Aquatic Toxicology最新文献_第4页

Multilevel toxicological impacts of industrial settleable particulate matter in a freshwater crustacean, Macrobrachium rosenbergii 罗氏沼虾（Macrobrachium rosenbergii）中工业可沉降颗粒物的多级毒理学影响

IF 4.3 2区环境科学与生态学 Q1 MARINE & FRESHWATER BIOLOGY

Aquatic Toxicology

Pub Date : 2026-01-13 DOI: 10.1016/j.aquatox.2026.107714

Michelly Pereira Soares , Carolina Fernandes De Angelis , Ludmila Mendes Silva , Beatriz Helena Montanari , Iara da Costa Souza , Magdalena V. Monferrán , Daniel A. Wunderlin , Marisa Narciso Fernandes , Cléo Alcantara Costa Leite

As integral components of aquatic food webs, crustaceans serve as pivotal conduits for energy transfer and sensitive bioindicators of environmental quality. This study characterizes the toxicological consequences of settleable atmospheric particulate matter (SePM)—a byproduct of industrial iron-ore processing—utilizing the freshwater shrimp Macrobrachium rosenbergii as a model organism. Experimental exposure demonstrated that SePM significantly enhances the aqueous solubility of both conventional (Fe, Al, Zn, Cu, Mn) and emergent (Cr, Ni, Sr, Sn, La, Ce) metals, establishing it as a potent vector for multi-elemental contamination. Exposed individuals bioaccumulated 24 metals, with predominant enrichment of Fe, Ba, Sr, Cu, and Zn; these accumulation profiles were modulated by both external concentration and element-specific uptake kinetics. Notably, ultrastructural characterization revealed significant metal sequestration within the exoskeleton, identifying an incidental pathway for contaminant cycling through discarded carapaces (ecdysis). Biochemical assessments indicated impairment of redox homeostasis, characterized by the exhaustion of enzymatic (CAT, SOD, GPx, GST) and non-enzymatic (GSH) defenses, alongside elevated lipid peroxidation and DNA strand breaks. While bioaccumulation had a dose-dependent progression, oxidative distress was manifest even at the lowest exposure levels, underscoring that the toxicity of SePM as a complex mixture cannot be accurately predicted by the additive impacts of its individual constituents. These findings highlight SePM as a critical, yet largely overlooked, driver of air-to-water cross-contamination. Our results underscore the urgent need to incorporate such atmospheric deposition into environmental monitoring frameworks and to expand regulatory criteria to address emergent metals and potential synergistic effects of metallic mixtures.

甲壳类动物是水生食物网的重要组成部分，是能量传递的重要通道，也是环境质量的敏感生物指标。本研究利用罗氏沼虾（Macrobrachium rosenbergii）作为模式生物，描述了可沉降大气颗粒物（SePM）的毒理学后果，SePM是工业铁矿石加工的副产品。实验表明，SePM显著增强了传统金属（Fe、Al、Zn、Cu、Mn）和新兴金属（Cr、Ni、Sr、Sn、La、Ce）的水溶性，使其成为多元素污染的有效载体。暴露个体生物积累了24种金属，以Fe、Ba、Sr、Cu和Zn富集为主；这些积累曲线受到外部浓度和元素特异性摄取动力学的调节。值得注意的是，超微结构表征揭示了外骨骼内显著的金属隔离，确定了污染物通过废弃甲壳循环的偶然途径（蜕皮）。生化评估显示氧化还原稳态受损，其特征是酶（CAT、SOD、GPx、GST）和非酶（GSH）防御衰竭，同时脂质过氧化和DNA链断裂升高。虽然生物积累具有剂量依赖的进展，但即使在最低暴露水平下，氧化应激也很明显，这强调了SePM作为复杂混合物的毒性不能通过其单个成分的加性影响来准确预测。这些发现强调了SePM是空气-水交叉污染的一个关键因素，但在很大程度上被忽视了。我们的研究结果强调，迫切需要将这种大气沉降纳入环境监测框架，并扩大监管标准，以解决新兴金属和金属混合物的潜在协同效应。

