Aquatic Toxicology最新文献_第5页

Comparative study on the reproduction toxicity of N-(1,3-dimethylbutyl)-N′-phenyl-p-phenylenediamine (6PPD) to Daphnia magna based on a 21-day short-term exposure and whole-life-stage exposure and the underlying toxic mechanisms N-（1,3-二甲基丁基）-N ' -苯基-对苯二胺（6PPD）对大水蚤21天短期和终生暴露生殖毒性的比较研究及其潜在毒性机制

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

Aquatic Toxicology

Pub Date : 2025-11-09 DOI: 10.1016/j.aquatox.2025.107640

Liu Yang , Xue Tang , Yongsheng Zhou , Shiniu Dai , Kexin Liu , Lina Shi , Xinli Wen

A common tire additive of N-(1,3-dimethylbutyl)-N′-phenyl-p-phenylenediamine (6PPD) is frequently detected in freshwater. To date, the toxicity of 6PPD to aquatic organisms has mainly been based on partial life-cycle test results. However, it remains unclear whether this approach leads to an underestimation of the true environmental risk of 6PPD. Here, the effects of environmentally relevant or greater concentrations of 6PPD on the reproduction and growth of Daphnia magna were specifically compared between day 21 and the day all the maternal daphnia died, with the underlying toxic mechanisms of 6PPD also explored. 6PPD at environmental or near-natural water concentrations (5.68 and/or 9.20 µg/L) significantly decreased the total number of offspring and net reproductive rate after whole-life-stage exposure. However, such adverse effects were not observed on day 21, indicating that environmental levels of 6PPD exerted reproductive toxicity on D. magna, and short-term exposure may underestimate the environmental risk of 6PPD. Elevated malondialdehyde levels in the 5.68, 9.20 and 44.58 µg/L treatment groups, coupled with reactive oxygen species (ROS) emerging as the dominant contributors to the biomarker response index, indicated that ROS overproduction induced by 6PPD triggered lipid peroxidation despite antioxidant capacity was enhanced. Downregulation of the vitellogenin expression in D. magna exposed to 5.68, 9.2 and 44.58 µg/L 6PPD, likely resulting from competitive binding to ecdysteroid receptor based on molecular docking and molecular dynamics simulation, might compromise nutrient provisioning during embryogenesis. Coupled with oxidative stress, these dual mechanisms appeared to mediate 6PPD-induced reproductive toxicity.

常见的轮胎添加剂N-（1,3-二甲基丁基）-N ' -苯基-对苯二胺（6PPD）在淡水中经常被检测到。迄今为止，6PPD对水生生物的毒性主要基于部分生命周期试验结果。然而，目前尚不清楚这种方法是否会导致低估6PPD的真实环境风险。本研究特别比较了环境相关或更高浓度的6PPD对大水蚤繁殖和生长的影响，从第21天到所有母水蚤死亡的那天，并探讨了6PPD的潜在毒性机制。6PPD在环境或接近自然的水中浓度（5.68和/或9.20µg/L）显著降低了后代总数和净繁殖率。然而，在第21天没有观察到这种不良反应，这表明环境水平的6PPD对大鼠有生殖毒性，短期暴露可能低估了6PPD的环境风险。5.68、9.20和44.58µg/L处理组丙二醛水平升高，加上活性氧（ROS）成为生物标志物反应指数的主要贡献者，表明6PPD诱导的ROS过量产生引发了脂质过氧化，尽管抗氧化能力增强。暴露于5.68、9.2和44.58µg/L 6PPD下的D. magna卵黄原蛋白表达下调，可能是基于分子对接和分子动力学模拟的卵黄原蛋白与表皮甾体受体的竞争性结合，可能影响胚胎发生过程中的营养供应。再加上氧化应激，这些双重机制似乎介导了6ppd诱导的生殖毒性。

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引用次数: 0

Temperature-dependent dopaminergic disruption by chlorpromazine in the rotifer Brachionus calyciflorus: Evidence from receptor gene expression and population response 氯丙嗪对萼花臂轮虫温度依赖性多巴胺能的破坏：来自受体基因表达和群体反应的证据

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

Aquatic Toxicology

Pub Date : 2025-11-04 DOI: 10.1016/j.aquatox.2025.107637

Sen Feng , Lingyun Zhu , Meng Li , Pengrui Xu , Chuhan Xu , Hairong Lian , Fan Gao , Xinfeng Cheng , Xianling Xiang

