity of MC-LR through the mechanisms of antagonizing oxidative stress, exhibiting anti-inflammatory and immunomodulatory effects, which may pave the way for AST being used in aquaculture and environmental health.

Amitriptyline (AMI), a commonly used tricyclic antidepressant, has been identified as a significant pharmaceutical contaminant in aquatic environments. Although parental exposure of zebrafish to AMI has been found to induce changes in the development, behavior, and gene expression of their F1 offspring, it is unclear whether such adverse effects will be further extended to subsequent generations. In the current study, we explored the effects of ancestral exposure to AMI at environmentally relevant concentrations (0 and 0.8 μg/L) on the early life stages of zebrafish F2 offspring. The results showed that ancestral exposure to AMI had no significant effect on the survival and development of the zebrafish F2 offspring. However, significant hyperactivity was observed in the F2 larvae in the ancestral AMI exposure group during the dark periods of a light-dark locomotion assay. Transcription analysis revealed that ancestral exposure to AMI significantly disrupted pathways associated with xenobiotic biodegradation and metabolism, as well as the metabolism of cofactors and vitamins. Furthermore, ancestral exposure to AMI significantly decreased the level of cytochrome P450 and the activity of glutathione S-transferase within the F2 larvae, which are critical enzymes involved in xenobiotic metabolism. These findings provide valuable insights into the multigenerational effects of AMI exposure in zebrafish, emphasizing the importance of assessing the risks posed by such pollutants to fish populations.

Thiamine (vitamin B1) deficiency is causative of reproductive failures and population declines in lake trout, Atlantic salmon, and other predatory fish species. Transketolase (TKT) is the rate-limiting enzyme of the non-oxidative phase of the pentose-phosphate pathway. TKT is critical for mediating the availability of sugars to return to glycolysis and for synthesizing NADPH and R5P, which are needed to maintain the cellular oxidation state and to produce biomolecules necessary for successful growth and reproduction. TKT activity provides a measure of functional thiamine availability since it requires thiamine diphosphate (TDP) as a coenzyme. Its activity is usually analyzed via a coupled enzyme reaction, including ribose-5-phosphate (R5P) and xylulose-5-phosphate (X5P) as substrates to permit the kinetic monitoring of the depletion of exogenous NADH. We developed a simplified, cost-effective procedure for quantifying TKT activity in fish liver to probe thiamine utilization and magnesium (Mg) dependence. Unlike previous protocols, the method omits costly X5P, relying instead on endogenous enzyme activity for in situ substrate generation. In two lake trout strains, TKT-specific activity correlated with TDP concentration while maximal activity reflected enzyme abundance and holoenzyme stability. By running samples with and without Mg and over a range of TDP concentrations, the assay framework allows for distinguishing a Mg limitation from a thiamine limitation and defines apparent EC and V values. This simplified and tunable assay provides a tool for evaluation of thiamine-related metabolic resistance under dietary or environmental stress across fish populations and species.

Macrobrachium rosenbergii, the giant freshwater prawn, is an important aquaculture species cultivated worldwide. As a catadromous species, it requires brackish water for early development (larval stages) and grows optimally under low-salinity conditions. This tolerance enables production using brackish groundwater or desalination concentrate, helping reduce disposal costs. However, aquaculture systems often accumulate nitrogenous waste such as ammonia, which can negatively affect growth, survival, and health. The interactive effects of ammonia and salinity on M. rosenbergii remained understudied, particularly during juvenile stages that coincide with the transition to brackish water. Therefore, we first determined the 3, 6, 24, and 48 h median lethal concentrations (LC) of total ammonia nitrogen (TAN) across three salinities (1, 5, and 10 ppt) at pH 8.2. Toxicity increased with both salinity and exposure time, with LC values ranging from 5.6 mg/L (95 % CI: 4.9-6.3) to 42 mg/L (95 % CI: 37-48) TAN. Based on these LC values, we tested how increasing waterborne ammonia concentrations affect the routine metabolic rate (RMR) of juvenile M. rosenbergii using static intermittent respirometry. Analysis by a linear mixed-effects model revealed a significant salinity × ammonia interaction where the positive relationship between ammonia concentration and RMR became steeper at higher salinities. The model also identified a significant main effect of ammonia, with RMR increasing as ammonia concentration rose, but no significant main effect of salinity. These findings inform aquaculture management of M. rosenbergii and demonstrate the potential for sentinel respirometry systems to detect real-time water quality changes by monitoring metabolic rates.

