Polycyclic aromatic hydrocarbons (PAHs) pose developmental risks, specifically craniofacial malformations in fish. This study assessed the effects of benzo [a]anthracene (BaA) and pyrene (Pyr) exposure on craniofacial chondrogenesis in Japanese medaka (Oryzias latipes) embryos, focusing on the roles of aryl hydrocarbon receptor (AhR) and cytochrome P450 (CYP). To explore the involvements with inhibiting craniofacial chondrogenesis, the CYP inhibitor (piperonyl butoxide [PBO]) and AhR antagonist (CH223191 [CH]) were used. Whole-mount Alcian blue staining of hatching larvae revealed that exposure of fish embryos to BaA partially impaired craniofacial chondrogenesis that was further exacerbated by BaA + PBO co-exposure, indicating synergistic effects of BaA under CYP inhibition. Those impairments were accompanied by the downregulation of collagen type II alpha 1a (Col2a1a) and sex-determining region Y-box9b (Sox9b). In contrast, although Pyr exposure also impaired craniofacial chondrogenesis, these effects were not associated with the downregulation of Col2a1a or Sox9b. Notably, both AhR and CYP inhibitions can attenuate Pyr-induced cartilage defects, suggesting that metabolic activation of Pyr is responsible for craniofacial effects. Overall, this study demonstrates that BaA and Pyr disrupt craniofacial chondrogenesis through different toxicological profiles.
{"title":"Differences of benzo[a]anthracene- and pyrene-induced disruption of craniofacial chondrogenesis in Japanese medaka","authors":"Shusaku Fukugami , Masatoshi Yamasaki , Emiko Kokushi , Seiichi Uno","doi":"10.1016/j.aquatox.2025.107696","DOIUrl":"10.1016/j.aquatox.2025.107696","url":null,"abstract":"<div><div>Polycyclic aromatic hydrocarbons (PAHs) pose developmental risks, specifically craniofacial malformations in fish. This study assessed the effects of benzo [a]anthracene (BaA) and pyrene (Pyr) exposure on craniofacial chondrogenesis in Japanese medaka (<em>Oryzias latipes</em>) embryos, focusing on the roles of aryl hydrocarbon receptor (AhR) and cytochrome P450 (CYP). To explore the involvements with inhibiting craniofacial chondrogenesis, the CYP inhibitor (piperonyl butoxide [PBO]) and AhR antagonist (CH223191 [CH]) were used. Whole-mount Alcian blue staining of hatching larvae revealed that exposure of fish embryos to BaA partially impaired craniofacial chondrogenesis that was further exacerbated by BaA + PBO co-exposure, indicating synergistic effects of BaA under CYP inhibition. Those impairments were accompanied by the downregulation of collagen type II alpha 1a (<em>Col2a1a</em>) and sex-determining region Y-box9b (<em>Sox9b</em>). In contrast, although Pyr exposure also impaired craniofacial chondrogenesis, these effects were not associated with the downregulation of <em>Col2a1a</em> or <em>Sox9b</em>. Notably, both AhR and CYP inhibitions can attenuate Pyr-induced cartilage defects, suggesting that metabolic activation of Pyr is responsible for craniofacial effects. Overall, this study demonstrates that BaA and Pyr disrupt craniofacial chondrogenesis through different toxicological profiles.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107696"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145845095","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}
Despite the increasing production and several applications of green plant-based-synthesized nanomaterials, their hazardous and transgenerational effects on aquatic organisms remain unknown. Thus, green copper oxide nanoparticles synthesized from Croton urucurana aqueous leaf extract (G-CuONPs) were evaluated for their transgenerational effects on the gastropod Biomphalaria glabrata across three generations (i.e., F0, F1, and F2). Adult snails (F0) were exposed for 7 days to G-CuONPs at sublethal concentrations (G-CuONP1 = 8.5 and G-CuONP2 = 21.0 µg L⁻¹) and to the aqueous extract (AqEx) used in G-CuONP synthesis (273.0 µg L⁻¹). Fecundity parameters (egg clutches per adult, eggs per egg clutch, and egg viability) and adult mortality were not affected in F0 and F1. However, changes in heart rate were observed in F1 and F2 from F0 exposure to AqEx and G-CuONP2, indicating the persistence of this effect even with a short parental exposure period. Notably, both F1 and F2 presented improved embryo development and hatching success, suggesting a positive carry-over effect. In contrast, there was a reduction in the period taken to return to normal for F1 from G-CuONP2 and an increase in this period for F2 from AqEx. These behavioral changes could compromise predator avoidance and, consequently, individual survival and population dynamics. The data suggest that while sublethal exposure to G-CuONPs may enhance early developmental outcomes in unexposed generations, it may simultaneously impair key survival behaviors over time. Further investigation is needed to elucidate the underlying mechanisms of these generational shifts and their ecological relevance.