Temperature-induced amplification of drug toxicity brings about mounting ecological risks, but the effects of neuroactive substances like chlorpromazine (CPZ) on non-target aquatic invertebrates under sudden temperature shifts remain unclear. We investigated the temperature-dependent neurotoxicity of CPZ in the freshwater rotifer Brachionus calyciflorus, focusing on dopaminergic signaling. We first identified and functionally validated the dopamine receptor gene BcDopR1 in B. calyciflorus, a receptor featuring a 1371-bp open reading frame (ORF) that encodes a 456-amino acid polypeptide with seven transmembrane domains. Heterologous expression in HEK293T cells showed dopamine significantly elevated intracellular cAMP in BcDopR1-transfected cells, while CPZ dose-dependently inhibited this DA-induced cAMP response, confirming BcDopR1 as a functional D1-like dopamine receptor and CPZ as its potent antagonist. Rotifers were exposed to CPZ (0–250 μg/L) under three ecologically relevant temperatures (18, 25 and 32 °C). The peak BcDopR1 expression was observed in the control group at 25 °C, and CPZ exposure inhibited its expression in a concentration- and temperature-dependent manner. As temperature increased from 18 to 32 °C, rotifers exhibited significant reductions (p < 0.05) in several morphological traits, including lorica length, posterior lateral spine length, body size, and egg size. At the population level, the maximum population density first increased and then decreased, whereas the population growth rate increased significantly (p < 0.05). Within 0–250 μg/L CPZ, rotifers at 18 and 25 °C (except 32 °C) showed a gradual increase in lorica length and body size, whereas their egg size and maximum population density first increased then decreased. These findings highlight the susceptibility of aquatic invertebrates to neuroactive contaminants and the compounding role of thermal stress in amplifying pharmaceutical ecotoxicity. BcDopR1 emerges as a promising molecular biomarker for assessing neuroactive pharmaceutical ecological risks under climate change, and advances understanding of zooplankton adaptation to multiple environmental stressors.

温度引起的药物毒性放大带来了越来越大的生态风险，但氯丙嗪（CPZ）等神经活性物质在温度突变下对非靶水生无脊椎动物的影响尚不清楚。我们研究了CPZ在淡水轮虫萼花臂轮虫中的温度依赖性神经毒性，重点是多巴胺能信号。我们首先鉴定并功能性验证了calyciflorus中多巴胺受体基因BcDopR1，该受体具有1371 bp的开放阅读框（ORF），编码456个氨基酸的多肽，具有7个跨膜结构域。HEK293T细胞中的异源表达显示，多巴胺显著升高了BcDopR1转染细胞的胞内cAMP，而CPZ剂量依赖性地抑制了这种da诱导的cAMP反应，证实了BcDopR1是一种功能性的d1样多巴胺受体，CPZ是其有效的拮抗剂。在3种生态相关温度（18、25和32℃）下，轮虫暴露于CPZ （0 ~ 250 μg/L）。对照组在25℃时BcDopR1表达达到峰值，CPZ暴露抑制其表达呈浓度和温度依赖关系。当温度从18℃升高到32℃时，轮虫的几个形态特征，包括门廓长度、后外侧棘长、体型和卵的大小，都有显著的降低（p < 0.05）。在种群水平上，最大种群密度先升高后降低，种群增长率显著升高（p < 0.05）。在0 ~ 250 μg/L CPZ范围内，除32°C外，在18°C和25°C条件下，轮虫的轮虫体长和体型逐渐增大，卵大小和最大种群密度先增大后减小。这些发现强调了水生无脊椎动物对神经活性污染物的易感性，以及热应激在放大药物生态毒性中的复合作用。BcDopR1作为气候变化下神经活性药物生态风险评估的重要分子生物标志物，促进了对浮游动物适应多种环境胁迫的认识。

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引用次数: 0

ROS production-related phenomena and biochemical reactions of the seaweed Ulva rigida in response to the effect of environmentally relevant Bisphenol A concentrations 海藻对环境相关双酚A浓度影响下ROS产生相关现象及生化反应

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

Aquatic Toxicology

Pub Date : 2025-11-04 DOI: 10.1016/j.aquatox.2025.107638

Paraskevi Malea , Maria-Markella Patronia , Marios Dermentzis , Alkistis Kevrekidou , Dimitrios Phaedon Kevrekidis