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引用次数: 0

Hepatic toxicity induced by exposure to glyphosate/aminomethylphosphonic acid and oxytetracycline alone or in combination in zebrafish: A novel mechanism of the gut-liver axis 斑马鱼暴露于草甘膦/氨基甲基膦酸和土霉素单独或联合引起的肝毒性：肠-肝轴的新机制

IF 4.3 2区环境科学与生态学 Q1 MARINE & FRESHWATER BIOLOGY

Aquatic Toxicology

Pub Date : 2026-01-12 DOI: 10.1016/j.aquatox.2026.107713

Junyue Zheng , Chen Wang , Miaomiao Teng , Tong Li , Jiazhen Jiang , Xiangguang Chen , Fengchang Wu

Glyphosate (Gly) is the most commonly used herbicide in the world. Glyphosate and its main degradation product, aminomethylphosphonic acid (AMPA), are often detected in aquatic environments and may pose a threat to the health of aquatic organisms. It is well established that Gly is mainly enriched in the intestine and degraded into AMPA. However, it remains unclear whether they disrupt the gut microbiota and cause liver health effects, as well as whether they have a synergistic effect with antibiotics. We investigated herein the effects of zebrafish exposure to Gly, AMPA and oxytetracycline (OTC) alone or in combination on the gut-liver axis. Our results suggest that Gly, AMPA, and OTC induce lipid accumulation, inflammatory response and oxidative damage in the liver, which is associated with a higher Firmicutes/Bacteroidetes ratio in the intestine and a higher levels of lipopolysaccharide in serum. Compared with the single exposure groups (OTC, Gly, and AMPA), the toxic effects of the gut-liver axis were more severe in the combined exposure groups (Gly+OTC, AMPA+OTC). Our results indicate that the health risks posed by Gly, AMPA and OTC through the gut microbiota of aquatic organisms are a neglected hot spots.

草甘膦（Gly）是世界上最常用的除草剂。草甘膦及其主要降解产物氨基甲基膦酸（AMPA）经常在水生环境中被检测到，并可能对水生生物的健康构成威胁。已经确定Gly主要富集于肠道并降解为AMPA。然而，目前尚不清楚它们是否会破坏肠道微生物群并导致肝脏健康影响，以及它们是否与抗生素有协同作用。本文研究了斑马鱼单独或联合暴露于Gly、AMPA和土霉素（OTC）对肠-肝轴的影响。我们的研究结果表明，Gly、AMPA和OTC诱导肝脏脂质积累、炎症反应和氧化损伤，这与肠道中厚壁菌门/拟杆菌门比例升高和血清中脂多糖水平升高有关。与单一暴露组（OTC、Gly、AMPA）相比，联合暴露组（Gly+OTC、AMPA+OTC）的肠肝轴毒性作用更为严重。我们的研究结果表明，Gly、AMPA和OTC通过水生生物肠道菌群构成的健康风险是一个被忽视的热点。

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引用次数: 0

Integrative proteomics and metabolomics approach to elucidate the multi-organ developmental toxicity of decabromodiphenyl ethane in zebrafish larvae 综合蛋白质组学和代谢组学方法研究十溴二苯乙烷对斑马鱼幼体多器官发育毒性

IF 4.3 2区环境科学与生态学 Q1 MARINE & FRESHWATER BIOLOGY

Aquatic Toxicology

Pub Date : 2026-01-12 DOI: 10.1016/j.aquatox.2026.107712

Ruiyang Zhang , Yue Zhang , Jinglong Xue , Ruxuan Zhang , Junhong Xie , Xinyue Luo , Xi Yang , Hongou Wang , Jianhui Liu , Jialiu Wei , Xianqing Zhou