尽管绿色植物合成纳米材料的产量和应用不断增加，但其对水生生物的危害和跨代影响尚不清楚。因此，研究了从巴豆水提取物（G-CuONPs）中合成的绿色氧化铜纳米颗粒对腹足动物（即F0， F1和F2）的跨代效应。成年蜗牛（F0）暴露在亚致死浓度的g - cuonp （g - cuonp1 = 8.5和g - cuonp2 = 21.0µg L -毒发展）和用于g - cuonp合成的水提取物（AqEx）中7天（273.0µg L -毒发展）。F0和F1对繁殖力参数（每窝卵数、每窝卵数和卵活力）和成虫死亡率没有影响。然而，F0暴露于AqEx和G-CuONP2后，F1和F2的心率发生了变化，这表明即使父母暴露时间较短，这种影响也会持续存在。值得注意的是，F1和F2的胚胎发育和孵化成功率都有所提高，表明存在正的结转效应。相比之下，G-CuONP2使F1恢复正常所需的时间缩短，AqEx使F2恢复正常所需的时间增加。这些行为变化可能会影响捕食者的躲避，从而影响个体生存和种群动态。数据表明，虽然亚致死暴露于G-CuONPs可能会增强未暴露代的早期发育结果，但随着时间的推移，它可能同时损害关键的生存行为。需要进一步的研究来阐明这些代际变化的潜在机制及其生态相关性。
{"title":"Carry-over effects of green copper oxide nanoparticles on three generations of the gastropod Biomphalaria glabrata","authors":"Cyntia Ayumi Yokota Harayashiki , Maxwell Batista Caixeta , Thiago Lopes Rocha","doi":"10.1016/j.aquatox.2025.107694","DOIUrl":"10.1016/j.aquatox.2025.107694","url":null,"abstract":"<div><div>Despite the increasing production and several applications of green plant-based-synthesized nanomaterials, their hazardous and transgenerational effects on aquatic organisms remain unknown. Thus, green copper oxide nanoparticles synthesized from <em>Croton urucurana</em> aqueous leaf extract (G-CuONPs) were evaluated for their transgenerational effects on the gastropod <em>Biomphalaria glabrata</em> across three generations (i.e., F0, F1, and F2). Adult snails (F0) were exposed for 7 days to G-CuONPs at sublethal concentrations (G-CuONP1 = 8.5 and G-CuONP2 = 21.0 µg L⁻¹) and to the aqueous extract (AqEx) used in G-CuONP synthesis (273.0 µg L⁻¹). Fecundity parameters (egg clutches per adult, eggs per egg clutch, and egg viability) and adult mortality were not affected in F0 and F1. However, changes in heart rate were observed in F1 and F2 from F0 exposure to AqEx and G-CuONP2, indicating the persistence of this effect even with a short parental exposure period. Notably, both F1 and F2 presented improved embryo development and hatching success, suggesting a positive carry-over effect. In contrast, there was a reduction in the period taken to return to normal for F1 from G-CuONP2 and an increase in this period for F2 from AqEx. These behavioral changes could compromise predator avoidance and, consequently, individual survival and population dynamics. The data suggest that while sublethal exposure to G-CuONPs may enhance early developmental outcomes in unexposed generations, it may simultaneously impair key survival behaviors over time. Further investigation is needed to elucidate the underlying mechanisms of these generational shifts and their ecological relevance.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107694"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145845096","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}
Hexabromocyclododecane (HBCD), a persistent brominated flame retardant, poses substantial ecological risks attributable to its bioaccumulation potential and toxicity. This study explored the toxic impacts of HBCD on the marine microalgae Chlorella salina using an integrated approach combining physiological, biochemical, and transcriptomic analyses. The microalgae was exposed to concentrations of 5, 50, and 100 μg·L⁻¹ of HBCD for 96 h. The results showed that HBCD significantly inhibited the growth of C. salina (p < 0.05), with a 21 % reduction in cell density at the highest concentration. Pigment analysis indicated that upon exposure to 100 μg·L⁻¹ HBCD, the levels of chlorophyll a, chlorophyll b, and carotenoids decreased by 17 %, 19 %, and 13 %, respectively (p < 0.05). Fourier transform infrared spectroscopy (FTIR) revealed concentration-dependent alterations in the composition, conformation, and functionality of key biomacromolecules. Specifically, lipid peroxidation was evidenced by decreased CH2/lipid, CH3/lipid, and olefinic=CH/lipid ratios, along with an increased carbonyl ester/lipid ratio. These findings were corroborated by elevated malondialdehyde (MDA) content and superoxide dismutase (SOD) activity. Alterations in the secondary structure of proteins were detected through decreased Amide I/Amide II and β-sheet/α-helix ratios. DNA damage involved a reversal of the B- to A-DNA transition and a shift from B- to Z-DNA conformational. Furthermore, transcriptomic analysis identified 4636 differentially expressed genes (DEGs) following exposure to 100 μg·L⁻¹ HBCD, which were predominantly enriched in pathways associated with fatty acid metabolism, energy metabolism, and cellular signaling. These findings provide mechanistic insights into the toxicity of HBCD in marine microalgae and highlight its potential ecological risks in marine environments.