The rotifer Brachionus sp. is of great importance for aquaculture, as the reproduction cycle under rearing conditions of many economically important species larvae depends on the use of rotifers as first live feed. Establishing a protocol that results in an improved tolerance of rotifers to environmental stressors will allow for a more stable rotifer production. The exposure to non-lethal heat shocks (NLHS) already proved to enhance the tolerance, not only to heat stress, but also to other stressors in several aquatic species, by activating the heat shock response and epigenetic mechanisms. This study aimed to determine the potential of a single NLHS to induce tolerance to different abiotic stressors in two strains of B. koreanus (MRS10 and IBA3) and to evaluate possible molecular mechanisms involved in the achievement of increased tolerance to hydrogen peroxide induced by NLHS. Cross-tolerance was achieved for both strains, namely to high salinity, cadmium chloride, and hydrogen peroxide. Scale-up tests resulted in increased tolerance to hydrogen peroxide only for MRS10. During the exposure to this substance, heat-shocked MRS10 rotifers showed an up-regulation of genes related to oxidative stress response and histone modifications, increased production of HSP70, and higher levels of total acetylation of histone H3. A single NLHS proved to induce epigenetic effects when rotifers were exposed to other stressor later in life. However, further studies should elucidate if the NLHS conditions used in this study can yield a persistent outcome, allowing the establishment of tolerant rotifer strain lines and, consequently, a more stable production.

The tire-derived antioxidant 6PPD (N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine), a ubiquitous environmental contaminant, poses significant risks to aquatic ecosystems, yet its sex-specific physiological impacts remain underexplored. This study investigated the effects of environmentally relevant 6PPD concentrations (20 μg/L) on feeding, digestion, absorption, and reproduction in adult zebrafish over 28 days. Results revealed pronounced male-specific impairments: 6PPD-exposed males exhibited reduced feeding speed and maximum food intake, alongside suppressed locomotor responses to food stimuli. Mechanistically, upregulation of intestinal cholecystokinin b (cckb) and delayed intestinal content emptying were identified as potential drivers of feeding inhibition in males. Concurrently, 6PPD induced intestinal oxidative stress in males, manifested through decreased activities of catalase (CAT) and superoxide dismutase (SOD), alongside elevated malondialdehyde (MDA) levels, and activated ferroptosis via dysregulation of critical genes (gpx4a, cybb, slc7a11, hmox1a, tfr1b and trf2). These disruptions correlated with shortened intestinal villi, goblet cell loss, and impaired nutrient absorption, leading to increased fecal output and diminished growth performance in males. In contrast, females displayed no significant structural damage to intestinal epithelium or declines in digestive and absorptive capacities. Notably, 6PPD caused no gonadal histopathological changes, hormonal dysregulation, reduced fertilization and hatching rates, nor transgenerational effects such as developmental abnormalities or locomotor deficits in offspring. This study provides the first evidence of male-selective feeding suppression and intestinal toxicity induced by 6PPD, highlighting sex-dependent vulnerability in aquatic species and underscoring the need for gender-specific risk assessments of tire-derived pollutants.

Copper (Cu), though essential as a micronutrient, can pose significant ecotoxicological risks when introduced into aquatic environments at elevated levels, primarily due to anthropogenic sources such as industrial discharge, agricultural runoff, and urban effluents. This study investigated the long-term effects of environmentally relevant copper concentrations (0, 5, 10, and 20 μg/L) on Japanese medaka (Oryzias latipes) over a six-month exposure period, focusing on reproductive toxicity, oxidative stress, immune response, and gut microbiota alterations. Histopathological analysis revealed gonadal impairments, including disrupted testicular and ovarian structures, impaired spermatogenesis, and reduced oocyte maturation. Additionally, hormonal changes revealed elevated levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and estradiol (E2), alongside reduced testosterone (T) levels, indicating interference with the hypothalamic-pituitary-gonadal (HPG) axis. Copper exposure also altered antioxidant enzyme activities, including sex-dependent modulation of superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) levels, indicating oxidative imbalance and compensatory defense responses, along with upregulation of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). Gut microbiota analysis via 16S rRNA sequencing revealed significant dysbiosis, characterized by marked reductions in alpha diversity indices and distinct beta diversity clustering. Taxonomic profiling showed a sharp decline in beneficial phyla such as Fusobacteriota, Firmicutes, and Actinobacteriota, coupled with an enrichment of potentially opportunistic Proteobacteria and shifts in Bacteroidota and Verrucomicrobiota, indicating compromised intestinal homeostasis. Collectively, these findings demonstrate that chronic exposure to copper ions induces multi-systemic toxicity in O. latipes, impairing reproductive function, provoking oxidative and inflammatory responses, and reshaping gut microbial communities in ways that may exacerbate host physiological stress.