Decabromodiphenyl ethane (DBDPE), as the novel brominated flame retardant, has been frequently detected in aquatic environments worldwide and has been confirmed to be harmful to aquatic organisms. Previous studies have mostly inferred potential damage to specific organs based on abnormal behaviors in zebrafish, but the multi-organ cross-toxicity of DBDPE and its underlying mechanisms remain to be elucidated. In this study, zebrafish (Danio rerio) embryos were exposed to DBDPE at concentrations of 5, 50, and 500 μg/L for 120 h. The results showed that DBDPE impaired embryonic development, causing cardiotoxicity, neurotoxicity, and visual toxicity. DBDPE induced excessive production of reactive oxygen species (ROS), accumulation of malondialdehyde (MDA), and depletion of glutathione (GSH), which in turn triggered phosphatidylethanolamine (PE) accumulation and ferroptosis-related proteins (ceruloplasmin, heme oxygenase 1, and autophagy-related protein 5) downregulation, accompanied by cardiac developmental abnormalities such as pericardial edema, increased heart rate, and prolonged sinoatrial-atrioventricular (SV-BA) distance. Beyond its cardiac effects, DBDPE exposure induced distinct neurotoxicity, including anxiety and aggression. Mechanistically, DBDPE directly interfered with lysophosphatidylcholine (LysoPC) metabolism and disrupted the normal localization of metabotropic glutamate receptor 5 (mGluR5), leading to neurobehavioral abnormalities. In addition, the phenomenon of ocular protrusion may be related to abnormal expression of retinol dehydrogenase 12 (RDH12) and glucuronosyltransferase (UGT1B2), key factors in retinol metabolism. This study firstly showed that DBDPE's multi-organ developmental toxicity is driven by an interconnected metabolic-protein network, which not only significantly advances the understanding of the complex toxic mechanisms of DBDPE, but also lays a solid scientific foundation for accurate environmental risk assessment and early health warning of such emerging pollutants.

十溴联苯乙烷（DBDPE）是一种新型的溴化阻燃剂，在世界范围内的水生环境中被频繁检测到，并已被证实对水生生物有害。以往的研究大多基于斑马鱼的异常行为推断其对特定器官的潜在损害，但DBDPE的多器官交叉毒性及其潜在机制仍有待阐明。在本研究中，斑马鱼（Danio rerio）胚胎暴露于浓度为5、50和500 μg/L的DBDPE中120小时。结果表明，DBDPE损害胚胎发育，引起心脏毒性、神经毒性和视觉毒性。DBDPE诱导活性氧（ROS）的过量产生、丙二醛（MDA）的积累和谷胱甘肽（GSH）的消耗，进而引发磷脂酰乙醇胺（PE）的积累和铁中毒相关蛋白（铜蓝蛋白、血红素加氧酶1和自噬相关蛋白5）的下调，并伴有心包水肿、心率增加和心房-房室（SV-BA）距离延长等心脏发育异常。除了对心脏的影响，DBDPE暴露还会引起明显的神经毒性，包括焦虑和攻击。机制上，DBDPE直接干扰溶血磷脂酰胆碱（LysoPC）代谢，破坏代谢性谷氨酸受体5 （mGluR5）的正常定位，导致神经行为异常。此外，眼球突出现象可能与视黄醇代谢关键因子视黄醇脱氢酶12 （RDH12）和葡萄糖醛基转移酶（UGT1B2）表达异常有关。本研究首次揭示了DBDPE的多器官发育毒性是由一个相互关联的代谢-蛋白质网络驱动的，这不仅显著推进了对DBDPE复杂毒性机制的认识，也为这类新兴污染物的准确环境风险评估和早期健康预警奠定了坚实的科学基础。

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引用次数: 0

Advances in three-dimensional fish cell models for aquatic toxicology 三维鱼类细胞模型在水生毒理学研究中的进展

