Nanoplastics and fluorides are widespread environmental pollutants, but their combined exposure risks to aquatic organisms and humans remain unclear. Studying their combined effect of inducing toxicity on the gut-liver axis at environmentally relevant concentrations is critical. Using zebrafish, this study evaluated toxic effects and mechanisms of single/combined exposure to 0.1 mg/L nanoplastics (NPs) and 15 mg/L sodium fluoride (NaF). Integrating network toxicology and in vivo validation, combined exposure significantly disrupted intestinal structure, increased permeability, and disturbed microbiota balance. Gut microbiota dysbiosis mediated hepatic lipid metabolism disorders via the gut-liver axis by activating the TLR4/NF-κB pathway, inducing liver inflammation, oxidative stress, and hepatocyte apoptosis. The observed toxic effects are consistent with gut-liver axis homeostasis disruption, though definitive causal links have not been established. This reveals their combined effect of inducing liver injury by interfering with gut-liver axis homeostasis, providing a theoretical basis for assessing ecological risks of compound pollutants and scientific references for pollution management and aquatic ecological protection.
{"title":"Combined toxicity of nanoplastics and sodium fluoride to zebrafish liver: Impact on gut-liver axis homeostasis and lipid metabolism","authors":"Zizheng Wang , Boran Zhou , Yingxue Zhang, Yufei Cao, Yiqiang Zhang, Xu Han, Yu Wang, Hongjing Zhao","doi":"10.1016/j.aquatox.2025.107682","DOIUrl":"10.1016/j.aquatox.2025.107682","url":null,"abstract":"<div><div>Nanoplastics and fluorides are widespread environmental pollutants, but their combined exposure risks to aquatic organisms and humans remain unclear. Studying their combined effect of inducing toxicity on the gut-liver axis at environmentally relevant concentrations is critical. Using zebrafish, this study evaluated toxic effects and mechanisms of single/combined exposure to 0.1 mg/L nanoplastics (NPs) and 15 mg/L sodium fluoride (NaF). Integrating network toxicology and in vivo validation, combined exposure significantly disrupted intestinal structure, increased permeability, and disturbed microbiota balance. Gut microbiota dysbiosis mediated hepatic lipid metabolism disorders via the gut-liver axis by activating the TLR4/NF-κB pathway, inducing liver inflammation, oxidative stress, and hepatocyte apoptosis. The observed toxic effects are consistent with gut-liver axis homeostasis disruption, though definitive causal links have not been established. This reveals their combined effect of inducing liver injury by interfering with gut-liver axis homeostasis, providing a theoretical basis for assessing ecological risks of compound pollutants and scientific references for pollution management and aquatic ecological protection.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107682"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145731136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-02DOI: 10.1016/j.aquatox.2026.107705
Xiaochen Wang , Kaiyu Fu , Jianghuan Hua , Mingyang Li , Lingzhi Tan , Lihua Yang , Jian Han , Weimin Xie , Bingsheng Zhou
Decabromodiphenyl ethane (DBDPE), a novel brominated flame retardant, has been widely detected in various environmental media and exhibits significant bioaccumulation potential. This study first analyzed the distribution characteristics of DBDPE in zebrafish tissues using a toxicokinetic model. The results revealed that DBDPE preferentially accumulated in the brain, with the concentration order being brain > liver > gonads, indicating a potential neurotoxic risk. Further research demonstrated that zebrafish chronically exposed to environmentally relevant concentrations of DBDPE exhibited abnormal social behaviors. Molecular analysis indicated that this neurobehavioral toxicity may be related to the disruption of neurotransmitter homeostasis and the upregulation of gene expression in the central nervous system induced by DBDPE. Notably, female zebrafish were found to be more sensitive to the neurotoxic effects of DBDPE. These findings not only clarify the tissue-specific accumulation characteristics of DBDPE but also reveal its sex-dependent neurotoxic differences, thereby providing important scientific evidence for the ecological risk assessment of this pollutant.