{"title":"Elucidating toxicity mechanisms of hexabromocyclododecane in marine microalga Chlorella salina: An integrated biomacromolecular and transcriptomic analysis","authors":"Fei Tian , Xuefeng Wang , Lihua Lai , Peng Shao , Zhenzhao Tang , Zhe Zhang , Qian Xiong , Linbao Zhang , Haigang Chen","doi":"10.1016/j.aquatox.2025.107662","DOIUrl":"10.1016/j.aquatox.2025.107662","url":null,"abstract":"<div><div>Hexabromocyclododecane (HBCD), a persistent brominated flame retardant, poses substantial ecological risks attributable to its bioaccumulation potential and toxicity. This study explored the toxic impacts of HBCD on the marine microalgae <em>Chlorella salina</em> using an integrated approach combining physiological, biochemical, and transcriptomic analyses. The microalgae was exposed to concentrations of 5, 50, and 100 μg·L⁻¹ of HBCD for 96 h. The results showed that HBCD significantly inhibited the growth of <em>C. salina</em> (<em>p</em> < 0.05), with a 21 % reduction in cell density at the highest concentration. Pigment analysis indicated that upon exposure to 100 μg·L⁻¹ HBCD, the levels of chlorophyll <em>a</em>, chlorophyll <em>b</em>, and carotenoids decreased by 17 %, 19 %, and 13 %, respectively (<em>p</em> < 0.05). Fourier transform infrared spectroscopy (FTIR) revealed concentration-dependent alterations in the composition, conformation, and functionality of key biomacromolecules. Specifically, lipid peroxidation was evidenced by decreased CH<sub>2</sub>/lipid, CH<sub>3</sub>/lipid, and olefinic=CH/lipid ratios, along with an increased carbonyl ester/lipid ratio. These findings were corroborated by elevated malondialdehyde (MDA) content and superoxide dismutase (SOD) activity. Alterations in the secondary structure of proteins were detected through decreased Amide I/Amide II and β-sheet/α-helix ratios. DNA damage involved a reversal of the B- to A-DNA transition and a shift from B- to Z-DNA conformational. Furthermore, transcriptomic analysis identified 4636 differentially expressed genes (DEGs) following exposure to 100 μg·L⁻¹ HBCD, which were predominantly enriched in pathways associated with fatty acid metabolism, energy metabolism, and cellular signaling. These findings provide mechanistic insights into the toxicity of HBCD in marine microalgae and highlight its potential ecological risks in marine environments.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107662"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145651099","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.2025.107691
Juliana Barros , Santosh Kumar , Sarra Ben Tanfous , Manuel Graça , Sahadevan Seena
Nanoplastics (NPs) are an emerging concern in freshwater ecosystems due to their persistence and potential to interact with persistent pollutants, such as metals. These combined stressors threaten freshwater ecosystems functioning, where leaf litter decomposition, primarily driven by aquatic hyphomycetes, supports energy transfer to higher trophic levels. A microcosm experiment was conducted to assess the joint impacts of polystyrene NPs (bare and carboxylated) at environmentally relevant (0.25 and 2.5 µg L⁻¹) and elevated (25 and 250 µg L⁻¹) concentrations in reference and metal-polluted stream waters. Fungal biomass, aquatic hyphomycetes sporulation and community composition, microbial leaf litter decomposition, as well as invertebrate feeding behaviour were quantified. Carboxylated NPs showed greater aggregation and surface alterations than bare NPs. Fungal biomass and sporulation declined significantly at 2.5 µg L⁻¹, with carboxylated NPs exerting stronger effects. Non-metric multidimensional scaling (NMDS) revealed clear shifts in fungal community structure across two water types (reference and metal-polluted) and NP concentrations. Metal pollution alone reduced decomposition by 17 %, with reductions reaching up to 24 % when combined with NPs, particularly carboxylated NPs. Invertebrate feeding was reduced by 27 % under metal pollution alone, with maximum inhibition (47 %) observed at the highest NP concentration, although NP type did not significantly alter feeding rates. Together, these results demonstrate that NPs, especially carboxylated forms, exacerbate the ecological impacts of metal pollution, impairing microbial processes and detritivore feeding. These findings underscore the importance of considering NPs surface chemistry and multiple stressors interactions in ecological risk assessments of polluted freshwater systems.