IF 4.3 2区环境科学与生态学 Q1 MARINE & FRESHWATER BIOLOGY

Aquatic Toxicology

Pub Date : 2026-01-10 DOI: 10.1016/j.aquatox.2026.107711

Ping-Ping Zhang , Chong-Rui Yao , Wen-Jun Shi , Ting Xu , Guang-Guo Ying

Aquatic ecosystems are increasingly threatened by diverse environmental pollutants, such as pharmaceuticals, personal care products, and persistent organic contaminants. While traditional in vivo fish models and two-dimensional (2D) cell cultures provide valuable mechanistic insights, they are limited by ethical concerns and insufficient ecological relevance. In contrast, three-dimensional (3D) fish cell culture systems, including spheroids, organoids, and organ-on-a-chip platforms, have been established as powerful tools in toxicology. These advanced models more accurately replicate native tissue architecture, maintain metabolic functions over extended periods, and facilitate long-term exposure studies, thereby enabling a comprehensive assessment of pollutant toxicity, bioaccumulation potential, and toxic mechanisms. The efficacy of 3D systems has been demonstrated in recent applications for evaluating endocrine-disrupting effects, pharmaceutical metabolism, host-pathogen interactions, and the chronic effects of organic pollutants. Notably, these models exhibit superior predictive capacity compared to conventional 2D assays. Despite significant advancements, challenges remain in standardizing protocols across fish species, improving analytical compatibility, and ensuring long-term culture stability. Advancing these innovative models through interdisciplinary collaboration will promote their integration into ecotoxicological testing and ecological risk assessment. Such progress is essential to support global initiatives aimed at advancing animal-free toxicology.

水生生态系统日益受到各种环境污染物的威胁，如药品、个人护理产品和持久性有机污染物。虽然传统的体内鱼模型和二维（2D）细胞培养提供了有价值的机制见解，但它们受到伦理问题和生态相关性不足的限制。相比之下，三维（3D）鱼细胞培养系统，包括球体、类器官和芯片上的器官平台，已经成为毒理学研究的有力工具。这些先进的模型更准确地复制了天然组织结构，在较长时间内维持代谢功能，并促进了长期暴露研究，从而能够全面评估污染物的毒性、生物蓄积潜力和毒性机制。3D系统的有效性已在最近的应用中得到证明，用于评估内分泌干扰效应、药物代谢、宿主-病原体相互作用和有机污染物的慢性效应。值得注意的是，与传统的二维分析相比，这些模型表现出优越的预测能力。尽管取得了重大进展，但在标准化鱼类协议、提高分析兼容性和确保长期培养稳定性方面仍然存在挑战。通过跨学科合作推进这些创新模型将促进它们与生态毒理学测试和生态风险评估的整合。这种进展对于支持旨在推进无动物毒理学的全球倡议至关重要。

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引用次数: 0

Crosstalk with the cholinergic pathway may be responsible for chlorpyrifos-induced reproductive toxicity in fish 与胆碱能通路的串扰可能是毒死蜱引起鱼类生殖毒性的原因

IF 4.3 2区环境科学与生态学 Q1 MARINE & FRESHWATER BIOLOGY

Aquatic Toxicology

Pub Date : 2026-01-09 DOI: 10.1016/j.aquatox.2026.107710

Aoxue Wang , Yujia Yan , Yuyao Jiang , Yanru Guan , Zexin Wen , Shengli Zhou , Yanmei Xu , Haisong Cui , Miqi Jin , Wenjun Gui , Shuying Li

Chlorpyrifos (CPF), a commonly applied organophosphate insecticide, is known to disrupt the endocrine systems of aquatic species. However, further research is required to elucidate the molecular mechanisms involved in the reproductive toxicity of fish. In the present study, zebrafish were exposed to environmentally relevant concentrations of CPF (1, 10, and 50 μg/L) for a 21-day period. Within the concentration range at which chlorpyrifos significantly inhibits the activity of acetylcholinesterase in zebrafish, there is a significant decrease in reproductive capacity of 31.65 %. The RNA-seq analysis has revealed that processes such as transporter activity, reproduction, and reproductive function are affected. Elevated FSH and LH levels in CPF-exposed females were observed at concentrations of 10 μg/L and 50 μg/L. Furthermore, the CPF treatment resulted in the upregulation of esr2b, hsd3b1, fshr, gnrh2, vtg1, and vtg2, while cyp19a1a was found to be downregulated. Co-exposure to cetrorelix acetate, a potent GnRH receptor antagonist, has been demonstrated to normalize gene expression and restore E₂ levels. These results suggest that CPF-induced reproductive toxicity involves crosstalk between cholinergic signaling and the HPG axis. These findings underscore the complex toxicity and ecological risks associated with CPF.