{"title":"Tissue uptake, distribution, elimination and neurotoxicity of decabromodiphenyl ethane (DBDPE) in adult zebrafish (Danio Rerio)","authors":"Xiaochen Wang , Kaiyu Fu , Jianghuan Hua , Mingyang Li , Lingzhi Tan , Lihua Yang , Jian Han , Weimin Xie , Bingsheng Zhou","doi":"10.1016/j.aquatox.2026.107705","DOIUrl":"10.1016/j.aquatox.2026.107705","url":null,"abstract":"<div><div>Decabromodiphenyl ethane (DBDPE), a novel brominated flame retardant, has been widely detected in various environmental media and exhibits significant bioaccumulation potential. This study first analyzed the distribution characteristics of DBDPE in zebrafish tissues using a toxicokinetic model. The results revealed that DBDPE preferentially accumulated in the brain, with the concentration order being brain > liver > gonads, indicating a potential neurotoxic risk. Further research demonstrated that zebrafish chronically exposed to environmentally relevant concentrations of DBDPE exhibited abnormal social behaviors. Molecular analysis indicated that this neurobehavioral toxicity may be related to the disruption of neurotransmitter homeostasis and the upregulation of gene expression in the central nervous system induced by DBDPE. Notably, female zebrafish were found to be more sensitive to the neurotoxic effects of DBDPE. These findings not only clarify the tissue-specific accumulation characteristics of DBDPE but also reveal its sex-dependent neurotoxic differences, thereby providing important scientific evidence for the ecological risk assessment of this pollutant.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107705"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-15DOI: 10.1016/j.aquatox.2026.107721
Dissanayakage Dilshan Sampath Dissanayaka , Fazel Abdolahpur Monikh , Jukka Kekäläinen , Hannu Huuskonen , Lan Dupuis , Matti Janhunen , Jussi VK Kukkonen , Wujun Xu , Vesa-Pekka Lehto , Raine Kortet
Polystyrene, a commonly used plastic, can have significant impacts on natural ecosystems where it accumulates via various ways. While the ecotoxicological effects of nanoparticles on freshwater fish are increasingly understood, charge-dependent toxicity has remained virtually unstudied. Here, we explored the effects of positively and negatively charged polystyrene nanoparticles (250 nm) on sperm quality and early embryo mortality in European whitefish, Coregonus lavaretus. Gametes were exposed to both positively and negatively charged nanoparticles during sperm activation and for three minutes after fertilization (medium concentrations for sperm motility: 0.1, 1 and 10 mg/L, and for embryo mortality, 0.1 and 1 mg/L). The motility parameters (curvilinear velocity, straight line velocity, straightness, linearity) and longevity of activated sperm were analysed by computer-assisted sperm analysis. The early mortality was studied in two family-based settings: 1) a full-factorial mating design of five males × three females, where embryos were incubated in a stable environment, taking into account parental effects in addition to possible PS-NPs induced toxicity, and 2) a single-pair mating design with five full-sib families incubated in a stressful environment (variable turbulence and oxygen conditions). There were no significant differences between the treatments in any of the sperm motility parameters or sperm longevity. In both incubation settings, the highest early embryo mortality was recorded in a group exposed to positively charged nanoparticles. However, the difference was statistically significant only in the stressful environment, where concentration-dependent toxicity of nanoparticles was observed. The present study suggests possible concentration-dependent toxicity effects of PS-NPs on early embryo mortality in whitefish. This study also emphasizes the significance of different incubation conditions, as possible ecotoxicological effects may sometimes be observed only in a stressful environment.
{"title":"Ecotoxicological effects of differently charged polystyrene nanoparticles on sperm motility and early embryo mortality in European whitefish","authors":"Dissanayakage Dilshan Sampath Dissanayaka , Fazel Abdolahpur Monikh , Jukka Kekäläinen , Hannu Huuskonen , Lan Dupuis , Matti Janhunen , Jussi VK Kukkonen , Wujun Xu , Vesa-Pekka Lehto , Raine Kortet","doi":"10.1016/j.aquatox.2026.107721","DOIUrl":"10.1016/j.aquatox.2026.107721","url":null,"abstract":"<div><div>Polystyrene, a commonly used plastic, can have significant impacts on natural ecosystems where it accumulates via various ways. While the ecotoxicological effects of nanoparticles on freshwater fish are increasingly understood, charge-dependent toxicity has remained virtually unstudied. Here, we explored the effects of positively and negatively charged polystyrene nanoparticles (250 nm) on sperm quality and early embryo mortality in European whitefish, <em>Coregonus lavaretus</em>. Gametes were exposed to both positively and negatively charged nanoparticles during sperm activation and for three minutes after fertilization (medium concentrations for sperm motility: 0.1, 1 and 10 mg/L, and for embryo mortality, 0.1 and 1 mg/L). The motility parameters (curvilinear velocity, straight line velocity, straightness, linearity) and longevity of activated sperm were analysed by computer-assisted sperm analysis. The early mortality was studied in two family-based settings: 1) a full-factorial mating design of five males × three females, where embryos were incubated in a stable environment, taking into account parental effects in addition to possible PS-NPs