Fish frequently face fluctuations in food availability and elevated metals levels, which can independently or interactively affect physiological functions. This study examined how nutritional status and zinc (Zn) exposure influence mitochondrial bioenergetics and redox balance in rainbow trout (Oncorhynchus mykiss). Fish were subjected to three nutritional regimes: seven-day satiation, seven-day starvation, or seven-day starvation followed by a 24-h refeeding. Liver and heart mitochondria were isolated and assessed for respiration and H₂O₂ emission during oxidation of glutamate-malate (complex I, CxI) and succinate (complex II; CxII), with and without Zn (0, 25, or 50 μM). Starvation decreased body and organ mass and suppressed CxI- and CxII-linked oxidative phosphorylation (OXPHOS), LEAK respiration, and respiratory control ratio (RCR) in both organs. Refeeding restored liver mitochondrial function but only partially recovered heart function. Zn effects were tissue-, substrate-, and concentration-dependent, with heart more sensitive than liver. In liver, low Zn mitigated starvation-induced OXPHOS suppression, while high Zn impaired respiration across all conditions. Zn elevated H₂O₂ emission in satiated liver mitochondria but reduced it in starved and refed fish. In contrast, heart mitochondria showed Zn-induced respiratory inhibition and a 4-5-fold increase in H₂O₂ emission regardless of nutritional state. Starvation and refeeding alone reduced H₂O₂ emission in heart but not liver. Succinate-supported mitochondria emitted more H₂O₂ than glutamate-malate, likely via enhanced reverse electron transport. Overall, nutritional status and Zn independently and interactively shape mitochondrial function in a tissue-specific manner, highlighting the importance of considering metabolic state in metals toxicity assessments and ecological risk evaluation.

Tributyltin (TBT) is an antiestrogenic endocrine disrupting compound used in the production of plastic, timber, and aquatic antifouling paints. Previous studies focusing on short-term effects of TBT exposure have identified immediate detrimental effects. Here, we evaluate whether a transient (24 h) exposure to TBT during development can cause persistent effects that remain after removal from treatment. Zebrafish (Danio rerio) larvae were exposed to environmentally relevant concentrations of TBT (0.04 and 0.4 μg/L) when they were either 3- or 7-days post-fertilization (dpf). After exposure, larvae were returned to recovery conditions and assessed 2-weeks, 4-weeks, or > 5 months postexposure. Exposure to 0.4 μg/L TBT at 3 dpf decreased total and distal retinal thicknesses. Adult (>5 month) photopic electroretinograms revealed physiological changes to photoreceptor a-wave and ON-bipolar cell b-wave components, with greater deficits in the 0.4 μg/L group. TBT exposure at 7 dpf significantly increased retinal inner plexiform layer thickness at 2-weeks, an effect that persisted to adulthood. Adult electroretinograms were also altered, with 0.04 μg/L TBT increasing and delaying a-wave and OFF-bipolar d-wave responses and increasing b-wave amplitude. Thus, the impact of TBT exposure depends on both concentration and exposure age, with retinal sequelae characterized by early anatomical and later physiological deficits. These data suggest that TBT exposure during critical periods of visual system development causes persistent age- and concentration-dependent deficits that are specific to the retina, revealing a previously unknown effect of this compound.