纳米塑料（NPs）由于其持久性和与持久性污染物（如金属）相互作用的潜力而成为淡水生态系统中一个新兴的问题。这些综合的压力源威胁着淡水生态系统的功能，在淡水生态系统中，主要由水生菌丝菌驱动的凋落叶分解支持能量向更高营养水平的转移。我们进行了一个微观实验，以评估聚苯乙烯NPs（裸的和羧化的）在环境相关（0.25和2.5µg L -⁻¹）和在参考和金属污染的溪流中浓度升高（25和250µg L -⁻¹）时的联合影响。对真菌生物量、水生菌丝菌产孢量和群落组成、微生物凋落叶分解以及无脊椎动物摄食行为进行了量化。羧基化NPs比裸NPs表现出更大的聚集和表面变化。在2.5µg L - 1时，真菌生物量和产孢量明显下降，羧化NPs的作用更强。非度量多维尺度（NMDS）揭示了两种水类型（参考水和金属污染水）和NP浓度下真菌群落结构的明显变化。仅金属污染就使分解率降低了17%，当与净污染物（特别是羧化净污染物）结合使用时，分解率可达24%。在金属污染下，无脊椎动物的摄食减少了27%，在最高NP浓度下观察到最大的抑制（47%），尽管NP类型没有显著改变摄食率。总之，这些结果表明，NPs，特别是羧基化形式，加剧了金属污染的生态影响，损害了微生物过程和营养物质的摄食。这些发现强调了在污染淡水系统生态风险评估中考虑NPs表面化学和多种应激源相互作用的重要性。
{"title":"Nanoplastics intensify metal-induced impacts in freshwater ecosystems","authors":"Juliana Barros , Santosh Kumar , Sarra Ben Tanfous , Manuel Graça , Sahadevan Seena","doi":"10.1016/j.aquatox.2025.107691","DOIUrl":"10.1016/j.aquatox.2025.107691","url":null,"abstract":"<div><div>Nanoplastics (NPs) are an emerging concern in freshwater ecosystems due to their persistence and potential to interact with persistent pollutants, such as metals. These combined stressors threaten freshwater ecosystems functioning, where leaf litter decomposition, primarily driven by aquatic hyphomycetes, supports energy transfer to higher trophic levels. A microcosm experiment was conducted to assess the joint impacts of polystyrene NPs (bare and carboxylated) at environmentally relevant (0.25 and 2.5 µg L⁻¹) and elevated (25 and 250 µg L⁻¹) concentrations in reference and metal-polluted stream waters. Fungal biomass, aquatic hyphomycetes sporulation and community composition, microbial leaf litter decomposition, as well as invertebrate feeding behaviour were quantified. Carboxylated NPs showed greater aggregation and surface alterations than bare NPs. Fungal biomass and sporulation declined significantly at 2.5 µg L⁻¹, with carboxylated NPs exerting stronger effects. Non-metric multidimensional scaling (NMDS) revealed clear shifts in fungal community structure across two water types (reference and metal-polluted) and NP concentrations. Metal pollution alone reduced decomposition by 17 %, with reductions reaching up to 24 % when combined with NPs, particularly carboxylated NPs. Invertebrate feeding was reduced by 27 % under metal pollution alone, with maximum inhibition (47 %) observed at the highest NP concentration, although NP type did not significantly alter feeding rates. Together, these results demonstrate that NPs, especially carboxylated forms, exacerbate the ecological impacts of metal pollution, impairing microbial processes and detritivore feeding. These findings underscore the importance of considering NPs surface chemistry and multiple stressors interactions in ecological risk assessments of polluted freshwater systems.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107691"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145796022","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.2025.107702
Jingjing Shi , Tianlie Luo , Zhuang Wang , Xi Ren , Yueyu Ran , Yuehan Peng , Guo Liu , Willie Peijnenburg
The liver plays a central role in xenobiotic metabolism and is consequently highly vulnerable to chemical-induced injury. Nevertheless, the mechanisms underlying diuron-induced hepatotoxicity remain poorly understood. Zebrafish (Danio rerio) were exposed to diuron at concentrations of 50 and 500 μg/L for 21 days, with subsequent analysis of the induced hepatotoxicity employing a combination of physiological, biochemical, and metabolomic techniques. Results showed that diuron significantly bioaccumulated in zebrafish, with bioconcentration factor (BCF) values ranging from 14.0 to 40.49 L/kg. Tissue distribution analysis indicated that the liver was the primary site of accumulation (491.48 ± 19.48 ng/g), while the brain also showed substantial accumulation (334.84 ± 10.90 ng/g) at an exposure concentration of 500 μg/L. Further examination of diuron metabolism in the liver identified 13 metabolites produced through demethylation, hydrolysis, oxidation, and C-N bond cleavage. These metabolic alterations correlated with histopathological damage, oxidative stress, and lipid peroxidation. Untargeted metabolomics further revealed a significant disruption in key metabolic pathways, particularly in arginine metabolism and the TCA cycle. Mechamistically, diuron-induced hepatotoxicity in zebrafish is characterized by the downregulation of key metabolites, namely gamma-Glutamyltyrosine, Leucylproline, and Malate, collectively contributing to the disruption of the tricarboxylic acid cycle alongside arachidonic acid, glutathione, and arginine metabolic pathways. These disturbances may represent the core mechanisms underlying hepatotoxicity. These findings will improve understanding of metabolic disorders in the liver and provide valuable insights into ecological risk assessments related to chemicals, and provide novel mechanistic insights into diuron induced hepatotoxicity.