induced toxicity, and 2) a single-pair mating design with five full-sib families incubated in a stressful environment (variable turbulence and oxygen conditions). There were no significant differences between the treatments in any of the sperm motility parameters or sperm longevity. In both incubation settings, the highest early embryo mortality was recorded in a group exposed to positively charged nanoparticles. However, the difference was statistically significant only in the stressful environment, where concentration-dependent toxicity of nanoparticles was observed. The present study suggests possible concentration-dependent toxicity effects of PS-NPs on early embryo mortality in whitefish. This study also emphasizes the significance of different incubation conditions, as possible ecotoxicological effects may sometimes be observed only in a stressful environment.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107721"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145995183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-13DOI: 10.1016/j.aquatox.2025.107685
Rafael Trevisan, Danielle Ferraz Mello, Adèle Le Gall, Charlotte Corporeau, Caroline Fabioux, Arnaud Huvet, Ika Paul-Pont
Climate change is significantly altering the thermal environment of marine species, causing shifts in animal metabolism through increased temperatures and more frequent marine heatwaves. These changes can impose additional physiological stress on coastal organisms, potentially worsening their sensitivity to environmental pollutants and metabolic disruptors such as plastics. Indeed, nanoplastics are concerning contaminants in marine ecosystems, with the potential to disrupt cellular metabolism and redox balance in aquatic organisms. This study examined if rising temperatures can influence the cellular toxicity of two model polystyrene nanoplastics (non-functionalized Plain-NanoPS and amino-functionalized NH₂-NanoPS) in primary cultures of Pacific oyster Crassostrea gigas (Magallana gigas) hemocytes. We exposed hemocytes to a range of nanoplastic concentrations (0.1 to 10 mg/L) at controlled temperatures from 16 °C to 28 °C and evaluated cellular responses using metabolic, oxidative, and viability biomarkers. This range of concentrations and temperatures reflects the NPs content in tissues and fluids, as well as temperature fluctuations in aquaculture sites and intertidal environments. Plain-NanoPS had minimal effects, while NH₂-NanoPS caused temperature-dependent toxicity, impairing ATP production, reducing metabolic activity, and increasing reactive oxygen species levels. Integrated cellular biomarker analysis showed a shift from an adaptive to a stress-dominated metabolic phenotype under combined NH₂-NanoPS exposure and warming conditions. Since both particle types exhibited similar surface charges in cell culture medium, factors other than surface charge might influence cellular toxicity. This research demonstrates that warming increases the metabolic toxicity of nanoplastics and can reduce the thermal resilience of oyster cells in vitro.
{"title":"Each temperature degree counts: warming enhances polystyrene nanoplastic toxicity via metabolic disruption in a marine cellular model","authors":"Rafael Trevisan, Danielle Ferraz Mello, Adèle Le Gall, Charlotte Corporeau, Caroline Fabioux, Arnaud Huvet, Ika Paul-Pont","doi":"10.1016/j.aquatox.2025.107685","DOIUrl":"10.1016/j.aquatox.2025.107685","url":null,"abstract":"<div><div>Climate change is significantly altering the thermal environment of marine species, causing shifts in animal metabolism through increased temperatures and more frequent marine heatwaves. These changes can impose additional physiological stress on coastal organisms, potentially worsening their sensitivity to environmental pollutants and metabolic disruptors such as plastics. Indeed, nanoplastics are concerning contaminants in marine ecosystems, with the potential to disrupt cellular metabolism and redox balance in aquatic organisms. This study examined if rising temperatures can influence the cellular toxicity of two model polystyrene nanoplastics (non-functionalized Plain-NanoPS and amino-functionalized NH₂-NanoPS) in primary cultures of Pacific oyster <em>Crassostrea gigas</em> (<em>Magallana gigas</em>) hemocytes. We exposed hemocytes to a range of nanoplastic concentrations (0.1 to 10 mg/L) at controlled temperatures from 16 °C to 28 °C and evaluated cellular responses using metabolic, oxidative, and viability biomarkers. This range of concentrations and temperatures reflects the NPs content in tissues and fluids, as well as temperature fluctuations in aquaculture sites and intertidal environments. Plain-NanoPS had minimal effects, while NH₂-NanoPS caused temperature-dependent toxicity, impairing ATP production, reducing metabolic activity, and increasing reactive oxygen species levels. Integrated cellular biomarker analysis showed a shift from an adaptive to a stress-dominated metabolic phenotype under combined NH₂-NanoPS exposure and warming conditions. Since both particle types exhibited similar surface charges in cell culture medium, factors other than surface charge might influence cellular toxicity. This research demonstrates that warming increases the metabolic toxicity of nanoplastics and can reduce the thermal resilience of oyster cells <em>in vitro</em>.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107685"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145753434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-11-26DOI: 10.1016/j.aquatox.2025.107658