Polycyclic aromatic hydrocarbons (PAHs) are persistent organic pollutants that pose a significant risk to aquatic ecosystems. This study evaluated metabolic responses in hepatopancreas, focusing on key enzymes of glycolysis and anaerobic glycolysis in the shrimp Penaeus vannamei exposed for 24 and 96 h to phenanthrene (PHE) and naphthalene (NAP). We analyzed the expression of two hexokinase genes (HK1 and HK2), and lactate dehydrogenase (LDH1 and LDH2 subunits), total enzymatic activity of HK and LDH, and intracellular glucose and lactate. NAP significantly induced the expression of HKs and LDHs at 96 h, while PHE had no significant effect. LDH2 expression was detected only in response to NAP, suggesting that this PAH enhances anaerobic metabolism, possibly due to a higher oxygen demand for NAP detoxification. Although no significant differences were detected in the total activities of HK and LDH due to exposure to the selected PAHs, a decreasing trend was detected in HK activity under NAP treatment at 24 h. Additionally, glucose decreased over time. In contrast, lactate levels increased at 24 h in response to NAP and PHE, suggesting an early shift toward anaerobic metabolism, and then returned to initial levels by 96 h. These findings highlight the effects of PAHs on energy metabolism disruption in shrimp and provide insights into the molecular responses of aquatic invertebrates to metabolic stress induced by organic pollutants.

The widespread use of plastic products has led to the global accumulation of microplastics (MPs) and nanoplastics (NPs) in aquatic and terrestrial environments, posing significant risks to ecosystems and human health. This study investigated the neurodevelopmental toxicity of polystyrene MPs (PS-MPs, 5 μm) and NPs (PS-NPs, 60 nm) in zebrafish (Danio rerio) and explored the underlying mechanisms. Zebrafish embryos were exposed to 0.05-50 mg/L PS-MPs/PS-NPs from 2 hour post-fertilization (hpf) to 7 days post-fertilization (dpf). Morphological, behavioral, and molecular endpoints were analyzed. Exposure to polystyrene MPs and NPs (PS-MNPs) induced dose-dependent developmental malformations, including spinal curvature, pericardial edema, and abnormal body pigmentation, accompanied by increased heart rate and body length. Behavioral assays revealed reduced spontaneous tail-coiling in embryos and hyperactive swimming in larvae, particularly under light stimulation. Mechanistic studies showed PS-MNPs disrupted neurotransmitter homeostasis (reduced dopamine, acetylcholine, GABA, and serotonin levels) and altered neurodevelopment-related gene expression (e.g., mbpa, ache, gfap). Oxidative stress was evident via elevated reactive oxygen species (ROS) and upregulated antioxidant genes (sod1, cat) in PS-NP-exposed larvae. These findings demonstrate that PS-MNPs induce neurodevelopmental toxicity in zebrafish through oxidative stress and neurotransmitter system dysfunction, highlighting the potential risks of plastic pollution to aquatic organisms and human health via trophic transfer.

Ammonia is a common environmental pollutant that is extremely toxic to aquatic animals. Therefore, there is an urgent need to increase ammonia tolerance in aquaculture animals to achieve high-quality development of the industry. Three treatments were designed to examine the effects of taurine on the large-scale loach (Paramisgurnus dabryanus). These were a control group (exposed to water and injected with physiological saline), an ammonia treatment group (exposed to 30 mmol/L NHCl solution and injected with physiological saline), and a taurine treatment group (exposed to 30 mmol/L NHCl solution and injected with taurine). Immune- and ammonia metabolism-related markers were measured at 12 h, 24 h, 48 h, and 96 h after treatment. The results showed that ammonia exposure significantly increased T-SOD activity and the level of IL-1β, significantly decreased IgM, C3, and TNF-α levels, and induced significantly high expression of immune-related genes (lyz, hsp70, tlr5, and myd88) in tissues. Intraperitoneal injection of taurine mitigated ammonia-induced disturbances in plasma glucose and osmotic pressure by regulating glucose metabolism and osmotic pressure balance. The results suggest that ammonia stress causes significant immune stimulation in large-scale loaches, and that taurine could alleviate this effect. Exposure to ammonia increases the concentration of ammonia in the gut, liver, kidneys, and gills of large-scale loach, significantly increases GDH and GS activity, and upregulates the expression levels of ammonia transporter-related genes such as aqps and rh. After taurine treatment, the concentration of ammonia in the somatic tissues of large-scale loaches significantly decreased, while the expression of ammonia transporter-related genes was inhibited, and the activities of GS was further enhanced. This indicates that large-scale loach initiate glutamine synthesis and upregulate ammonia transporter proteins to cope with the stress of highly concentrated ammonia, and that taurine can promote glutamine synthesis to decrease the in vivo ammonia concentration. The results can deepen our understanding of the toxicological effects of ammonia and the mechanisms by which taurine promotes ammonia tolerance in fishes, offering a basis for taurine application in aquaculture.