毒死蜱（CPF）是一种常用的有机磷杀虫剂，已知会破坏水生物种的内分泌系统。然而，还需要进一步的研究来阐明鱼类生殖毒性的分子机制。在本研究中，斑马鱼暴露于环境相关浓度的CPF（1、10和50 μg/L）中21天。在毒死蜱显著抑制斑马鱼乙酰胆碱酯酶活性的浓度范围内，斑马鱼的繁殖能力显著下降31.65%。RNA-seq分析揭示了转运蛋白活性、繁殖和生殖功能等过程受到影响。cpf暴露的雌性在浓度为10 μg/L和50 μg/L时FSH和LH水平升高。此外，CPF处理导致esr2b、hsd3b1、fshr、gnrh2、vtg1和vtg2上调，而cyp19a1a下调。共同暴露于醋酸cetrorelix（一种有效的GnRH受体拮抗剂）已被证明可以使基因表达正常化并恢复E2水平。这些结果表明cpf诱导的生殖毒性涉及胆碱能信号和HPG轴之间的串扰。这些发现强调了CPF相关的复杂毒性和生态风险。

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引用次数: 0

Sex-specific differences are shown in western mosquitofish (Gambusia affinis) following life cycle exposure to steroid compounds 在西方食蚊鱼（Gambusia affinis）的生命周期暴露于类固醇化合物后，显示出性别特异性差异

IF 4.3 2区环境科学与生态学 Q1 MARINE & FRESHWATER BIOLOGY

Aquatic Toxicology

Pub Date : 2026-01-05 DOI: 10.1016/j.aquatox.2026.107708

Chen-Si Wang , Guo-Yong Huang , Dong-Qiao Lei , Guang-Guo Ying

Steroid hormones, such as androstadienedione (ADD), androstenedione (AED), and estrone (E1), are widespread and persistent in various aquatic environments. However, their combined effects on aquatic organisms remain poorly understood. In this study, western mosquitofish (Gambusia affinis) were exposed throughout their life cycle to low and high concentrations of ADD (100 and 10000 ng/L), AED (100 and 10000 ng/L), E1 (100 and 5000 ng/L), and binary mixtures of each androgen (ADD or AED) with E1 at their respective low and high concentrations. The effects of these treatments on sex ratio, condition factors, gonadal development, sexual dimorphism, and hypothalamic-pituitary-gonadal-liver axis-related gene transcription were assessed. A high concentration of ADD or AED significantly increased male-biased sex ratios (1.2-fold increase); however, this effect was attenuated in combination with a high concentration of E1. Notably, in males, a high concentration of ADD acted synergistically with E1, increasing the proportion of immature spermatocytes and downregulating amh transcriptional expression, thereby exacerbating testicular damage and reproductive toxicity. In contrast, in females, ADD or AED may antagonize E1, reducing oocyte degeneration rates and mitigating steroid-mediated disruption in fish. Overall, exposure to these hormones, whether alone or in combination, impairs gene expression and gonad development in G. affinis, but these effects exhibit sex-specific differences. These findings highlight the complex and sex-specific nature of endocrine disruption caused by steroid hormone mixtures in aquatic environments.

类固醇激素，如雄甾二酮（ADD）、雄甾二酮（AED）和雌酮（E1），在各种水生环境中广泛存在并持续存在。然而，它们对水生生物的综合影响仍然知之甚少。本研究将西食蚊鱼（Gambusia affinis）一生暴露于低浓度和高浓度的ADD（100和10000 ng/L）、AED（100和10000 ng/L）、E1(100和5000 ng/L)，以及每种雄激素（ADD或AED）与E1在各自的低浓度和高浓度的混合物中。评估这些治疗对性别比、病情因素、性腺发育、两性二态性和下丘脑-垂体-性腺-肝轴相关基因转录的影响。高浓度的ADD或AED显著增加了男性偏倚性比率（增加1.2倍）；然而，与高浓度E1结合后，这种作用减弱。值得注意的是，在雄性中，高浓度的ADD与E1协同作用，增加未成熟精母细胞的比例，下调amh的转录表达，从而加剧睾丸损伤和生殖毒性。相反，在雌性中，ADD或AED可以拮抗E1，降低卵母细胞变性率，减轻类固醇介导的破坏。总的来说，暴露在这些激素中，无论是单独的还是联合的，都会损害G. affinis的基因表达和性腺发育，但这些影响表现出性别特异性差异。这些发现强调了水生环境中类固醇激素混合物引起的内分泌干扰的复杂性和性别特异性。