Bisphenol A (BPA) is an extensively used synthetic compound that has causes various hazardous effects on aquatic primary producers. Research on BPA impacts on marine macrophytes and especially on Ulva spp. is limited. BPA-induced oxidative stress in Ulva rigida determined even at environmentally relevant concentrations (Low Effect Concentration, LOEC: 0.3 μg L^-1, Terminal Day, TD: 7) and it was higher on 7-11D. Increases in superoxide dismutase (SOD) and ascorbate peroxidise (APX) activities on specific days and concentrations may suggest the activation of an antioxidant mechanism in response to BPA-induced oxidative stress. On 1-5D, BPA-induced oxidative stress did not sufficiently activate SOD. On 7D at 0.1 μg L^-1, SOD activity decreases the Corrected Total Cell Fluorescence (CTCF) values to the control level, whereas at 0.3 and 1 μg L^-1, both enzymes may not be able to scavenge the oxidative stress. Protein content decreases, from 7D onwards at 0.3–3 μg L^-1, which may indicate oxidative injury in these biomolecules, as the antioxidant mechanism was unable to equilibrate the oxidative stress. Oxidative stress goes hand in hand with lipid peroxidation (malondialdehyde, MDA) at 0.3 on 7D and at 0.3–3 μg L^-1 on 3D The chlorophyll (Chls), pheophytin (Phs) and carotenoid (χ+c) contents decreased on 5D at 0.1–3 μg L^-1 of BPA (LOECs: 0.1 for Chls and χ+c, 1 μg L^-1 for Phs, TD: 5). BPA toxicity, based on the thalli surface area, seemed to be BPA dose-dependent and it was more pronounced at 3D (LOEC: 0.1 μg L^-1, TD: 3). U. rigida is among the most sensitive marine macrophytes against BPA, as it can cause adverse effects on various ‘biomarkers’, even at environmental concentrations.

双酚A （BPA）是一种广泛使用的合成化合物，对水生初级生产者造成各种有害影响。关于双酚a对海洋大型植物，特别是对藻属植物的影响的研究很少。即使在环境相关浓度（低效浓度，LOEC: 0.3 μg L-1，终末日，TD: 7）下，bpa诱导的刚性木藻氧化应激也会发生，并且在7- 11d上更高。在特定的时间和浓度下，超氧化物歧化酶（SOD）和抗坏血酸过氧化物（APX）活性的增加可能表明，bpa诱导的氧化应激激活了一种抗氧化机制。在1-5D， bpa诱导的氧化应激不能充分激活SOD。当浓度为0.1 μg L-1时，第7D SOD活性使校正总细胞荧光（CTCF）值降低至对照水平，而在0.3和1 μg L-1时，两种酶均不能清除氧化应激。在0.3-3 μ L-1时，蛋白质含量从7D开始下降，这可能表明这些生物分子存在氧化损伤，因为抗氧化机制无法平衡氧化应激。当BPA浓度为0.1 - 3 μ L-1时（Chls的LOECs为0.1，χ+c的LOECs为1 μ L-1， ph的LOECs为1 μ L-1， TD为5），5D时叶绿素（Chls）、叶绿素素（Phs）和类胡萝卜素（χ+c）含量降低。基于菌体表面积的BPA毒性似乎是剂量依赖性的，并且在3D （LOEC: 0.1 μg L-1, TD: 3）时更为明显。硬藻是对双酚a最敏感的海洋大型植物之一，因为即使在环境浓度下，它也会对各种“生物标志物”产生不利影响。

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引用次数: 0

Co-exposure effects of arsenite and bisphenol A on zebrafish: A focus on gut microbiota’s role in arsenobetaine biosynthesis-related toxicity 亚砷酸盐和双酚A对斑马鱼的共同暴露效应：肠道微生物群在砷甜菜碱生物合成相关毒性中的作用

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

Aquatic Toxicology

Pub Date : 2025-11-04 DOI: 10.1016/j.aquatox.2025.107639

Le Zhang, Weitian Liu, Yingying Tang, Peng Zhang, Huosheng Li, Jianyou Long, Wei Zhang

The biotransformation of arsenite (As(III)) into the less toxic or nontoxic form arsenobetaine (AsB) is crucial for mitigating arsenic (As)-induced toxicity. Co-contaminants like bisphenol A (BPA) could interfere with this process, although their precise roles and underlying mechanisms remain elusive. Here, we demonstrate that BPA co-exposure in zebrafish disrupts the gut microbiota, thereby inhibiting AsB biosynthesis and exacerbating As toxicity. After 28 days of co-exposure to As(III) and BPA, total As and As(V) levels increased significantly, while AsB concentrations in muscle tissue markedly decreased. This was accompanied by pronounced intestinal damage, which was strongly and positively correlated with As(V) accumulation. Mechanistically, BPA-induced gut microbial dysbiosis suppressed AsB production, resulting in elevated toxic As(V) burden, impaired intestinal barrier integrity, and enhanced inflammatory responses. Transcriptomic analysis further revealed that BPA upregulated pathways related to drug metabolism–cytochrome P450 and arachidonic acid metabolism, which may act synergistically with microbiota dysbiosis to amplify toxicity. Overall, our findings demonstrate that BPA potentiates As toxicity by disrupting its gut microbiota-mediated detoxification, revealing a novel ‘metabolic interference’ mechanism with important implications for chemical mixture risk assessment.