Xiaomei Chen , Hanyi Zhu , Yinliang Zhong , Jun Guo , Huiqiang Lu , Jian Yang
Tetrachlorobisphenol A (TCBPA), a prevalent halogenated flame retardant detected in human serum and breast milk, poses significant exposure risks during developmental windows. While recognized for reproductive toxicity, its impact on craniofacial development remains unexplored. This study investigated the effects of TCBPA (0.5, 0.6, and 0.7 mg/L) on zebrafish cartilage development during craniofacial bone development (11–96 h post-fertilization). At experimental concentrations, TCBPA induced a range of developmental issues, notably significant craniofacial deformities, which were characterized by abnormal specifications and morphology of Meckel’s and ceratohyal cartilages. Additionally, qPCR results revealed that TCBPA exposure led to the down-regulation of genes related to cartilage development. Moreover, it antagonized retinoid X receptor subtype beta-a (RXRba), a key receptor in the retinoic acid (RA) signaling pathway, leading to suppressed expression of downstream target genes essential for cartilage development. TUNEL staining further demonstrated that TCBPA exposure triggered excessive apoptosis of zebrafish craniofacial chondrocytes, a finding corroborated by qPCR results indicating altered expression of apoptosis-related genes. This phenomenon may be attributed to the collaborative involvement of RXRs and peroxisome proliferator-activated receptor gamma (PPARγ) in regulating cell survival, differentiation, and apoptosis. The antagonism of TCBPA on RXRba was also validated in a rescue experiment using Bexarotene, a high affinity agonist of RXRs. In conclusion, TCBPA inhibits the expression of genes crucial to cartilage development by antagonizing RXRba activity. It also induces abnormal apoptosis of chondrocytes through other signaling pathways mediated by RXRs, resulting in craniofacial cartilage toxicity in zebrafish.
四氯双酚A （TCBPA）是一种普遍存在于人类血清和母乳中的卤化阻燃剂，在发育窗口期具有显著的暴露风险。虽然被认为具有生殖毒性，但其对颅面发育的影响仍未被探索。本实验研究了0.5、0.6和0.7 mg/L TCBPA对斑马鱼颅面骨发育（受精后11-96 h）期间软骨发育的影响。在实验浓度下，TCBPA诱导了一系列发育问题，特别是显著的颅面畸形，其特征是梅克尔软骨和角状软骨的规格和形态异常。此外，qPCR结果显示，TCBPA暴露导致与软骨发育相关的基因下调。此外，它拮抗维甲酸（RA）信号通路中的关键受体类视黄酸X受体亚型β -a (RXRba)，导致软骨发育必需的下游靶基因的表达受到抑制。TUNEL染色进一步证实TCBPA暴露引发斑马鱼颅面软骨细胞过度凋亡，qPCR结果证实了这一发现，表明凋亡相关基因表达改变。这种现象可能归因于RXRs和过氧化物酶体增殖激活受体γ (PPARγ)协同参与调节细胞存活、分化和凋亡。TCBPA对RXRba的拮抗作用也在使用高亲和力RXRs激动剂Bexarotene的救援实验中得到了验证。总之，TCBPA通过拮抗RXRba活性抑制软骨发育关键基因的表达。它还通过RXRs介导的其他信号通路诱导软骨细胞异常凋亡，导致斑马鱼颅面软骨毒性。
{"title":"Toxicity of tetrachlorobisphenol A interfering with craniofacial cartilage development by inhibiting RXR activity in zebrafish","authors":"Xiaomei Chen , Hanyi Zhu , Yinliang Zhong , Jun Guo , Huiqiang Lu , Jian Yang","doi":"10.1016/j.aquatox.2025.107658","DOIUrl":"10.1016/j.aquatox.2025.107658","url":null,"abstract":"<div><div>Tetrachlorobisphenol A (TCBPA), a prevalent halogenated flame retardant detected in human serum and breast milk, poses significant exposure risks during developmental windows. While recognized for reproductive toxicity, its impact on craniofacial development remains unexplored. This study investigated the effects of TCBPA (0.5, 0.6, and 0.7 mg/L) on zebrafish cartilage development during craniofacial bone development (11–96 h post-fertilization). At experimental concentrations, TCBPA induced a range of developmental issues, notably significant craniofacial deformities, which were characterized by abnormal specifications and morphology of Meckel’s and ceratohyal cartilages. Additionally, qPCR results revealed that TCBPA exposure led to the down-regulation of genes related to cartilage development. Moreover, it antagonized retinoid X receptor subtype beta-a (RXRba), a key receptor in the retinoic acid (RA) signaling pathway, leading to suppressed expression of downstream target genes essential for cartilage development. TUNEL staining further demonstrated that TCBPA exposure triggered excessive apoptosis of zebrafish craniofacial chondrocytes, a finding corroborated by qPCR results indicating altered expression of apoptosis-related genes. This phenomenon may be attributed to the collaborative involvement of RXRs and peroxisome proliferator-activated receptor gamma (PPARγ) in regulating cell survival, differentiation, and apoptosis. The antagonism of TCBPA on RXRba was also validated in a rescue experiment using Bexarotene, a high affinity agonist of RXRs. In conclusion, TCBPA inhibits the expression of genes crucial to cartilage development by antagonizing RXRba activity. It also induces abnormal apoptosis of chondrocytes through other signaling pathways mediated by RXRs, resulting in craniofacial cartilage toxicity in zebrafish.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107658"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145609030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-13DOI: 10.1016/j.aquatox.2025.107683
Bruna da Silva , Adriana Oliveira Medeiros , William Gabriel Borges , Bárbara Lopes Körner , Amanda Cristina Ninov Pazini , Raquel de Brito , Cássia Alves Lima-Rezende , Cristiano Ilha , Jacir Dal Magro , Renan de Souza Rezende