{"title":"A metabolomics study unravels the hepatotoxic mechanism of diuron in zebrafish: Disruption of glutathione synthesis and mitochondrial energy metabolism","authors":"Jingjing Shi , Tianlie Luo , Zhuang Wang , Xi Ren , Yueyu Ran , Yuehan Peng , Guo Liu , Willie Peijnenburg","doi":"10.1016/j.aquatox.2025.107702","DOIUrl":"10.1016/j.aquatox.2025.107702","url":null,"abstract":"<div><div>The liver plays a central role in xenobiotic metabolism and is consequently highly vulnerable to chemical-induced injury. Nevertheless, the mechanisms underlying diuron-induced hepatotoxicity remain poorly understood. Zebrafish (<em>Danio rerio</em>) were exposed to diuron at concentrations of 50 and 500 μg/L for 21 days, with subsequent analysis of the induced hepatotoxicity employing a combination of physiological, biochemical, and metabolomic techniques. Results showed that diuron significantly bioaccumulated in zebrafish, with bioconcentration factor (BCF) values ranging from 14.0 to 40.49 L/kg. Tissue distribution analysis indicated that the liver was the primary site of accumulation (491.48 ± 19.48 ng/g), while the brain also showed substantial accumulation (334.84 ± 10.90 ng/g) at an exposure concentration of 500 μg/L. Further examination of diuron metabolism in the liver identified 13 metabolites produced through demethylation, hydrolysis, oxidation, and C-N bond cleavage. These metabolic alterations correlated with histopathological damage, oxidative stress, and lipid peroxidation. Untargeted metabolomics further revealed a significant disruption in key metabolic pathways, particularly in arginine metabolism and the TCA cycle. Mechamistically, diuron-induced hepatotoxicity in zebrafish is characterized by the downregulation of key metabolites, namely gamma-Glutamyltyrosine, Leucylproline, and Malate, collectively contributing to the disruption of the tricarboxylic acid cycle alongside arachidonic acid, glutathione, and arginine metabolic pathways. These disturbances may represent the core mechanisms underlying hepatotoxicity. These findings will improve understanding of metabolic disorders in the liver and provide valuable insights into ecological risk assessments related to chemicals, and provide novel mechanistic insights into diuron induced hepatotoxicity.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107702"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893692","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: 2025-12-03DOI: 10.1016/j.aquatox.2025.107672
Tiantian Chen , Jiaqi Chen , Wenlong Dong , Shuqun Song , Weijun Tian , Caiwen Li
As emerging contaminants, benzotriazole ultraviolet stabilizers (BUVSs) have been frequently detected in aquatic environments, which usually co-occur with heavy metals and cause complex toxicity to aquatic organisms. However, the specific role of BUVSs in the combined toxicity remains poorly understood. Herein, a harmful marine dinoflagellate Akashiwo sanguinea was used to explore the individual and combined toxicities of UV-234 and cadmium (Cd2+). Exposure to UV-234 at an environmental concentration (10 μg L−1) slightly inhibited algal growth (P > 0.05). Individual exposure to both low (1.77 mg L−1) and high (5.30 mg L−1) concentrations of Cd2+ significantly impaired algal photosynthesis by altering photosynthetic pigments, disrupting energy absorption, dissipation and trapping, reaction center activation, and electron transport, thereby inducing oxidative stress, and up-regulated pyruvate metabolism and the tricarboxylic acid cycle. Notably, co-exposure with UV-234 mitigated the toxic effects induced by Cd2+, and caused weaker inhibition of algal growth via inducing less substantial oxidative damage. These findings highlight the significant influence of UV-234 and Cd2+ co-exposure on marine dinoflagellates, providing new insights into the joint toxicity mechanisms and a scientific basis for environmental risk assessment of emerging BUVSs.
{"title":"Combined effects of benzotriazole ultraviolet stabilizers and cadmium on physiological performance of marine dinoflagellate Akashiwo sanguinea","authors":"Tiantian Chen , Jiaqi Chen , Wenlong Dong , Shuqun Song , Weijun Tian , Caiwen Li","doi":"10.1016/j.aquatox.2025.107672","DOIUrl":"10.1016/j.aquatox.2025.107672","url":null,"abstract":"<div><div>As emerging contaminants, benzotriazole ultraviolet stabilizers (BUVSs) have been frequently detected in aquatic environments, which usually co-occur with heavy metals and cause complex toxicity to aquatic organisms. However, the specific role of BUVSs in the combined toxicity remains poorly understood. Herein, a harmful marine dinoflagellate <em>Akashiwo sanguinea</em> was used to explore the individual and combined toxicities of UV-234 and cadmium (Cd<sup>2+</sup>). Exposure to UV-234 at an environmental concentration (10 μg L<sup>−1</sup>) slightly inhibited algal growth (<em>P</em> > 0.05). Individual exposure to both low (1.77 mg L<sup>−1</sup>) and high (5.30 mg L<sup>−1</sup>) concentrations of Cd<sup>2+</sup> significantly impaired algal photosynthesis by altering photosynthetic pigments, disrupting energy absorption, dissipation and trapping, reaction center activation, and electron transport, thereby inducing oxidative stress, and up-regulated pyruvate metabolism and the tricarboxylic acid cycle. Notably, co-exposure with UV-234 mitigated the toxic effects induced by Cd<sup>2+</sup>, and caused weaker inhibition of algal growth via inducing less substantial oxidative damage. These findings highlight the significant influence of UV-234 and Cd<sup>2+</sup> co-exposure on marine dinoflagellates, providing new insights into the joint toxicity mechanisms and a scientific basis for environmental risk assessment of emerging BUVSs.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107672"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145689956","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: 2025-11-29DOI: 10.1016/j.aquatox.2025.107661
Guixiang Wang , Jiangbing Qiu , Ruolin Wu , Aifeng Li , Ying Ji
The lipophilic phycotoxins gymnodimine-A (GYM-A) and okadaic acid (OA) are frequently detected in shellfish globally, posing a potential threat to human health through combined dietary exposure. Thus, this study aimed to evaluate the combined cytotoxicity of GYM-A and OA on Caco-2 cells and to elucidate their interactive mechanisms through analyses of calcium homeostasis, apoptosis, oxidative stress, DNA damage, and cell cycle arrest. The OA was 10 times more cytotoxic than GYM-A, as indicated by their respective IC₅₀ values. Notably, the combined exposure to both toxins resulted in a synergistic reduction in cell viability. Mechanistic investigations showed that both GYM-A and OA elevated intracellular calcium ion (Ca2+) levels and induced apoptosis, with GYM-A exerting a more pronounced pro-apoptotic effect. Moreover, OA significantly increased ROS accumulation, which was further amplified in the presence of low concentrations of GYM-A. Both toxins induced significant DNA damage, and greater damage was observed in the mixture group. While GYM-A had minimal influence on cell cycle progression, OA induced G2/M phase arrest, which was significantly exacerbated by co-exposure to GYM-A. Collectively, these findings demonstrated that co-exposure to both toxins exerted synergistic cytotoxicity in Caco-2 cells through the coordinated disruption of calcium homeostasis and oxidative stress, thereby inducing DNA damage and aggravating cell cycle arrest. This study provides mechanistic insights into the combined toxicity of marine phycotoxins and offers a foundation for future ecological risk assessment and exploration of potential biomedical applications of GYM-A and OA.