亚砷酸盐（As(III)）转化为毒性较小或无毒的砷甜菜碱（AsB）对于减轻砷（As）诱导的毒性至关重要。双酚A （BPA）等共污染物可能会干扰这一过程，尽管它们的确切作用和潜在机制尚不清楚。在这里，我们证明了BPA在斑马鱼中的共同暴露会破坏肠道微生物群，从而抑制AsB的生物合成并加剧As的毒性。As（III）和BPA共暴露28 d后，肌肉组织中总As和As(V)水平显著升高，AsB浓度显著降低。同时伴有明显的肠道损伤，这与As(V)的积累密切相关。从机制上说，bpa诱导的肠道微生物生态失调抑制了AsB的产生，导致毒性As(V)负担升高，肠道屏障完整性受损，炎症反应增强。转录组学分析进一步表明，BPA上调了药物代谢相关通路-细胞色素P450和花生四烯酸代谢，这可能与微生物群失调协同作用，放大毒性。总的来说，我们的研究结果表明，BPA通过破坏其肠道微生物群介导的解毒来增强As毒性，揭示了一种新的“代谢干扰”机制，对化学混合物的风险评估具有重要意义。

{"title":"Co-exposure effects of arsenite and bisphenol A on zebrafish: A focus on gut microbiota’s role in arsenobetaine biosynthesis-related toxicity","authors":"Le Zhang, Weitian Liu, Yingying Tang, Peng Zhang, Huosheng Li, Jianyou Long, Wei Zhang","doi":"10.1016/j.aquatox.2025.107639","DOIUrl":"10.1016/j.aquatox.2025.107639","url":null,"abstract":"<div><div>The biotransformation of arsenite (As(III)) into the less toxic or nontoxic form arsenobetaine (AsB) is crucial for mitigating arsenic (As)-induced toxicity. Co-contaminants like bisphenol A (BPA) could interfere with this process, although their precise roles and underlying mechanisms remain elusive. Here, we demonstrate that BPA co-exposure in zebrafish disrupts the gut microbiota, thereby inhibiting AsB biosynthesis and exacerbating As toxicity. After 28 days of co-exposure to As(III) and BPA, total As and As(V) levels increased significantly, while AsB concentrations in muscle tissue markedly decreased. This was accompanied by pronounced intestinal damage, which was strongly and positively correlated with As(V) accumulation. Mechanistically, BPA-induced gut microbial dysbiosis suppressed AsB production, resulting in elevated toxic As(V) burden, impaired intestinal barrier integrity, and enhanced inflammatory responses. Transcriptomic analysis further revealed that BPA upregulated pathways related to drug metabolism–cytochrome P450 and arachidonic acid metabolism, which may act synergistically with microbiota dysbiosis to amplify toxicity. Overall, our findings demonstrate that BPA potentiates As toxicity by disrupting its gut microbiota-mediated detoxification, revealing a novel ‘metabolic interference’ mechanism with important implications for chemical mixture risk assessment.</div></div>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"290 ","pages":"Article 107639"},"PeriodicalIF":4.3,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145442023","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}

引用次数: 0

Transcriptomic and physiological insights into Diethylstilbestrol toxicity in Phaeodactylum tricornutum 三角褐指藻（Phaeodactylum tricornutum）中己烯雌酚毒性的转录组学和生理学研究

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

Aquatic Toxicology

Pub Date : 2025-11-03 DOI: 10.1016/j.aquatox.2025.107636

Dong-Sheng Zhao , Xiao-Li Liu , Yu-Ting Chen , Huan Yang , Muhammad Ahsan Farooq , Xiufeng Yan , Hui-Xi Zou

Diethylstilbestrol (DES), an emerging pollutant, poses a threat to marine ecosystems, but its toxic effects on marine phytoplankton and the underlying mechanisms are not well understood. To address this knowledge gap, this study systematically investigated the physiological and molecular responses of the marine diatom Phaeodactylum tricornutum to DES exposure, aiming to uncover its toxicological mechanisms. DES significantly reduced chlorophyll content and photosynthetic efficiency, impaired the PSII core, and decreased both photosynthesis and respiration rates. The diatom responded by enhancing antioxidant defenses, including superoxide dismutase and catalase activities. DES was also partially removed from the water column, with removal rates of 9–18 %. Transcriptomic analysis revealed extensive changes in genes involved in porphyrin metabolism and carbon fixation, which were closely linked to the observed physiological impairments. In summary, these findings reveal a core toxicological mechanism whereby DES disrupts photosynthesis through inhibition of carbon fixation and porphyrin metabolism, providing new insights into how emerging pollutants impair marine primary producers and offering a scientific basis for the ecological risk assessment of DES contamination.