Low-order streams provide critical ecosystem services but are increasingly threatened by agricultural intensification and agrochemical pollution. Atrazine and 2,4-D are among the most widely used herbicides worldwide; however, their combined effects on non-target microbial decomposers, particularly aquatic hyphomycetes that sustain detritus-based food webs, remain poorly understood. Here, we experimentally (25-day of incubation) evaluated the individual and interactive effects of atrazine, 2,4-D, and their mixture (1, 50, and 100 µg L⁻¹) at environmentally relevant concentrations on sporulation, richness, and community composition of aquatic hyphomycetes colonizing Inga vera leaves. Herbicide exposure affected fungal reproduction in a nonlinear and context-dependent manner, with the strongest reduction in sporulation (∼50 %) occurring in the mixture at medium concentration, while higher concentrations did not consistently intensify the response. Community ordination analyses revealed significant pollutant × dose interactions, with shifts in species assemblages driven by the proliferation of tolerant taxa such as Lunulospora curvula and Heliscella stellata. The observed decoupling between fungal function and structure supports the hypothesis of functional redundancy but also points to impaired colonization and reduced organic matter mineralization efficiency under chemical stress. Our findings demonstrate that sublethal endpoints, such as sporulation, provide early warning signals of agrochemical contamination, this study advances the ecological risk assessment of pesticide mixtures. It underscores the need to integrate functional microbial indicators into biomonitoring frameworks for tropical freshwater systems.
{"title":"Effects of atrazine and 2,4-D mixtures on aquatic fungi: Functional decline and community reorganization in subtropical streams","authors":"Bruna da Silva , Adriana Oliveira Medeiros , William Gabriel Borges , Bárbara Lopes Körner , Amanda Cristina Ninov Pazini , Raquel de Brito , Cássia Alves Lima-Rezende , Cristiano Ilha , Jacir Dal Magro , Renan de Souza Rezende","doi":"10.1016/j.aquatox.2025.107683","DOIUrl":"10.1016/j.aquatox.2025.107683","url":null,"abstract":"<div><div>Low-order streams provide critical ecosystem services but are increasingly threatened by agricultural intensification and agrochemical pollution. Atrazine and 2,4-D are among the most widely used herbicides worldwide; however, their combined effects on non-target microbial decomposers, particularly aquatic hyphomycetes that sustain detritus-based food webs, remain poorly understood. Here, we experimentally (25-day of incubation) evaluated the individual and interactive effects of atrazine, 2,4-D, and their mixture (1, 50, and 100 µg L⁻¹) at environmentally relevant concentrations on sporulation, richness, and community composition of aquatic hyphomycetes colonizing <em>Inga vera</em> leaves. Herbicide exposure affected fungal reproduction in a nonlinear and context-dependent manner, with the strongest reduction in sporulation (∼50 %) occurring in the mixture at medium concentration, while higher concentrations did not consistently intensify the response. Community ordination analyses revealed significant pollutant × dose interactions, with shifts in species assemblages driven by the proliferation of tolerant taxa such as <em>Lunulospora curvula</em> and <em>Heliscella stellata</em>. The observed decoupling between fungal function and structure supports the hypothesis of functional redundancy but also points to impaired colonization and reduced organic matter mineralization efficiency under chemical stress. Our findings demonstrate that sublethal endpoints, such as sporulation, provide early warning signals of agrochemical contamination, this study advances the ecological risk assessment of pesticide mixtures. It underscores the need to integrate functional microbial indicators into biomonitoring frameworks for tropical freshwater systems.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107683"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145731135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-21DOI: 10.1016/j.aquatox.2025.107690
Gustavo Axel Elizalde-Velázquez , Selene Elizabeth Herrera-Vázquez , Niki Tagkalidou , Melissa Faria , Irene Romero-Alfano , Eva Prats , Ariadna Verdaguer , Cristian Gómez-Canela , Leobardo Manuel Gómez-Oliván , Demetrio Raldúa
Aluminum (Al) is a widespread aquatic neurotoxic pollutant, yet its brain accumulation is seldom quantified in fish neurotoxicity studies. Here, we investigated the neurobehavioral and molecular consequences of acute waterborne Al exposure in adult zebrafish (n = 227). Fish were exposed for 96 h to 50 mg/L AlCl₃ at pH 5.0 and then transferred to clean water for a 7-day depuration period. Despite the absence of statistically significant Al accumulation in either brain or carcass, exposed animals exhibited consistent neurobehavioral impairments, including reduced non-associative learning (short-term habituation of the acoustic startle response), anxiety- and depression-like phenotypes (positive geotaxis and negative scototaxis), and increased aggressive-like behavior. All behavioral alterations were fully reversed after depuration, indicating a transient effect. Brain oxidative stress markers (catalase, superoxide dismutase, lipid peroxidation), neurotransmitter levels, and acetylcholinesterase activity remained largely unchanged, arguing against a direct, generalized disruption of brain biochemistry. In contrast, brain expression of appa, gfap, and cat was significantly upregulated immediately after exposure and returned to control levels after depuration, suggesting an early but reversible stress and glial response. Overall, these findings show that short-term acidic Al exposure can induce reversible cognitive and affective disturbances in zebrafish in the absence of detectable brain accumulation, highlighting the importance of transient molecular stress pathways in acute aluminum neurotoxicity.