全球贝类中经常检测到亲脂藻毒素裸子氨基酚- a （gymnodimine-A）和冈田酸（OA），通过联合饮食暴露对人类健康构成潜在威胁。因此，本研究旨在通过对钙稳态、凋亡、氧化应激、DNA损伤和细胞周期阻滞的分析，评估GYM-A和OA对Caco-2细胞的联合细胞毒性，并阐明它们的相互作用机制。OA的细胞毒性是GYM-A的10倍，正如它们各自的IC₅0值所示。值得注意的是，两种毒素的联合暴露导致细胞活力的协同降低。机制研究表明，GYM-A和OA均能提高细胞内钙离子（Ca2+）水平并诱导细胞凋亡，其中GYM-A具有更明显的促凋亡作用。此外，OA显著增加了ROS的积累，在低浓度的GYM-A存在下，ROS的积累进一步增强。两种毒素均引起显著的DNA损伤，且混合毒素组损伤更大。虽然gyma对细胞周期进程的影响很小，但OA诱导G2/M期阻滞，共同暴露于gyma会显著加剧这种阻滞。总的来说，这些发现表明，共同暴露于这两种毒素通过协调破坏钙稳态和氧化应激，在Caco-2细胞中发挥协同细胞毒性，从而诱导DNA损伤并加重细胞周期阻滞。本研究提供了海洋藻毒素联合毒性的机制见解，并为未来的生态风险评估和探索gyma和OA的潜在生物医学应用奠定了基础。
{"title":"Synergistic cytotoxicity of gymnodimine-A and okadaic acid in Caco-2 cells through coordinated disruption of calcium homeostasis and oxidative stress","authors":"Guixiang Wang , Jiangbing Qiu , Ruolin Wu , Aifeng Li , Ying Ji","doi":"10.1016/j.aquatox.2025.107661","DOIUrl":"10.1016/j.aquatox.2025.107661","url":null,"abstract":"<div><div>The lipophilic phycotoxins gymnodimine-A (GYM-A) and okadaic acid (OA) are frequently detected in shellfish globally, posing a potential threat to human health through combined dietary exposure. Thus, this study aimed to evaluate the combined cytotoxicity of GYM-A and OA on Caco-2 cells and to elucidate their interactive mechanisms through analyses of calcium homeostasis, apoptosis, oxidative stress, DNA damage, and cell cycle arrest. The OA was 10 times more cytotoxic than GYM-A, as indicated by their respective IC₅₀ values. Notably, the combined exposure to both toxins resulted in a synergistic reduction in cell viability. Mechanistic investigations showed that both GYM-A and OA elevated intracellular calcium ion (Ca<sup>2+</sup>) levels and induced apoptosis, with GYM-A exerting a more pronounced pro-apoptotic effect. Moreover, OA significantly increased ROS accumulation, which was further amplified in the presence of low concentrations of GYM-A. Both toxins induced significant DNA damage, and greater damage was observed in the mixture group. While GYM-A had minimal influence on cell cycle progression, OA induced G2/M phase arrest, which was significantly exacerbated by co-exposure to GYM-A. Collectively, these findings demonstrated that co-exposure to both toxins exerted synergistic cytotoxicity in Caco-2 cells through the coordinated disruption of calcium homeostasis and oxidative stress, thereby inducing DNA damage and aggravating cell cycle arrest. This study provides mechanistic insights into the combined toxicity of marine phycotoxins and offers a foundation for future ecological risk assessment and exploration of potential biomedical applications of GYM-A and OA.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107661"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145613642","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: 2026-01-03DOI: 10.1016/j.aquatox.2026.107706
Marius Bidon , Takaya Saito , Kaja H. Skjaerven , Philip Antony Jesu Prabhu , Cécile Heraud , Jérôme Roy , Claudia Marchán-Moreno , Zoyne Pedrero-Zayas , Stéphanie Fontagné-Dicharry
Methylmercury (MeHg) is a pervasive neurotoxicant threatening aquatic ecosystems. Selenium (Se) has been reported to protect fish against the adverse MeHg toxicity, yet molecular investigations of their interaction in the brain remain scarce. This study investigated the molecular effects of dietary MeHg and whether organic Se, in the form of selenomethionine (SeMet), could mitigate MeHg-induced change in the brain of rainbow trout (Oncorhynchus mykiss). A 6-month feeding trial was conducted with diets containing low basal Se (0.3 mg/kg) and no mercury (Hg), supplemented with 2 mg Hg/kg diet as MeHg, alone or combined with 1.5 mg Se/kg diet as SeMet. Gene methylation (reduced representation bisulfite sequencing) and expression (RNA sequencing) were assessed, alongside biochemical quantification of DNA methylation-related metabolites (S-adenosylmethionine, SAM, and S-adenosylhomocysteine, SAH) and oxidative stress-related metabolites (reduced glutathione, GSH, and oxidized glutathione, GSSG). SeMet did not prevent MeHg-induced changes in SAM/SAH levels but mitigated MeHg-induced alterations in DNA methylation of genes related to the glutamatergic system, inflammation, and immune response. Transcriptomic analysis revealed antagonistic effects of MeHg and SeMet on energy metabolism pathways, with hypoxia-inducible factor 1 subunit alpha-like 2 identified as a potential key regulator. Although this molecular interaction may reflect SeMet-mediated attenuation of oxidative stress, biochemical data did not confirm changes in GSH/GSSG levels. These findings provide novel insights into the molecular mechanisms underlying MeHg neurotoxicity and its modulation by SeMet in fish brain, highlighting a potential protective role of organic Se against MeHg-induced molecular alterations.