己烯雌酚（DES）是一种新兴污染物，对海洋生态系统构成威胁，但其对海洋浮游植物的毒性作用及其机制尚不清楚。为了解决这一知识空白，本研究系统地研究了海洋硅藻褐藻对DES暴露的生理和分子反应，旨在揭示其毒理学机制。DES显著降低了叶绿素含量和光合效率，损害了PSII核心，降低了光合速率和呼吸速率。硅藻的反应是增强抗氧化防御，包括超氧化物歧化酶和过氧化氢酶的活性。DES也被部分从水柱中去除，去除率为9 ~ 18%。转录组学分析显示，参与卟啉代谢和碳固定的基因发生了广泛的变化，这与观察到的生理损伤密切相关。综上所述，这些发现揭示了DES通过抑制固碳和卟啉代谢破坏光合作用的核心毒理学机制，为了解新兴污染物对海洋初级生产者的危害提供了新的见解，并为DES污染的生态风险评估提供了科学依据。

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引用次数: 0

Identification of Fentin chloride -induced scoliosis in zebrafish through the regulation of adrenaline by metabolomics and network pharmacology 通过代谢组学和网络药理学鉴定氯化芬丁对肾上腺素的调节对斑马鱼脊柱侧凸的影响

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

Aquatic Toxicology

Pub Date : 2025-11-03 DOI: 10.1016/j.aquatox.2025.107635

Hao Cheng , Shanshan Zhu , Wenyan Liu , Fasheng Liu , Jing Hu , Xinwei Xu , Xinjun Liao , Xiaowen Shi , Huiqiang Lu

Fentin chloride (TPTC) is an organotin compound used extensively in hull construction due to its excellent resistance to corrosion. To explore the biotoxicity of TPTC, In this study, the molecular mechanism of TPTC-induced scoliosis was investigated in the zebrafish model by combining metabolomics and network pharmacology. TPTC exposure causes scoliosis and neurotoxicity in zebrafish, and leads to increasing curvature angles with the increase in concentration. Metabolomic analysis identified 366 significant differential metabolites associated with TPTC-induced scoliosis. Network pharmacology revealed 32 intersecting targets between TPTC and scoliosis, and Kyoto Encyclopedia of Genes and Genomes pathway analysis demonstrated that these targets were mainly enriched in pathways, such as, neuroreceptor-ligand interactions, cGMP-PKG signaling, and adrenergic signaling. The combined analysis identified adrenergic receptors as the key targets of TPTC. ELISA revealed increased levels of adrenaline with the increase in TPTC concentrations. RT-qPCR showed that the expression levels of the Urotensin-Related Peptide genes (Urp1, Urp2) and their receptor genes (Utrs2r1), which regulate body axis curvature, are significantly increased downstream of the adrenaline signaling pathway. The use of an adrenaline inhibitor mitigated TPTC-induced scoliosis and the level of Urp1, Urp2 and Utrs2r1 nearly recovered to normal levels. Therefore, TPTC induces scoliosis by acting on adrenergic receptors to interfere with epinephrine and up-regulating the expression of downstream Urotensin-Related Peptide genes.

氯化芬丁（TPTC）是一种有机锡化合物，因其优异的耐腐蚀性而广泛应用于船体结构中。为了探讨TPTC的生物毒性，本研究采用代谢组学和网络药理学相结合的方法，在斑马鱼模型中研究TPTC诱导脊柱侧凸的分子机制。TPTC暴露导致斑马鱼脊柱侧凸和神经毒性，并导致弯曲角度随着浓度的增加而增加。代谢组学分析确定了366种与tptc诱导的脊柱侧凸相关的显著差异代谢物。网络药理学揭示了TPTC与脊柱侧凸之间的32个交叉靶点，京都基因与基因组百科全书通路分析表明，这些靶点主要富集于神经受体-配体相互作用、cGMP-PKG信号通路和肾上腺素能信号通路。综合分析发现肾上腺素能受体是TPTC的关键靶点。ELISA结果显示肾上腺素水平随着TPTC浓度的升高而升高。RT-qPCR结果显示，在肾上腺素信号通路下游，调节体轴曲率的尿紧张素相关肽基因（Urp1、Urp2）及其受体基因（Utrs2r1）的表达水平显著升高。肾上腺素抑制剂的使用减轻了tptc诱导的脊柱侧凸，Urp1、Urp2和Utrs2r1的水平几乎恢复到正常水平。因此，TPTC通过作用于肾上腺素能受体，干扰肾上腺素，上调下游尿紧张素相关肽基因的表达，从而诱导脊柱侧凸。

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引用次数: 0

Endocrine disruptive effects and mechanisms of isothiazolinone analogs in marine medaka (Oryzias melastigma) embryos and H295R cells 异噻唑啉酮类似物对海洋medaka胚胎和H295R细胞的内分泌干扰作用及其机制