{"title":"Transient cognitive and affective impairments following short-term aluminum exposure in adult zebrafish","authors":"Gustavo Axel Elizalde-Velázquez , Selene Elizabeth Herrera-Vázquez , Niki Tagkalidou , Melissa Faria , Irene Romero-Alfano , Eva Prats , Ariadna Verdaguer , Cristian Gómez-Canela , Leobardo Manuel Gómez-Oliván , Demetrio Raldúa","doi":"10.1016/j.aquatox.2025.107690","DOIUrl":"10.1016/j.aquatox.2025.107690","url":null,"abstract":"<div><div>Aluminum (Al) is a widespread aquatic neurotoxic pollutant, yet its brain accumulation is seldom quantified in fish neurotoxicity studies. Here, we investigated the neurobehavioral and molecular consequences of acute waterborne Al exposure in adult zebrafish (<em>n</em> = 227). Fish were exposed for 96 h to 50 mg/L AlCl₃ at pH 5.0 and then transferred to clean water for a 7-day depuration period. Despite the absence of statistically significant Al accumulation in either brain or carcass, exposed animals exhibited consistent neurobehavioral impairments, including reduced non-associative learning (short-term habituation of the acoustic startle response), anxiety- and depression-like phenotypes (positive geotaxis and negative scototaxis), and increased aggressive-like behavior. All behavioral alterations were fully reversed after depuration, indicating a transient effect. Brain oxidative stress markers (catalase, superoxide dismutase, lipid peroxidation), neurotransmitter levels, and acetylcholinesterase activity remained largely unchanged, arguing against a direct, generalized disruption of brain biochemistry. In contrast, brain expression of <em>appa, gfap</em>, and <em>cat</em> was significantly upregulated immediately after exposure and returned to control levels after depuration, suggesting an early but reversible stress and glial response. Overall, these findings show that short-term acidic Al exposure can induce reversible cognitive and affective disturbances in zebrafish in the absence of detectable brain accumulation, highlighting the importance of transient molecular stress pathways in acute aluminum neurotoxicity.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107690"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145813783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-17DOI: 10.1016/j.aquatox.2025.107688
Maëva Marimoutou , Gilles Bareille , Mathieu Milhe-Poutingon , Clémentine Gelber , Patrick Baldoni-Andrey , Nicholas Bagger Gurieff , Hélène Tabouret , Sandra Mounicou , Séverine Le Faucheur
Cobalt (Co) is central to the development of new low-carbon energies, becoming an element of emerging concern for the environment. Gastropods are widely distributed in aquatic ecosystems and represent the largest group of the phylum Mollusca. However very few studies have focused on Co impacts on gastropods. We thus aimed to examine the internal handling of Co in gastropods and its excretion into the shell in order to better understand its toxic actions and how these organisms cope with Co stress. To that end, Ampullaceana balthica was exposed to increasing Co concentrations (6, 30 and 60 μg·L−1) using outdoor flow-through mesocosms for 28 days in June and October. They were analyzed for their growth, reproduction and Co accumulation in the soft bodies and the outer shell part every week. Cobalt distribution in soft tissues and its subcellular distribution were further examined.
Cobalt induced a decrease in the egg mass number and a delay in their hatching. Its accumulation in the soft tissue and the outer shell exhibited distinct seasonal patterns. Linear relationships with the ambient Co concentrations were only evident in the soft tissues in June and in the shell in October. For both periods, Co was mainly distributed in the hepatopancreas and the mantle, particularly in their mitochondria and granules fractions. We thus discussed the possible pathways of Co from the soft tissues to the shell involving granules. The present results demonstrate that using shells as bioindicators of metal exposure has certain limitations, depending on the organism life cycle.
