Community rescue enables ecological communities to persist under otherwise lethal environmental stress through adaptive changes. The present study addresses what community attributes may predict the chance of rescue, and the ecological consequences associated with community rescue. Replicate aquatic microcosms were set up from each of 20 base planktonic communities, and were exposed to a gradient of concentrations of an herbicide. Planktonic respiration rate was measured as a surrogate of community activity, to infer the potential of community rescue. We found that the rescue potential depended on planktonic taxonomical composition but not diversity per se. We then studied in detail planktonic communities that rescued from a specific high concentration of herbicide pollution. Community rescue was accompanied with multiple ecological costs, including reduced taxonomical diversity and primary productivity, as well as simplified planktonic interaction networks. A shift from producer-dominated toward decomposer-dominated taxa was observed; specifically, certain heterotrophic bacteria and fungi became more abundant at the expense of microalgae. A number of taxa highly resistant to glyphosate were identified. Our results highlight that community rescue under severe herbicide pollution may be associated with unwanted ecological costs, and studies of this kind may help to search for microbial taxa capable of pollutant biodegradation.

The presence of prednisone in aquatic ecosystems poses risks to aquatic organisms. However, the impact of prednisone on the intestinal microbiota of aquatic organisms is still poorly understood. In the present study, zebrafish (Danio rerio) were exposed to environmentally realistic concentrations of prednisone (5.0, 50.0, and 500.0 ng/L) over 60 days. The effects of prednisone on zebrafish intestines were thoroughly evaluated using multidimensional approaches, combining histopathological observations, transcriptomic analysis, and 16S rRNA sequencing. The studies we have performed showed that prednisone exposure induced significant intestinal tissue damage, characterized by a reduction in intestinal muscularis thickness and decreased density of goblet cells. These pathological alterations might contribute to the inhibited growth in prednisone-treated zebrafish. Transcriptomic analysis revealed that prednisone exposure modulated pathways associated with starch and sucrose metabolism. Furthermore, 16S rRNA sequencing indicated that prednisone significantly altered the composition and function of gastrointestinal microbiota. In conclusion, the current study reveals the mechanisms driving prednisone-induced intestinal damage, reveals the health effects of prednisone exposure on aquatic organisms, while supplying core perspectives on the molecular basis of intestinal injury and corresponding ecotoxic threats.

Per- and polyfluoroalkyl substances (PFASs) have raised global concern due to their persistence and potential long-term ecological effects, prompting the use of alternatives such as perfluoroether sulfonates (PFESAs). However, ecotoxicological data for PFESA compounds, particularly regarding long-term impacts, remain scarce. This study systematically evaluated the acute, chronic, and multigenerational toxicity of potassium perfluoro(4-methyl-3,6-dioxaoctane) sulfonate (PFMDS) using Daphnia magna as a freshwater model. Acute toxicity testing revealed relatively low toxicity, accompanied by variable reactive oxygen species (ROS) responses. In contrast, chronic and continuous multigenerational exposure (F0-F2) affected multiple life-history traits, including somatic growth, reproductive timing, and offspring production. In F0, exposure at 15.0-20.0 mg/L significantly reduced fecundity and inhibited growth. Reproductive output also showed a decreasing tendency in F2 at 10.0 mg/L, while molting frequency remained largely unchanged despite growth impairment. Transcriptional analysis revealed significant downregulation of vitellogenin-related genes in F0 adults and juvenile hormone esterase in both F0 and F2 adults, suggesting alterations in endocrine-related regulatory processes. Together, these findings demonstrate that chronic PFMDS exposure can affect multiple life-history and molecular endpoints across successive generations, highlighting the importance of multigenerational approaches for identifying the potential hazards of emerging PFESA alternatives.