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

Aquatic Toxicology

Pub Date : 2025-11-01 DOI: 10.1016/j.aquatox.2025.107633

Jiali Li , Lizhu Tang , Jing Li , Chenyan Hu , Jiahui Cao , Wenbing Zhang , Lianguo Chen

The application of isothiazolinones as antimicrobial agents has caused prevalent pollution of marine environment. However, the developmental toxicity and endocrine disrupting effects of different isothiazolinone analogs to marine organisms remain largely elusive. In the present study, marine medaka embryos were exposed to 0, 1, 3, and 10 μg/L of six representative isothiazolinone analogs, including isothiazole, methylisothiazolinone (MIT), methylchloroisothiazolinone (MCI), octylisothiazolinone (OIT), benzisothiazolinone (BIT), and dichlorocthylisothiazolinone (DCOIT), after which the anomalies in early embryogenesis and endocrine homeostasis were examined. In vivo results showed that OIT, BIT, and DCOIT were potently estrogenic, which was characterized by the higher estradiol (E₂) content and remarkable elevation of E₂/testosterone ratio in larval medaka. Correlation analysis found significantly positively relationship among OIT, BIT, and DCOIT, indicating their similar modes of toxicity. Besides, in vitro exposure using H295R cells was performed to gain more insights into endocrine disrupting mechanisms, further confirming the multiple disturbances of DCOIT in reproductive endocrine cascades, consisting of MAPK proteins, aromatase, and sex hormones. Overall, the present findings underscore the high susceptibility of marine organisms to the developmental and endocrine toxicity of isothiazolinones, especially during early embryonic stages. In the future, the marine ecological risks of isothiazolinones need to be evaluated urgently, thus facilitating chemical lifecycle management.

异噻唑啉酮类抗菌药物的应用对海洋环境造成了普遍的污染。然而，不同的异噻唑啉酮类似物对海洋生物的发育毒性和内分泌干扰作用在很大程度上仍然是难以捉摸的。本研究采用0、1、3、10 μg/L的异噻唑啉酮、甲基异噻唑啉酮（MIT）、甲基氯异噻唑啉酮（MCI）、辛基异噻唑啉酮（OIT）、苄基异噻唑啉酮（BIT）、二氯辛基异噻唑啉酮（DCOIT）等6种代表性异噻唑啉酮类似物对海洋medaka胚胎进行了早期胚胎发育异常和内分泌稳态的检测。体内实验结果表明，OIT、BIT和DCOIT具有强雌激素作用，其特点是雌二醇（E2）含量较高，E2/睾酮比显著升高。相关分析发现，OIT、BIT和DCOIT三者之间呈显著正相关，表明它们的毒性模式相似。此外，利用H295R细胞进行体外暴露，进一步了解内分泌干扰机制，进一步证实DCOIT在由MAPK蛋白、芳香化酶和性激素组成的生殖内分泌级联中的多重干扰。总的来说，目前的研究结果强调了海洋生物对异噻唑啉酮的发育和内分泌毒性的高度敏感性，特别是在早期胚胎阶段。未来，迫切需要对异噻唑啉酮类化合物的海洋生态风险进行评估，从而促进化学品生命周期管理。

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引用次数: 0

Biochemical and molecular stress responses to enrofloxacin in Mytilus galloprovincialis: transient or lasting effects? 对恩诺沙星的生化和分子应激反应：短暂或持久的影响？

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

Aquatic Toxicology

Pub Date : 2025-10-29 DOI: 10.1016/j.aquatox.2025.107626

J. Giannessi , C. Pretti , V. Meucci , L. Intorre , L. De Marchi , B. Gabbrielli , M. Baratti

Antibiotic contamination is an emerging threat in marine environments due to its potential to alter key physiological processes in non-target organisms. Among veterinary antibiotics, enrofloxacin (ENR), a widely used fluoroquinolone, is frequently detected in coastal waters. This study investigated the biological effects of ENR exposure in the Mediterranean mussel Mytilus galloprovincialis using an integrated approach combining gene expression, biochemical, and bioenergetic endpoints. Mussels were exposed to two environmentally relevant concentrations of ENR (5 and 500 ng/L) for 7 days (EXP7) and 14 days (EXP14), followed by a 14-day recovery period (REC). Gill tissues were analyzed for transcriptional changes in genes related to detoxification, oxidative stress, apoptosis, and energy metabolism. In addition, energy reserves, mitochondrial activity, and indicators of genotoxicity and antioxidant responses were measured. Results showed that ENR exposure modulated the expression of several genes, including early upregulation of abcb and cyp4y1, and downregulation of pkpyr and icdh, indicating activation of detoxification pathways and energy metabolism shifts. Biochemical analyses revealed increased mitochondrial activity (ETS), mobilization of energy reserves, and sustained elevation of GST activity, while DNA strand break levels confirmed a potential genotoxic effect. Despite the removal of the contaminant, most stress responses did not fully revert during recovery. These findings demonstrate that even low concentrations of ENR can disrupt mussel physiology at multiple levels, with effects persisting beyond exposure. The study underscores the importance of incorporating sub-lethal biomarkers into environmental risk assessments and supports the inclusion of veterinary antibiotics like ENR in marine monitoring programs to protect coastal ecosystem health.