{"title":"Internal handling, shell accumulation and effects of cobalt on the gastropod Ampullaceana balthica","authors":"Maëva Marimoutou , Gilles Bareille , Mathieu Milhe-Poutingon , Clémentine Gelber , Patrick Baldoni-Andrey , Nicholas Bagger Gurieff , Hélène Tabouret , Sandra Mounicou , Séverine Le Faucheur","doi":"10.1016/j.aquatox.2025.107688","DOIUrl":"10.1016/j.aquatox.2025.107688","url":null,"abstract":"<div><div>Cobalt (Co) is central to the development of new low-carbon energies, becoming an element of emerging concern for the environment. Gastropods are widely distributed in aquatic ecosystems and represent the largest group of the phylum Mollusca. However very few studies have focused on Co impacts on gastropods. We thus aimed to examine the internal handling of Co in gastropods and its excretion into the shell in order to better understand its toxic actions and how these organisms cope with Co stress. To that end, <em>Ampullaceana balthica</em> was exposed to increasing Co concentrations (6, 30 and 60 μg·L<sup>−1</sup>) using outdoor flow-through mesocosms for 28 days in June and October. They were analyzed for their growth, reproduction and Co accumulation in the soft bodies and the outer shell part every week. Cobalt distribution in soft tissues and its subcellular distribution were further examined.</div><div>Cobalt induced a decrease in the egg mass number and a delay in their hatching. Its accumulation in the soft tissue and the outer shell exhibited distinct seasonal patterns. Linear relationships with the ambient Co concentrations were only evident in the soft tissues in June and in the shell in October. For both periods, Co was mainly distributed in the hepatopancreas and the mantle, particularly in their mitochondria and granules fractions. We thus discussed the possible pathways of Co from the soft tissues to the shell involving granules. The present results demonstrate that using shells as bioindicators of metal exposure has certain limitations, depending on the organism life cycle.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107688"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-04DOI: 10.1016/j.aquatox.2025.107671
Helena Costa, Maud Van Essche, Juliane A. Riedel, Akash Gupta, Audun H. Rikardsen, Anders Goksøyr, Pierre Blévin, Mikael Harju, Laura Pirard, Susan Bengston Nash, Sofie Sødestrøm, Courtney A. Waugh
Killer whales (Orcinus orca) accumulate high levels of persistent organic pollutants (POPs), which have been linked to immunomodulation. Over the past decades, large-scale mortality events associated with cetacean morbillivirus (CeMV) have affected cetacean populations, and concerns have been raised about the role of contaminants in exacerbating these outbreaks. However, establishing cause-effect relationships in free-roaming cetaceans remains a significant challenge. In vitro approaches present unique potential for furthering our understanding of the effects of multiple environmental stressors in marine mammal health. In this study, we used primary fibroblasts cultured from wild Norwegian killer whale skin biopsies (n = 6) to assess how exposure to POP mixtures affects cell viability and CeMV replication. Our findings demonstrate that CeMV successfully replicates in killer whale fibroblasts, with the viral replication significantly increasing over the duration of the experiment. POP exposure led to a concentration-dependent decrease in cell viability and a significant increase in viral replication. These results validate killer whale primary fibroblasts as a valuable in vitro tool for the study of co-exposure of POPs and morbillivirus on toothed cetaceans. Moreover, these findings support the need for further research to confirm the role of contaminants in intensifying the severity of CeMV infections in the wild.