Climate-driven warming and pharmaceutical residues, including nonsteroidal anti-inflammatory drugs (NSAIDs), are increasingly concurrent in wastewater-impacted freshwater systems, although their combined physiological effects in fish remain insufficiently characterized. This study evaluated hematological, serum biochemical, hepatic oxidative, immune, cortisol, neurotoxic, and reproductive responses in Nile tilapia (Oreochromis niloticus) following 14- day exposure to control conditions (27 °C), thermal stress (35 °C), diclofenac (DCF, 0.5 mg/L nominal), or their combination. Co- exposure produced the most pronounced changes, and two-way ANOVA indicated predominantly additive effects of heat stress and DCF. Red blood cell counts (0.94 vs 1.30 × 10[6]/µl), hemoglobin (8.3 vs 9.1 g/dL), and hematocrit (15.4 vs 17.1%) were significantly reduced, whereas leukocyte (128.5 vs 116.5 × 10[3]/µl) and thrombocyte (294.8 vs 285.3 × 10[3]/µl) counts increased significantly. Serum glucose (165.8 vs 95.4 mg/dL), total protein, aspartate transaminase, alanine transaminase, and alkaline phosphatase levels increased significantly, indicating hepatic strain. Hepatic superoxide dismutase activity decreased significantly to 19.5 U/mg protein, while malondialdehyde increased significantly to 29.8 nmol/mg protein. Respiratory burst, myeloperoxidase, immunoglobulin M, and tumour necrosis factor-α levels increased significantly, while cortisol rose to 340% of control. Gonadotropin-releasing hormone, vitellogenin, and acetylcholinesterase activity decreased significantly to 45%, 30%, and 35% of control, respectively. A significant more-than-additive temperature × DCF interaction was observed only for IgM, TNF-α, and cortisol, suggesting that warming exacerbated immune and cortisol-related stress responses to DCF. These findings raise concern for subtropical freshwaters receiving inadequately treated pharmaceutical effluent and highlighting the need to incorporate warming into ecological risk assessments of pharmaceuticals.

Pyrethroid pesticides, widely applied in agriculture and public health, frequently contaminate aquatic ecosystems and pose substantial risks to teleost fish due to their lipophilicity and bioaccumulation potential. This review synthesizes recent advances in understanding pyrethroid-induced multisystem toxicity in teleosts, covering neurotoxicity via voltage-gated sodium channel disruption, cardiovascular impairment, reproductive and endocrine disruption, immunotoxicity, and metabolic dysfunction. Oxidative stress emerges as a common mediator across these effects. Toxicity is modulated by abiotic factors (temperature, salinity, sediment organic matter), biotic factors (species, developmental stage, sex), and co-exposure with other contaminants. Detoxification strategies include physical/chemical remediation, microbial biodegradation, and nutritional or immunomodulatory interventions that enhance endogenous antioxidant defenses. Despite progress, critical knowledge gaps remain regarding chronic low-level exposure, metabolite toxicity, transgenerational epigenetic effects, and climate-change interactions. Future research should integrate molecular, organismal, and environmental data to develop predictive risk assessment frameworks and field-applicable mitigation measures, ensuring sustainable pyrethroid use while safeguarding fish health and aquatic biodiversity.

Climate warming and nutrient imbalance in coastal areas are considered key drivers of harmful algal blooms formation, yet their influence on the toxicity of these harmful organisms remains poorly understood. This study investigated the lethal and sub-lethal effects of the toxin-producing dinoflagellate A. carterae on the brine shrimp Artemia franciscana using different exposure matrices (live cells, cell lysates and cell-free supernatants), two temperature regimes (19 and 24 °C), and nitrogen-enriched conditions. Mortality assays revealed clear dose-response relationships, with cell lysates being markedly more toxic than live cells, indicating that most bioactive compounds are intracellular. In contrast, exposure to live cells caused significant sub-lethal effects, including a dose-dependent reduction in swimming activity, with behavioural impairment occurring at concentrations considerably below lethal thresholds. A binary exposure experiment demonstrated that elevated temperature (24 °C) significantly amplified sub-lethal toxicity of A. carterae, resulting in reduced motility, and increased lipid peroxidation and DNA damage on A. franciscana. Similar responses were observed when A. carterae was grown under nitrogen-enriched conditions. LC-HRMS analysis revealed the presence of amphidinol-related compounds and cytotoxic macrolides, supporting a membrane-active mode of action underlying the observed effects. Overall, these findings demonstrate that A. carterae induces significant sub-lethal effects in a model organism A. franciscana at cell densities comparable to those reported during A. carterae proliferations, and suggest that climate warming combined with nitrogen-enriched conditions may increase the hazard potential of this dinoflagellate under future coastal conditions. These results highlight the importance of incorporating sub-lethal endpoints and multi-stressor scenarios into hazard and risk assessment of harmful algal blooms under future coastal conditions.