抗生素污染是海洋环境中一个新兴的威胁，因为它有可能改变非目标生物的关键生理过程。在兽用抗生素中，恩诺沙星（ENR）是一种广泛使用的氟喹诺酮类药物，在沿海水域中经常被检测到。本研究采用结合基因表达、生化和生物能量终点的综合方法，研究了ENR暴露对地中海贻贝（Mytilus galloprovincialis）的生物学效应。将贻贝暴露于两种环境相关浓度的ENR（5和500 ng/L）中7天（EXP7）和14天（EXP14），然后进行14天的恢复期（REC）。分析鳃组织中与解毒、氧化应激、细胞凋亡和能量代谢相关的基因的转录变化。此外，还测量了能量储备、线粒体活性、遗传毒性和抗氧化反应指标。结果表明，ENR暴露可调节多个基因的表达，包括abcb和cyp4y1的早期上调，pkpyr和icdh的下调，表明解毒途径的激活和能量代谢的改变。生化分析显示线粒体活性（ETS）增加，能量储备动员，GST活性持续升高，而DNA链断裂水平证实了潜在的遗传毒性作用。尽管去除了污染物，但大多数应激反应在恢复过程中并没有完全恢复。这些发现表明，即使是低浓度的ENR也会在多个层面上破坏贻贝的生理机能，其影响持续到暴露后。该研究强调了将亚致死生物标志物纳入环境风险评估的重要性，并支持将兽医抗生素（如ENR）纳入海洋监测计划，以保护沿海生态系统的健康。

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引用次数: 0

Marine ecotoxicity evaluation of 10 per- and poly-fluoroalkyl acids using three USEPA short-term chronic bioassays 使用三种USEPA短期慢性生物测定法评价10种单氟和多氟烷基酸的海洋生态毒性

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

Aquatic Toxicology

Pub Date : 2025-10-28 DOI: 10.1016/j.aquatox.2025.107625

Nicholas T. Hayman , Zacharias Pandelides , Josiah Discar , Marienne A. Colvin , Gunther Rosen , Jennifer Arblaster , Jason Conder

Effects data for per- and poly-fluoroalkyl substances (PFAS) for marine aquatic life are lacking, limiting the assessment of site-specific ecological risks in marine ecosystems and development of marine water quality criteria. In this study, the toxicity of 10 PFAS (PFBA, PFHxA, PFOA, PFDA, PFBS, PFHxS, PFOS, PFDS, 6:2 FTS, and 8:2 FTS) were evaluated with three standard marine toxicity testing species: Mediterranean mussel (Mytilus galloprovincialis); purple sea urchin (Strongylocentrotus purpuratus); and giant kelp (Macrocystis pyrifera). Many tests failed to elicit responses exceeding 50 % adverse effect levels, despite approaching solubility limits. EC₅₀ values were able to be derived in only 43 % of the toxicity tests, and were generally above 1 mg/L, except for PFOS and PFDA based on the most sensitive of the three species (S. purpuratus and M. galloprovincialis), with EC₅₀s in the approximate 0.1 to 1 mg/L range. M. pyrifera, the macroalgae, was less sensitive than either invertebrate species. EC₅₀ values for all three species decreased with perfluoroalkyl carbon chain length, as increasing toxicity was observed in longer chained compounds, and a statistically significant relationship between chain length and EC₅₀ was detected for M. galloprovincialis. A number of other toxicological metrics (NOECs, LOECs, EC₁₀s, and EC₂₀s) were also generated. NOECs for sublethal endpoints were in the 0.01 to 100 mg/L range and were orders of magnitude higher than environmentally relevant concentrations. Based on the results in this study, adverse effects on these species and endpoints would not be expected to occur in the PFAS-impacted marine environment.