Phenol is a common aquatic contaminant originating from industrial discharge, plastics, and personal care products, and is frequently detected due to its high solubility and environmental persistence. Although its acute toxicity is well documented, the effects of phenol at environmentally relevant concentrations on cellular mechanisms linked to tumor progression remain underexplored. In this study, we investigated the impact of phenol exposure (0-125 μM) on cancer-related cellular behaviors using B16F10 melanoma and LL2 lung carcinoma cells, as well as zebrafish xenograft models, which serve as an integrated aquatic toxicology platform. Phenol exposure activated extracellular signal-regulated kinase (ERK) and p38 pathways, upregulated hypoxia-inducible factor 1α (HIF-1α), increased vascular endothelial growth factor (VEGF) expression, and induced epithelial-mesenchymal transition (EMT). These molecular events collectively enhanced tumor cell migration and angiogenesis both in vitro and in vivo. Our findings provide mechanistic evidence that environmentally relevant phenol exposure can modulate conserved stress and signaling pathways associated with tumor-related phenotypes. This work underscores the importance of combining molecular biomarkers with aquatic vertebrate models to assess the ecological and toxicological risks of persistent organic pollutants such as phenol.

Diaphanosoma celebensis, a marine water flea, has gained recognition as a valuable model organism in marine ecotoxicology, ecophysiology, and epigenetics. This review highlights the significance of D. celebensis in environmental research, emphasizing its high-quality genomic and transcriptomic resources, adaptability to environmental stressors, and sensitivity to pollutants. The species' utility in studying molecular responses to contaminants such as microplastics, heavy metals, and endocrine disruptors is underscored by its ability to provide insights into detoxification pathways, stress response mechanisms, and epigenetic modifications. Diaphanosoma celebensis serves as a critical tool for advancing our understanding of the ecological impacts of pollution and the adaptive capacities of marine invertebrates. This review synthesizes existing research, explores the species' strengths as a research model, and identifies future research directions. All evidence suggests D. celebensis can complement traditional freshwater models and enhance our capacity to monitor and protect marine health.

Azamethiphos and hydrogen peroxide are active ingredients (AI) of formulations used as water-bath pesticides in Atlantic salmon aquaculture to remove ectoparasitic copepods. Despite their long-term use, unknowns and concerns are still present, particularly regarding the toxicity towards non-target commercially and ecologically important species in Atlantic Canada, and potential differences in toxicity between the AI and the formulated product. Here, we tested the acute effects of azamethiphos and hydrogen peroxide on five marine species. Hazard data (half maximal effective and lethal concentrations, respectively EC50 and LC50) were determined for 10 endpoints, assessed at various timepoints, during the exposure of Stage I larval American lobster Homarus americanus, green sea urchin Strongylocentrotus droebachiensis gametes, haemocytes and adults of blue mussel Mytilus edulis, common periwinkle snail Littorina littorea, and copepod Acartia tonsa. To investigate whether formulations had the same effect as the AI, for azamethiphos, both the AI and the formulation (Salmosan® Vet) were tested. For hydrogen peroxide, potential differences in the toxicity of three formulations (purchased solutions 50 %, 35 %, and 3 %) were compared. Results suggest no differences between the azamethiphos and Salmosan® Vet, with similar L/EC50 values. Little differences were found among the three hydrogen peroxide formulations. For azamethiphos, the most sensitive species was the American lobster, followed by sea urchin, whereas for hydrogen peroxide, sea urchin was the most sensitive, followed by A. tonsa. L. littorea was the least sensitive species tested. Overall, results showed that all the endpoints were greater than the Environmental Quality Standard previously determined for the two compounds.