Cadmium (Cd) and micro/nanoplastics frequently coexist in aquatic environments, yet how plastic particles modulate heavy metal toxicity in microalgae remains poorly understood. Here, the freshwater microalga Chlamydomonas reinhardtii was employed to investigate the interaction between polystyrene nanoplastics (PS-NPs) and Cd at physiological, biochemical, ultrastructural, and molecular levels. Among the tested particle sizes, 500 nm PS-NPs exhibited the strongest observed growth inhibition under Cd co-exposure and were therefore selected for subsequent mechanistic investigation. Cd-NPs co-exposure caused pronounced growth inhibition, pigment disturbance, oxidative damage, and chloroplast ultrastructural disruption. Notably, EDTA-resistant cellular Cd accumulation was lower under simultaneous Cd-NPs co-exposure than under Cd exposure alone, indicating that the greater biological impairment observed under co-exposure was not attributable to an increased EDTA-resistant cellular Cd burden. Integrated transcriptomic and metabolomic analyses revealed coordinated disturbances in metal/redox homeostasis, membrane lipid remodeling, pigment metabolism, nitrogen redistribution, and central carbon metabolism. These findings support a model in which NPs modify Cd-associated biological responses without increasing EDTA-resistant cellular Cd retention. This study provides new insights into how nanoplastics may modify metal toxicity outcomes in freshwater microalgae and highlights the potential importance of incorporating organism-level stress responsiveness into ecological risk assessment of emerging aquatic contaminants.

The accumulation of microorganisms and macroorganisms on aquatic surfaces poses economic and ecological challenges, particularly in maritime transport. Traditional antifouling methods, such as biocidal coatings containing toxic compounds like tributyltin (TBT) and copper, are effective but harmful to the environment. This study investigates the ecotoxicological hazards of two nature-inspired compounds (NIAFs), previously investigated for antifouling applications: the polyphenol GBA and the dihydrochalcone DH345, derived from polyphenols and flavonoids, respectively. The ecotoxicity of these compounds was evaluated using standardized assays with various species, including embryos of Danio rerio (zebrafish) (OECD TG 236), the algae Raphidocelis subcapitata (OECD TG 201), and the bacteria Aliivibrio fischeri (ISO 11348-2), along with nuclear receptor transactivation assays in Mytilus galloprovincialis (Mediterranean mussel). Gallic acid derivative GBA and 24h-transformation products showed low toxicity in zebrafish embryos, while dihydrochalcone DH345 inflicted developmental toxicity in zebrafish at 1 mg/L and above. Comparatively, tralopyril, a commercial biocide, exhibited significant toxicity at lower concentrations. Transcriptomic analysis of zebrafish embryos treated with GBA revealed selective gene modulation related to stress response, ion transport, and protein synthesis. Both GBA and DH345 were shown to inhibit algae growth at 0.1 mg/L. Aliivibrio fischeri assay showed no toxic effects for any of the tested compounds. Nuclear receptor transactivation assays conducted with GBA revealed no activation of PPAR (Peroxisome Proliferator-Activated Receptor) or PXR (Pregnane X Receptor) receptors. These findings suggest that GBA and DH345 may represent potential antifouling candidates with lower toxicity than tralopyril, under the tested conditions. However, further research is needed to evaluate their potential long-term ecological impacts, particularly chronic toxicity across various organisms, and environmental risk. This study advances the pursuit of sustainable antifouling solutions that prioritize environmental protection.

Prometryn, a triazine herbicide detected in near-shore waters, sorbs strongly to and persists in sediments, yet its toxicity to marine benthic organisms remains poorly characterised. We assessed acute (96-h, waterborne) and chronic (28-d, spiked-sediment microcosm) toxicity to the Manila clam (Ruditapes philippinarum), the nereid (Perinereis aibuhitensis) and the ghost shrimp (Callianassa japonica) using procedures adapted from OECD and U.S. EPA guidance. Experimental toxicity endpoints are based on nominal concentrations because exposure concentrations were not verified throughout the tests. Effects may therefore occur at actual concentrations below the nominal effect concentrations reported here. The 96-h LC50 values were 25.3, 11.8 and 2.40 mg/L and the 28-d LC50 values were 8.67, 3.51 and 1.42 mg/kg dry weight, respectively. Growth responses occurred together with substantial mortality at the lowest sediment concentrations tested for the nereid and ghost shrimp, so a consistent ordering of growth and survival sensitivity could not be established across species. An exploratory acute-data species sensitivity distribution for 21 marine species yielded an HC5 of 2.06 µg/L, with primary producers more sensitive than the animals tested. Screening quotients reached 0.31 for marine or coastal water and 0.064 for marine sediment, whereas fresh or estuarine sediment reached 1.2 and a freshwater agricultural drainage canal 2.1. On the marine data alone, therefore, no quotient approaches 1; but the only marine sediment survey available covers nine stations in a single bay, and the sediment benchmark itself rests on an extrapolated ghost-shrimp growth EC10. In both settings, the margin between the most sensitive laboratory threshold and the highest reported concentration was several-fold narrower in sediment than in the water column: about 1000-fold versus about 3800-fold for marine observations, and about 50-fold versus about 550-fold once river-estuary and freshwater observations are included. Sediment therefore requires explicit, compartment-specific treatment in the risk assessment of prometryn.