{"title":"Selenomethionine mitigation of methylmercury-induced epigenetic and transcriptomic alterations in rainbow trout brain: A toxicogenomic survey","authors":"Marius Bidon , Takaya Saito , Kaja H. Skjaerven , Philip Antony Jesu Prabhu , Cécile Heraud , Jérôme Roy , Claudia Marchán-Moreno , Zoyne Pedrero-Zayas , Stéphanie Fontagné-Dicharry","doi":"10.1016/j.aquatox.2026.107706","DOIUrl":"10.1016/j.aquatox.2026.107706","url":null,"abstract":"<div><div>Methylmercury (MeHg) is a pervasive neurotoxicant threatening aquatic ecosystems. Selenium (Se) has been reported to protect fish against the adverse MeHg toxicity, yet molecular investigations of their interaction in the brain remain scarce. This study investigated the molecular effects of dietary MeHg and whether organic Se, in the form of selenomethionine (SeMet), could mitigate MeHg-induced change in the brain of rainbow trout (<em>Oncorhynchus mykiss</em>). A 6-month feeding trial was conducted with diets containing low basal Se (0.3 mg/kg) and no mercury (Hg), supplemented with 2 mg Hg/kg diet as MeHg, alone or combined with 1.5 mg Se/kg diet as SeMet. Gene methylation (reduced representation bisulfite sequencing) and expression (RNA sequencing) were assessed, alongside biochemical quantification of DNA methylation-related metabolites (S-adenosylmethionine, SAM, and S-adenosylhomocysteine, SAH) and oxidative stress-related metabolites (reduced glutathione, GSH, and oxidized glutathione, GSSG). SeMet did not prevent MeHg-induced changes in SAM/SAH levels but mitigated MeHg-induced alterations in DNA methylation of genes related to the glutamatergic system, inflammation, and immune response. Transcriptomic analysis revealed antagonistic effects of MeHg and SeMet on energy metabolism pathways, with <em>hypoxia-inducible factor 1 subunit alpha-like 2</em> identified as a potential key regulator. Although this molecular interaction may reflect SeMet-mediated attenuation of oxidative stress, biochemical data did not confirm changes in GSH/GSSG levels. These findings provide novel insights into the molecular mechanisms underlying MeHg neurotoxicity and its modulation by SeMet in fish brain, highlighting a potential protective role of organic Se against MeHg-induced molecular alterations.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107706"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893691","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: 2025-12-01DOI: 10.1016/j.aquatox.2025.107663
Sazal Kumar , Wayne A. O’Connor , Allison C. Luengen , Frederic D.L. Leusch , Steve D. Melvin , Chenglong Ji , Junfei Zhan , Geoff R. MacFarlane
In estuaries, aquatic organisms are often exposed to estrogenic endocrine disrupting chemicals (EEDCs), including 17β-estradiol (E2) and nonylphenol (NP), which affect physiology and metabolism. This study evaluated metabolic profiles of Sydney rock oysters (Saccostrea glomerata) using 1HNMR -based metabolomics after acute (14 days), pulse (14 days exposure followed by 14 days depuration), and chronic (28 days) exposure of E2 at 200 ng/L and NP at 5000 ng/L. Only acute exposure to both E2 and NP led to marked metabolic perturbations. Energy and stress-related metabolites including adenosine monophosphate, succinate, acetoacetate, and glutamate significantly increased in acute treatments compared to controls, suggesting heightened energy demand to cope with oxidative and osmotic stress. However, the metabolites from pulse and chronic exposure treatments were not significantly different from the control. Such responses highlight a time-dependent adaptation of molluscs, similar to depuration. E2 is expected to be more rapidly metabolised in molluscs than NP, leading to comparatively slower metabolic adaptation of molluscs to NP exposure. Finally, this study emphasizes that oysters have a time-dependent adaptive mechanism to cope with EEDC exposure.