The inflammatory response is a core protective physiological process against stimuli like infection or injury, and can be initiated by autoimmune disorders. It is primarily characterized by neutrophil-dominated leukocytosis and may lead to multiple organ dysfunction in severe cases. Environmental factors play an important role in the inflammatory response. Rare earth elements are not essential elements for living organisms. However, owing to large-scale mining and use, their concentrations in the environment have increased. Thus, rare earth elements are now considered emerging environmental pollutants, and the risks that rare earth elements pose to human health need further investigation. In this study, zebrafish were used as experimental animals, and zebrafish embryos were exposed to the different concentrations of lanthanum chloride (0, 5, 15, and 25 mg/L) to analyze its effect on embryo development and immune system. The number and distribution of zebrafish neutrophils as well as changes in oxidative stress and the expression of genes related to inflammation were analyzed. The results indicated that lanthanum chloride exposure reduced the heart rate, shortened the body length, and increased the yolk area of zebrafish embryos. In addition, exposure to lanthanum chloride caused the diffusion of neutrophils, leading to inflammation in zebrafish. Concurrently, the exposure led to the accumulation of reactive oxygen species in zebrafish, which subsequently resulted in the upregulation of malondialdehyde, catalase, and superoxide dismutase levels. Further experiments revealed that exposure to lanthanum chloride led to the upregulation of several inflammation-related genes, such as il-6, il-8, il-10, and cxcl-c1c, as well as certain TLR4/NF-κB signaling-related genes, including tlr4, myd88, nf-κb p65, il-1β, and tnf-α. The TLR4/NF-κB signaling pathway inhibitor andrographolide can alleviate the inflammatory response induced by lanthanum chloride exposure. In conclusion, lanthanum chloride induced inflammation in zebrafish by activating the TLR4/NF-κB signaling pathway. The study results can provide a reference for evaluating the health risks of rare earth elements in humans.

Ammonia (NH) is a widespread environmental pollutant with significant ecological and physiological impacts on aquatic organisms. While ammonia plays a key role in nitrogen cycling, excessive amounts disrupt homeostasis and cause toxic effects in various species. Its toxicity is influenced by environmental conditions such as pH, temperature, and salinity, with un-ionized ammonia being especially harmful due to its high membrane permeability. High ammonia levels impair ion balance, disturb nitrogen metabolism, trigger oxidative stress, affect neurophysiological functions at the intracellular level. Furthermore, ammonia can damage vital tissues, eliciting species-specific differential responses (fish, invertebrates, and amphibians), and impair survival, development, reproductive ability, and even movement. In addition, ammonia can alter the microorganisms' composition and metabolic functions. These findings highlight a complex relationship between microbial changes and host health conditions. Therefore, this review can aid in understanding the profound toxicity of ammonia, which affects both organisms and microorganisms, while emphasizing the need for monitoring and management strategies. As climate change intensifies environmental variability, a more profound understanding of ammonia toxicity is essential for protecting aquatic biodiversity and maintaining ecosystem stability.

In vivo and in vitro experiments were conducted to test whether copper (Cu) uptake occurs via sodium (Na) transporters in the gills of Callinectes sapidus acclimated to dilute seawater (2 ppt), a condition in which the species hyper-osmoregulates. Specific inhibitors targeting Na/H exchangers (amiloride, 100 μM) and Na, K, 2 Cl cotransporters (NKCC) (furosemide, 120 μM) were used. In vivo, adult crabs were exposed for 6 h to 1 μM radiolabeled Cu (Cu) in artificial seawater or Na-free media, both at 2 ppt. In vitro, isolated posterior gills were perfused with hemolymph-like saline and exposed to external solutions containing Cu. Na uptake was first validated using radiolabeled Na (Na) and the inhibitors: in vivo Na uptake was significantly reduced by amiloride (68 %) and furosemide (23 %) and in vitro amiloride reduced Na uptake by 40 %. Cu uptake, however, remained unaffected by the Na presence/absence or by the inhibitors in both experimental approaches. The Cu accumulated mainly in the carapace (49 %) and posterior gills (22 %), regardless of Na availability. The findings clearly demonstrate that Cu uptake, irrespective of the uptake pathway, proceeds independently of Na.