Microbial biofilms respond to environmental stress and drive key biogeochemical processes in streams, underpinning ecosystem services such as toxicant removal, carbon fixation, and nutrient cycling. 1H-benzotriazole (B1H) is a ubiquitous emerging pollutant with known effects on microorganisms, plants and animals, that frequently co-occurs with nutrient enrichment in effluent-impacted freshwaters. Using fluvial microcosms, we evaluated the effects of B1H below reported toxicity thresholds (nominal: 200µg/L; measured 175±12µg/L, mean±SD) on epilithic biofilm structure and functioning under dynamic fish-mediated nutrient enrichment, using mosquitofish (Gambusia holbrooki) as contaminant recipients and nutrient sources. Structural responses were limited, with B1H increasing protein content in the extracellular polymeric substance (EPS) matrix but producing no significant effects on biomass-related endpoints. In contrast, several functional processes were affected by B1H exposure. B1H particularly reduced phosphorus uptake and biomass-specific community metabolism, indicating lower functional efficiency of epilithic biofilms. Nitrification and heterotrophic carbon utilisation effects were found after prolonged exposure. Progressive fish-mediated ammonium enrichment and phosphorus depletion generated severe stoichiometric imbalance in all treatments that also interacted with B1H exposure to shape biofilm responses. By week 3, exposed and unexposed biofilms converged through partial recovery of some responses in B1H-exposed biofilms, together with declining functional performance in unexposed biofilms under nutrient imbalance. Overall, our findings indicate that contaminant effects on freshwater biofilms depend on the ecological context. B1H illustrates that contaminants can modify freshwater ecosystem functioning through interacting direct and indirect pathways even at concentrations below standard toxicity thresholds, highlighting the importance of incorporating ecological interactions into freshwater ecological risk assessment.

River-dominated estuaries are particularly vulnerable to mercury (Hg) pollution, yet field evidence on how the large estuarine gradients modulate the spatial heterogeneity of Hg distribution and bioaccumulation in zooplankton remains limited. Based on a comprehensive field investigation along a transect from the Yangtze River estuary (YRE) to the East China Sea (ECS) inner shelf, this study reveals distinct spatial patterns of total Hg (THg, mainly as inorganic Hg) and methylmercury (MeHg) distribution in water columns and zooplankton bioaccumulation. Dissolved THg in surface and bottom waters fluctuated along the transect, whereas dissolved MeHg and the proportion of MeHg to THg (%MeHg) were notably elevated within the estuarine turbidity maximum zone. Particulate THg and partitioning coefficients of THg decreased seaward, mainly driven by salinity-induced desorption. THg concentrations were higher in small-sized zooplankton owing to greater inorganic Hg adsorption, and decreased at marine sites due to salinity-induced inhibition on Hg bioavailability via speciation modulation. Conversely, MeHg concentrations were higher in larger zooplankton due to biomagnification, and MeHg bioaccumulation was elevated within the estuarine mixing zone, likely driven by site-specific MeHg production and dietary shifts toward bacterial food sources as evidenced by fatty acid biomarkers. Our findings demonstrate contrasting biogeochemical controls on the fate and ecological risks of inorganic Hg versus MeHg, providing crucial insights for Hg pollution risk assessment in large river-dominated estuarine systems.

Endocrine disruptors (EDs) are widely distributed in terrestrial and aquatic ecosystemsand are increasingly recognized for their potential impacts on organism health. Exposure to EDs is known to affect endocrine systems, such as the thyroid hormone system (THS), but can also manipulate the immune system (IS) of organisms. This study aimed to investigate the potential impact of the ED sodium fluoride (NaF) on the THS and pathogen resistance in rainbow trout exposed for seven months to 1.5 or 5 mg/L of fluoride (F[-]). Viral resistance was assessed by subjecting the fish to an infectious challenge with the infectious hematopoietic necrosis virus (IHNV). Mortality was monitored daily for six weeks following infection. Exposure to sodium fluoride (NaF), particularly at 5 mg F[-]/L, significantly increased the susceptibility of juvenile fish to viral infections, nearly doubling cumulative mortality rates. While early viral replication was not affected, NaF caused lasting changes to cellular immunity, including a reduction in circulating immune cells, disrupted leucocyte profiles and an intensified inflammatory response. The link to thyroid disruption could be drawn by showing that NaF induced temporary disruption of thyroid function (T3 and T4 concentrations) during infection and caused persistent structural changes in the thyroid gland, indicating a lasting physiological vulnerability even after hormonal levels appeared to recover.