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引用次数: 0

Zebrafish Abcg2a mutant line as an in vivo model for evaluation of the interaction of Abcg2a with drugs and contaminants 以斑马鱼Abcg2a突变系为体内模型，评价Abcg2a与药物和污染物的相互作用

IF 4.3 2区环境科学与生态学 Q1 MARINE & FRESHWATER BIOLOGY

Aquatic Toxicology

Pub Date : 2026-01-05 DOI: 10.1016/j.aquatox.2026.107709

Jovica Lončar , Roko Žaja , Ivan Mihaljević , Jelena Dragojević Višević , Lana Vujica , Marin Kutnjak , Cecile Otten , Tvrtko Smital

As a member of the ABC transporter superfamily, ABCG2 is a half transporter that mediates the translocation of various xenobiotic substrates across cell membranes, playing an essential role in cellular detoxification. With the aim of developing a reliable in vivo model to study the role of ABCG2 and its interaction with drugs and environmental contaminants, in this study we used the CRISPR/Cas9 gene-editing technology to develop a zebrafish (Danio rerio) Abcg2a mutant line. The generated Abcg2a mutants developed normally to adulthood with no visible phenotype changes, abcg2a gene expression was reduced by more than 90% in the mutant larvae up to 5 days-post-fertilization, and overexpression of transcripts of functionally related ABC genes was detected in three out of eight monitored genes. The accumulation pattern of the specific Abcg2 fluorescent substrate pheophorbide A differed between mutants and wildtypes with a dominant signal in the gallbladder and intestine, respectively. Upon exposure to the model toxicants MLN7243 and mitoxantrone, the mutant larvae showed increased mortality compared to the wildtypes. The addition of the specific inhibitor Ko143 increased the mortality rate of the wildtype larvae to that of the mutants, indicating that the protective effect of Abcg2a had been abolished. The developed Abcg2a mutant line could be used as a reliable in vivo model in both pharmacology and ecotoxicology to further elucidate the function of Abcg2a in different tissues and cell compartments and to better understand the interaction of Abcg2a with different physiological or xenobiotic compounds.

作为ABC转运蛋白超家族的一员，ABCG2是一种半转运蛋白，可介导各种外源底物跨细胞膜的易位，在细胞解毒中发挥重要作用。为了建立可靠的体内模型来研究ABCG2的作用及其与药物和环境污染物的相互作用，本研究采用CRISPR/Cas9基因编辑技术构建了斑马鱼（Danio rerio） Abcg2a突变系。产生的Abcg2a突变体正常发育至成年，没有明显的表型变化，在受精后5天，突变体幼虫的Abcg2a基因表达减少了90%以上，8个监测基因中有3个检测到功能相关的ABC基因转录物过表达。特异的Abcg2荧光底物嗜磷素A的积累模式在突变型和野生型之间存在差异，分别在胆囊和肠道中具有显性信号。暴露于模型毒物MLN7243和米托蒽醌后，突变幼虫的死亡率高于野生型。特异性抑制剂Ko143的加入使野生型幼虫的死亡率高于突变体，表明Abcg2a的保护作用已经被消除。构建的Abcg2a突变系可作为可靠的体内模型，在药理学和生态毒理学上进一步阐明Abcg2a在不同组织和细胞区室中的功能，更好地了解Abcg2a与不同生理或外源化合物的相互作用。

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引用次数: 0

Selenomethionine mitigation of methylmercury-induced epigenetic and transcriptomic alterations in rainbow trout brain: A toxicogenomic survey 硒代蛋氨酸缓解甲基汞诱导虹鳟鱼脑的表观遗传和转录组改变：一项毒性基因组学调查

IF 4.3 2区环境科学与生态学 Q1 MARINE & FRESHWATER BIOLOGY

Aquatic Toxicology

Pub Date : 2026-01-03 DOI: 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.