缺乏单氟烷基物质和多氟烷基物质对海洋水生生物的影响数据，限制了对海洋生态系统中特定地点生态风险的评估和海洋水质标准的制定。在这项研究中,10个pfa的毒性(PFBA PFHxA, PFOA、PFDA可以,PFHxS,卵圆孔未闭,pdf, 6:2 FTS,宣告FTS)进行评估和三个标准的海洋物种毒性测试:地中海贻贝(Mytilus galloprovincialis);紫海胆（strongylocentrrotus purpuratus）；巨藻（Macrocystis pyrifera）。尽管接近溶解度极限，但许多试验未能引起超过50%的不良反应水平。只有43%的毒性试验能够得出EC50值，一般都在1毫克/升以上，除了全氟辛烷磺酸和全氟辛烷磺酸，这是基于三种物种中最敏感的一种（紫癜脓毒杆菌和加洛省脓毒杆菌），EC50值大约在0.1至1毫克/升之间。大型藻类M. pyrifera的敏感性低于两种无脊椎动物。所有三种物种的EC50值都随着全氟烷基碳链长度的增加而降低，因为观察到链长化合物的毒性增加，并且在链长度与加galloprovincialis的EC50之间检测到具有统计学意义的关系。还生成了许多其他毒理学指标（noec、loec、ec10和ec20）。亚致死终点noec在0.01至100 mg/L范围内，比环境相关浓度高几个数量级。根据本研究的结果，在受pfas影响的海洋环境中，预计不会对这些物种和端点产生不利影响。

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引用次数: 0

Effects of pyrethroid insecticides on sex ratios in agile frogs (Rana dalmatina) 拟除虫菊酯类杀虫剂对敏捷蛙性比的影响

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

Aquatic Toxicology

Pub Date : 2025-10-28 DOI: 10.1016/j.aquatox.2025.107624

Emese Balogh , Szabolcs Hócza , Nikolett Ujhegyi , Andrea Kásler , Dóra Holly , Dávid Herczeg , János Ujszegi , Zoltán Gál , Orsolya I. Hoffmann , Veronika Bókony , Zsanett Mikó

Environmental pollutants have the potential to alter sex ratios in wildlife through sex-biased mortality. Furthermore, endocrine disruptors may cause sex reversal during early ontogeny in ectothermic vertebrates, resulting in a phenotypic sex that is not concordant with the genotypic sex encoded by the sex chromosomes. Despite the wide-ranging implications of these sex-ratio biasing effects, they are rarely studied in ecotoxicology, especially in a way that allows for disentangling the two mechanisms. We investigated these effects of two synthetic pyrethroids, deltamethrin and etofenprox, that are commonly used insecticides and have been linked to adverse effects on fish and amphibian biodiversity. We assessed the effects of environmentally relevant concentrations of these two pyrethroids on phenotypic sex ratio, sex-dependent mortality, and sex reversal in agile frogs (Rana dalmatina). Tadpoles from field-collected eggs were reared in mesocosms until metamorphosis by adding 0.03 or 0.3 μg/L of deltamethrin or etofenprox three times to the water. We observed no effect in three of the four treatment groups. However, in the lower-concentration etofenprox treatment, phenotypic sex ratio was male-biased two months post-metamorphosis, and genotypic sexing revealed that this was due to female-biased mortality during metamorphosis and not to sex reversal. Although the estimation certainty of these effects was somewhat limited, they highlight that not all sex-ratio distorting effects are caused by sex reversal. Therefore, ecotoxicological studies aiming to understand the endocrine distruptor effects of environmental contaminants should strive to separate the effects on sex determination and sex-dependent mortality.

环境污染物有可能通过性别偏向性死亡率改变野生动物的性别比例。此外，内分泌干扰物可能在变温脊椎动物的早期个体发育过程中引起性别逆转，导致表现型性别与性染色体编码的基因型性别不一致。尽管这些性别比例偏倚效应具有广泛的影响，但它们很少在生态毒理学中进行研究，特别是以一种允许分离这两种机制的方式。我们研究了两种合成拟除虫菊酯（溴氰菊酯和乙醚菊酯）的这些影响，这两种杀虫剂是常用的，并与对鱼类和两栖动物生物多样性的不利影响有关。我们评估了这两种拟除虫菊酯的环境相关浓度对敏捷蛙（Rana dalmatina）表型性比、性别依赖性死亡率和性别逆转的影响。将田间采卵的蝌蚪置于中胚层中饲养，分别在水中添加0.03或0.3 μg/L的溴氰菊酯或乙醚菊酯3次，直至蜕变。我们观察到四个治疗组中有三个没有效果。然而，在低浓度的乙托芬prox治疗中，表型性别比例在变态后两个月偏向于男性，基因型性别分析显示，这是由于变态期间的死亡率偏向于女性，而不是性别逆转。虽然这些影响的估计确定性有些有限，但他们强调，并非所有的性别比例扭曲效应都是由性别逆转引起的。因此，生态毒理学研究旨在了解环境污染物对内分泌干扰物的影响，应努力将其对性别决定和性别依赖性死亡率的影响分开。

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引用次数: 0