{"title":"Acute disturbance, but chronic re-equilibration of the oyster metabolome to 17β-estradiol and nonylphenol exposure","authors":"Sazal Kumar , Wayne A. O’Connor , Allison C. Luengen , Frederic D.L. Leusch , Steve D. Melvin , Chenglong Ji , Junfei Zhan , Geoff R. MacFarlane","doi":"10.1016/j.aquatox.2025.107663","DOIUrl":"10.1016/j.aquatox.2025.107663","url":null,"abstract":"<div><div>In estuaries, aquatic organisms are often exposed to estrogenic endocrine disrupting chemicals (EEDCs), including 17β-estradiol (E2) and nonylphenol (NP), which affect physiology and metabolism. This study evaluated metabolic profiles of Sydney rock oysters (<em>Saccostrea glomerata</em>) using <sup>1</sup>HNMR -based metabolomics after acute (14 days), pulse (14 days exposure followed by 14 days depuration), and chronic (28 days) exposure of E2 at 200 ng/L and NP at 5000 ng/L. Only acute exposure to both E2 and NP led to marked metabolic perturbations. Energy and stress-related metabolites including adenosine monophosphate, succinate, acetoacetate, and glutamate significantly increased in acute treatments compared to controls, suggesting heightened energy demand to cope with oxidative and osmotic stress. However, the metabolites from pulse and chronic exposure treatments were not significantly different from the control. Such responses highlight a time-dependent adaptation of molluscs, similar to depuration. E2 is expected to be more rapidly metabolised in molluscs than NP, leading to comparatively slower metabolic adaptation of molluscs to NP exposure. Finally, this study emphasizes that oysters have a time-dependent adaptive mechanism to cope with EEDC exposure.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107663"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145650842","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: 2025-12-09DOI: 10.1016/j.aquatox.2025.107681
Tao Zhang , Biqing Wen , Xunjie Huo , Jiayuan Ren , Xuerui Ge , Xiaocong Chen
This study exposed female Portunus trituberculatus crabs (developmental stages III-IV) to microplastics (MPs) and bisphenol A (BPA) individually or combined for 21 days. Assessments included growth, histology, enzyme/gene expression, and metabolomics. Both MPs and BPA caused hepatopancreatic damage and lipid accumulation but via distinct mechanisms. MPs groups showed downregulated acetyl-CoA carboxylase (ACC) gene expression and upregulated fatty acid transport protein (FATP) genes, with reduced N-acetyl-d-glucosamine synthesis, suggesting disrupted energy metabolism (e.g., nucleotide sugar synthesis and ABC transport). BPA groups showed similarly downregulated ACC but upregulated FATP and Fatty Acid-Binding Protein (FABP) genes. Metabolomic shifts included decreased uric acid/prostaglandin F2α and increased glycochenodeoxycholic acid/inositol-1,3-bisphosphate, indicating estrogenic effects and hormonal imbalance. Combined exposure exacerbates hepatopancreatic injury and lipid metabolism disorders through complex mechanisms of action, highlighting heightened risks to aquatic ecosystems and potential human health impacts. The study underscores MPs and BPA as dual threats with unique and compounded toxicity pathways.
{"title":"Microplastics and bisphenol A exposure induce hepatopancreatic damage and lipid metabolism disorders in Portunus trituberculatus","authors":"Tao Zhang , Biqing Wen , Xunjie Huo , Jiayuan Ren , Xuerui Ge , Xiaocong Chen","doi":"10.1016/j.aquatox.2025.107681","DOIUrl":"10.1016/j.aquatox.2025.107681","url":null,"abstract":"<div><div>This study exposed female <em>Portunus trituberculatus</em> crabs (developmental stages III-IV) to microplastics (MPs) and bisphenol A (BPA) individually or combined for 21 days. Assessments included growth, histology, enzyme/gene expression, and metabolomics. Both MPs and BPA caused hepatopancreatic damage and lipid accumulation but via distinct mechanisms. MPs groups showed downregulated acetyl-CoA carboxylase (<em>ACC</em>) gene expression and upregulated fatty acid transport protein (<em>FATP</em>) genes, with reduced N-acetyl-<span>d</span>-glucosamine synthesis, suggesting disrupted energy metabolism (e.g., nucleotide sugar synthesis and ABC transport). BPA groups showed similarly downregulated <em>ACC</em> but upregulated <em>FATP</em> and Fatty Acid-Binding Protein (<em>FABP</em>) genes. Metabolomic shifts included decreased uric acid/prostaglandin F2α and increased glycochenodeoxycholic acid/inositol-1,3-bisphosphate, indicating estrogenic effects and hormonal imbalance. Combined exposure exacerbates hepatopancreatic injury and lipid metabolism disorders through complex mechanisms of action, highlighting heightened risks to aquatic ecosystems and potential human health impacts. The study underscores MPs and BPA as dual threats with unique and compounded toxicity pathways.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"291 ","pages":"Article 107681"},"PeriodicalIF":4.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145731137","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}
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