甲基汞（MeHg）是一种普遍存在的神经毒物，威胁着水生生态系统。据报道，硒（Se）可以保护鱼类免受甲基汞的不良毒性，但它们在大脑中相互作用的分子研究仍然很少。本研究旨在研究饲料中甲基汞的分子效应，以及硒代蛋氨酸（SeMet）形式的有机硒是否能减轻甲基汞在虹鳟鱼（Oncorhynchus mykiss）脑内引起的变化。试验采用低基础硒（0.3 mg/kg）、无汞（Hg）饲粮，以2 mg Hg/kg饲粮为MeHg，单独或与1.5 mg Se/kg饲粮联合作为SeMet，饲喂6个月。评估基因甲基化（亚硫酸盐还原测序）和表达（RNA测序），以及DNA甲基化相关代谢物（s-腺苷蛋氨酸，SAM和s-腺苷同型半胱氨酸，SAH）和氧化应激相关代谢物（还原性谷胱甘肽，GSH和氧化性谷胱甘肽，GSSG）的生化定量。SeMet不能阻止mehg诱导的SAM/SAH水平的变化，但减轻了mehg诱导的与谷氨酸系统、炎症和免疫反应相关的基因DNA甲基化的改变。转录组学分析显示MeHg和SeMet对能量代谢途径具有拮抗作用，其中缺氧诱导因子1亚基α样2被确定为潜在的关键调节因子。虽然这种分子相互作用可能反映了semet介导的氧化应激衰减，但生化数据并未证实GSH/GSSG水平的变化。这些发现为甲基汞神经毒性的分子机制及其在鱼脑中由SeMet调节提供了新的见解，强调了有机硒对甲基汞诱导的分子改变的潜在保护作用。

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引用次数: 0

Environmentally relevant 6PPD-quinone drives personality-specific behavioral abnormalities in juvenile grouper through interplay between neuroinflammation and gut microbial dysbiosis 环境相关的6ppd醌通过神经炎症和肠道微生物生态失调之间的相互作用驱动幼石斑鱼个性特异性行为异常

IF 4.3 2区环境科学与生态学 Q1 MARINE & FRESHWATER BIOLOGY

Aquatic Toxicology

Pub Date : 2026-01-03 DOI: 10.1016/j.aquatox.2026.107707

Liuqingqing Liu , Wenting Zhao , Xianxiang Luo , Xiuhui Tan , Linjia Liu , Liyan Huang , Zixi Yuan , Zhiying Li , Fengmin Li , Hao Zheng

The lethal impacts of N-(1,3-dimethylbutyl)-N’-phenyl-p-phenylenediamine-quinone (6PPD-Q), a transformation product of tire wear antioxidant 6PPD, on salmonids pose great threats to “Ocean Health” within One Health frame. However, its sublethal effects on non-sensitive fish, especially the behaviors and the underlying mechanisms, remain poorly understood. Therefore, juvenile pearl gentian grouper (♀Epinephelus fuscoguttatus × ♂Epinephelus lanceolatus), one of the ecologically and economically important marine species, was selected to compare the effects of 6PPD-Q and 6PPD at an environmentally relevant concentration (10 µg L^-1) on the personality behaviors and brain-gut axis regulation mechanism. After 30 days of exposure, 6PPD-Q significantly reduced the time spent in the thigmotaxis zone and locomotor activity by 19.40% and 14.03%, respectively, while 6PPD showed little effect, indicating that 6PPD-Q increased risk-taking propensity and decreased activity, thereby disrupting personality behavioral homeostasis in the non-sensitive fish. Mechanistically, 6PPD-Q exposure mediated the neurotoxic effects through inducing persistent neuroinflammatory responses, increasing blood-brain barrier permeability, and decreasing neuronal activity. These neurotoxic effects were associated with the downregulated DNA damage repair gene (gadd45ba) and anti-inflammatory regulator (dusp1). In parallel, 6PPD-Q impaired intestinal physicochemical barrier integrity, reduced beneficial bacteria (e.g., Muribaculaceae) and enriched pathogenic bacteria (e.g., Nautella), thereby disturbing gut microbial homeostasis and brain–gut axis regulation. From “brain–gut” axis perspective, this study elucidated the mechanisms by which 6PPD-Q at environmentally relevant concentration disrupts personality behavioral balance in non-sensitive marine fish, providing new insight for ecological risk assessment and early warning of emerging tire-derived contaminants in marine ecosystems.