Glyphosate is the most widely used herbicide worldwide and impacts non-target aquatic organisms through leaching processes. Previous studies have shown that this pesticide induces oxidative stress, however, the mechanisms responsible for mitigating ROS production and the associated cellular damage remain poorly understood. Therefore, the aim of this study was to examine the effects of Roundup® on the gene expression of uncoupling proteins (UCP2 and UCP3), its impact on ROS production, as well as the involvement of the Nrf2-ARE pathway in these processes. To this end, hepatocyte-like cells (ZF-L cell line) were exposed to three concentrations of Roundup (65 μg L[-1], 650 μg L[-1], and 6500 μg L[-1]), along with a control group, for 24 and 48 h. The results indicate that exposure led to a significant increase in ROS levels only at the highest concentration after 24 h, with no sustained effect observed at 48 h. This result is consistent with the data observed for the Nrf2 and ucp3 genes, whose expression increased only after 24 h. Additionally, the ARE sequence was identified in this study in the promoter regions of the Nrf2 and ucp3 gene. Significant oxidative DNA damage was observed at the highest concentration after 24 h, and damage remained elevated after 48 h compared to the control. These findings indicate that Roundup elevates ROS levels, with this effect being attenuated after 48 h, possibly as a result of Nrf2 and ucp3 activation. However, DNA damage persisted after 48 h, even when ROS levels and gene expression no longer differed from the control.

The ocean is increasingly exposed to multiple stressors, including rising temperatures and metal pollution. Zooplankton are central components of the marine food web and understanding lethal responses and underpinning molecular mechanisms across species from different habitats is essential for predicting ecosystem resilience. This study compares two zooplankton species from an Arctic fjord, the near surface-dwelling Acartia longiremis and the lipid-rich, deeper-dwelling Calanus finmarchicus, for their molecular responses to acute and sub-acute temperature and copper (Cu) stress. Endpoints were mortality, DNA damage measured with the fast micromethod assay, and expression of selected genes. Elevated temperature (11 °C) and Cu (20 µg/L), separately and in combination, resulted in species-specific responses. The individual stressors caused greater mortality in A. longiremis than in C. finmarchicus. Significant temperature-induced DNA damage was detected in C. finmarchicus but not A. longiremis. Genotoxicity of the combined stress probably reflects DNA strand breaks and cross-links, and transcriptomic changes indicated oxidative stress and impaired DNA defence and repair mechanisms. A. longiremis was more sensitive to both Cu and temperature at acute levels, while C. finmarchicus was more susceptible to sublethal genotoxic effects. These findings demonstrate that zooplankton with distinct habitat preferences within the same Arctic ecosystem can exhibit different stress sensitivities, response patterns, and defence mechanisms. Accounting for species-specific variation is therefore essential when predicting ecosystem responses to climate change and pollution.

The continuous expansion of the pharmaceutical sector has intensified aquatic contamination, as persistent active compounds enter water bodies through urban, industrial, and agricultural runoff. Among these contaminants, sulfamethoxazole (SMX)-a widely used sulphonamide antibiotic-raises ecological concerns due to its persistence and potential for bioaccumulation. To evaluate its ecotoxicological risks, this study conducted an integrated assessment combining biodegradability assays, multi-trophic acute toxicity screening, and tissue-specific sublethal biomarker analyses across the trophic chain: microalgae (Selenastrum capricornutum), crustaceans (Daphnia magna and Heterocypris incongruens), and fish (Cyprinus carpio). Although SMX exhibited moderate biodegradability, acute exposure assays revealed strong species-specific sensitivities. Microalgae proved particularly susceptible, exhibiting an EC50 of 24.77 ± 6.43 mg/L, whereas no acute mortality was observed in crustaceans or fish at concentrations up to 100 mg/L. However, a 14-day sublethal exposure of Cyprinus carpio to 10 µg/L and 100 µg/L demonstrated that the absence of acute lethality does not equal biological safety. While hepatic and gonadal indices remained unaffected, SMX triggered marked metabolic disruption. The biochemical assays across the gills, intestine, and liver showed a significant, dose-dependent modulation of key antioxidant enzymes-superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione S-transferase-alongside altered transaminase activity. By linking degradation potential with multi-trophic responses and organ-specific enzymatic profiles, this work demonstrates that SMX exposure can induce biochemical stress without visible physiological damage. These findings emphasise that assessing pharmaceutical contamination in receiving surface waters requires sensitive tissue-level biomarkers alongside traditional lethality metrics to predict cumulative ecological risks accurately.