{"title":"A whale in a well: Co-exposure of a persistent organic pollutant mixture and cetacean morbillivirus on killer whale (Orcinus orca) primary fibroblasts","authors":"Helena Costa, Maud Van Essche, Juliane A. Riedel, Akash Gupta, Audun H. Rikardsen, Anders Goksøyr, Pierre Blévin, Mikael Harju, Laura Pirard, Susan Bengston Nash, Sofie Sødestrøm, Courtney A. Waugh","doi":"10.1016/j.aquatox.2025.107671","DOIUrl":"10.1016/j.aquatox.2025.107671","url":null,"abstract":"<div><div>Killer whales (<em>Orcinus orca</em>) accumulate high levels of persistent organic pollutants (POPs), which have been linked to immunomodulation. Over the past decades, large-scale mortality events associated with cetacean morbillivirus (CeMV) have affected cetacean populations, and concerns have been raised about the role of contaminants in exacerbating these outbreaks. However, establishing cause-effect relationships in free-roaming cetaceans remains a significant challenge. <em>In vitro</em> approaches present unique potential for furthering our understanding of the effects of multiple environmental stressors in marine mammal health. In this study, we used primary fibroblasts cultured from wild Norwegian killer whale skin biopsies (<em>n</em> = 6) to assess how exposure to POP mixtures affects cell viability and CeMV replication. Our findings demonstrate that CeMV successfully replicates in killer whale fibroblasts, with the viral replication significantly increasing over the duration of the experiment. POP exposure led to a concentration-dependent decrease in cell viability and a significant increase in viral replication. These results validate killer whale primary fibroblasts as a valuable <em>in vitro</em> tool for the study of co-exposure of POPs and morbillivirus on toothed cetaceans. Moreover, these findings support the need for further research to confirm the role of contaminants in intensifying the severity of CeMV infections in the wild.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107671"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145689955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-23DOI: 10.1016/j.aquatox.2025.107693
Xunyue Liu , Junyao Ge , Haojie Zhu , Peng Liu , Huidi Zhang , Qiong Rao , Wenze He , Jianqiang Sun
Spirotetramat is a novel, tetrahydrofuran-based broad-spectrum insecticide. It is widely used in global agriculture due to its high insecticidal activity. However, its long-term and extensive use causes environmental accumulation, making its toxicity to non-target organisms a key issue in environmental risk assessments. Previous studies have confirmed that it causes oxidative damage in zebrafish embryos and gonads. The toxic effects and mechanisms of spirotetramat in the zebrafish intestine remain unclear, despite its importance in digestion and absorption, immune defense, and microbiota-host interactions. This study systematically investigated the toxic effects of spirotetramat on zebrafish intestine using multidimensional approaches, including histopathological observation, detection of oxidative stress-related gene expression, and analysis of intestinal microbiota. This study found that gene expression levels of sod, cat, and gpx increased in the 0.08 mg/L group but decreased in the 2 mg/L group, indicating that low concentrations activate the intestinal antioxidant system, while high concentrations cause significant overload. Histopathological analysis revealed intestinal damage, including villus fragmentation and epithelial detachment, in the 2 mg/L treatment group. The increased alkaline phosphatase activity in the 2 mg/L group may be associated with compensatory repair. Microbiota analysis revealed an elevated quantity and diversity of intestinal flora in the treatment groups, with altered abundance of specific bacteria in the 2 mg/L treatment group. Functional prediction of the microbiota suggested that spirotetramat exposure induced changes in metabolic functions. In conclusion, spirotetramat induced intestinal oxidative stress in zebrafish, leading to intestinal barrier damage and microbiota dysbiosis. This study provides a theoretical basis for the comprehensive assessment of spirotetramat's ecological risks.
{"title":"Intestinal toxicity and microbiota dysbiosis in zebrafish exposed to spirotetramat","authors":"Xunyue Liu , Junyao Ge , Haojie Zhu , Peng Liu , Huidi Zhang , Qiong Rao , Wenze He , Jianqiang Sun","doi":"10.1016/j.aquatox.2025.107693","DOIUrl":"10.1016/j.aquatox.2025.107693","url":null,"abstract":"<div><div>Spirotetramat is a novel, tetrahydrofuran-based broad-spectrum insecticide. It is widely used in global agriculture due to its high insecticidal activity. However, its long-term and extensive use causes environmental accumulation, making its toxicity to non-target organisms a key issue in environmental risk assessments. Previous studies have confirmed that it causes oxidative damage in zebrafish embryos and gonads. The toxic effects and mechanisms of spirotetramat in the zebrafish intestine remain unclear, despite its importance in digestion and absorption, immune defense, and microbiota-host interactions. This study systematically investigated the toxic effects of spirotetramat on zebrafish intestine using multidimensional approaches, including histopathological observation, detection of oxidative stress-related gene expression, and analysis of intestinal microbiota. This study found that gene expression levels of <em>sod, cat</em>, and <em>gpx</em> increased in the 0.08 mg/L group but decreased in the 2 mg/L group, indicating that low concentrations activate the intestinal antioxidant system, while high concentrations cause significant overload. Histopathological analysis revealed intestinal damage, including villus fragmentation and epithelial detachment, in the 2 mg/L treatment group. The increased alkaline phosphatase activity in the 2 mg/L group may be associated with compensatory repair. Microbiota analysis revealed an elevated quantity and diversity of intestinal flora in the treatment groups, with altered abundance of specific bacteria in the 2 mg/L treatment group. Functional prediction of the microbiota suggested that spirotetramat exposure induced changes in metabolic functions. In conclusion, spirotetramat induced intestinal oxidative stress in zebrafish, leading to intestinal barrier damage and microbiota dysbiosis. This study provides a theoretical basis for the comprehensive assessment of spirotetramat's ecological risks.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107693"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145823033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号