轮胎磨损抗氧化剂6PPD的转化产物N-（1,3-二甲基丁基）-N ' -苯基-对苯二胺醌（6PPD- q）对鲑鱼的致命影响对One Health框架内的“海洋健康”构成了巨大威胁。然而，其对非敏感鱼类的亚致死效应，特别是其行为和潜在机制仍知之甚少。因此，本研究选择具有重要生态和经济意义的海洋物种之一——龙胆石斑鱼幼鱼（♀Epinephelus fuscoguttatus ×♂Epinephelus lanceolatus），比较6PPD- q和环境相关浓度（10µg L-1） 6PPD对其人格行为和脑肠轴调节机制的影响。暴露30天后，6PPD- q显著减少了移动性区和运动活动的时间，分别减少了19.40%和14.03%，而6PPD作用不大，说明6PPD- q增加了冒险倾向，减少了活动，从而破坏了非敏感鱼的人格行为稳态。在机制上，6PPD-Q暴露通过诱导持续的神经炎症反应、增加血脑屏障通透性和降低神经元活性来介导神经毒性作用。这些神经毒性作用与下调的DNA损伤修复基因（gadd45ba）和抗炎调节剂（dusp1）有关。同时，6PPD-Q破坏肠道物理化学屏障完整性，减少有益菌（如Muribaculaceae），丰富致病菌（如Nautella），从而扰乱肠道微生物稳态和脑肠轴调节。本研究从“脑肠”轴的角度，阐明了环境相关浓度下6PPD-Q破坏非敏感海洋鱼类人格行为平衡的机制，为海洋生态系统中新出现的轮胎衍生污染物的生态风险评估和预警提供了新的视角。

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引用次数: 0

A metabolomics study unravels the hepatotoxic mechanism of diuron in zebrafish: Disruption of glutathione synthesis and mitochondrial energy metabolism 代谢组学研究揭示了diuron对斑马鱼的肝毒性机制：破坏谷胱甘肽合成和线粒体能量代谢

IF 4.3 2区环境科学与生态学 Q1 MARINE & FRESHWATER BIOLOGY

Aquatic Toxicology

Pub Date : 2026-01-02 DOI: 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.

肝脏在外源代谢中起着核心作用，因此极易受到化学物质引起的损伤。然而，二恶龙引起肝毒性的机制仍然知之甚少。将斑马鱼（Danio rerio）暴露在浓度为50和500 μg/L的diuron环境中21天，随后采用生理、生化和代谢组学相结合的方法分析其诱导的肝毒性。结果表明，在斑马鱼体内，diuron具有显著的生物蓄积性，生物富集系数（BCF）在14.0 ~ 40.49 L/kg之间。组织分布分析表明，暴露浓度为500 μg/L时，肝脏为主要蓄积部位（491.48±19.48 ng/g），脑组织也有大量蓄积（334.84±10.90 ng/g）。进一步检查狄乌隆在肝脏中的代谢，鉴定出13种代谢物通过去甲基化、水解、氧化和C-N键裂解产生。这些代谢改变与组织病理损伤、氧化应激和脂质过氧化有关。非靶向代谢组学进一步揭示了关键代谢途径的显著破坏，特别是精氨酸代谢和TCA循环。从机制上说，二乌龙诱导的斑马鱼肝毒性的特点是下调关键代谢物，即γ -谷氨酰基酪氨酸、赖氨酸和苹果酸，共同促进三羧酸循环与花生四烯酸、谷胱甘肽和精氨酸代谢途径的破坏。这些紊乱可能是肝毒性的核心机制。这些发现将提高对肝脏代谢紊乱的认识，为化学物质相关的生态风险评估提供有价值的见解，并为迪乌隆诱导的肝毒性提供新的机制见解。

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引用次数: 0