Comparative Biochemistry and Physiology C-toxicology & Pharmacology最新文献_第6页

Early life tributyltin exposure has long term physiological effects on the zebrafish (Danio rerio) visual system 幼年接触三丁基锡对斑马鱼的视觉系统有长期的生理影响。

IF 4.3 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2026-03-01 Epub Date: 2025-11-28 DOI: 10.1016/j.cbpc.2025.110416

Jennifer S. Jensen , Peyman Owrang , Avery Sherffius , Claire Selby , Nathaniel R. Fleming , Logan Ouellette , Matthew Hartings , Victoria P. Connaughton

Tributyltin (TBT) is an antiestrogenic endocrine disrupting compound used in the production of plastic, timber, and aquatic antifouling paints. Previous studies focusing on short-term effects of TBT exposure have identified immediate detrimental effects. Here, we evaluate whether a transient (24 h) exposure to TBT during development can cause persistent effects that remain after removal from treatment. Zebrafish (Danio rerio) larvae were exposed to environmentally relevant concentrations of TBT (0.04 and 0.4 μg/L) when they were either 3- or 7-days post-fertilization (dpf). After exposure, larvae were returned to recovery conditions and assessed 2-weeks, 4-weeks, or > 5 months postexposure. Exposure to 0.4 μg/L TBT at 3 dpf decreased total and distal retinal thicknesses. Adult (>5 month) photopic electroretinograms revealed physiological changes to photoreceptor a-wave and ON-bipolar cell b-wave components, with greater deficits in the 0.4 μg/L group. TBT exposure at 7 dpf significantly increased retinal inner plexiform layer thickness at 2-weeks, an effect that persisted to adulthood. Adult electroretinograms were also altered, with 0.04 μg/L TBT increasing and delaying a-wave and OFF-bipolar d-wave responses and increasing b-wave amplitude. Thus, the impact of TBT exposure depends on both concentration and exposure age, with retinal sequelae characterized by early anatomical and later physiological deficits. These data suggest that TBT exposure during critical periods of visual system development causes persistent age- and concentration-dependent deficits that are specific to the retina, revealing a previously unknown effect of this compound.

三丁基锡（TBT）是一种抗雌激素内分泌干扰化合物，用于生产塑料、木材和水生防污涂料。以前的研究关注的是接触TBT的短期影响，已经确定了直接的有害影响。在这里，我们评估了在发育期间短暂（24 h）暴露于TBT是否会在停止治疗后造成持续影响。斑马鱼（Danio rerio）幼虫在受精后3 d和7 d分别暴露于环境相关浓度的TBT（0.04和0.4 μg/L）中。暴露后，将幼虫放回恢复状态，并在暴露后2周、4周或 > 5 个月进行评估。在3 dpf时暴露于0.4 μg/L TBT可降低视网膜总厚度和远端厚度。成人（bbb50 月）视网膜光电图显示光感受器a波和on双极细胞b波组分的生理变化，0.4 μg/L组缺陷更大。7 dpf时的TBT暴露在2周时显著增加了视网膜内丛状层的厚度，这种影响持续到成年。成人视网膜电图也发生改变，0.04 μg/L TBT增加和延迟a波和off双极d波反应，增加b波振幅。因此，TBT暴露的影响取决于浓度和暴露年龄，视网膜后遗症以早期解剖和后期生理缺陷为特征。这些数据表明，在视觉系统发育的关键时期接触TBT会导致视网膜特异性的持续年龄和浓度依赖性缺陷，揭示了这种化合物以前未知的作用。

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引用次数: 0

Concurrent endoplasmic reticulum stress and demyelination in DEHP-exposed zebrafish larvae at the early developmental stages 暴露于dehp的斑马鱼幼体在早期发育阶段并发内质网应激和脱髓鞘。

IF 4.3 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2026-03-01 Epub Date: 2025-11-19 DOI: 10.1016/j.cbpc.2025.110394

Garima Jindal , Anuradha Mangla , Mehjbeen Javed , Mohd. Anas Saifi , Iqra Mazahir , Padmshree Mudgal , Shiekh Raisuddin

Di-ethylhexyl phthalate (DEHP) is an endocrine disruptor with established neurotoxic as well as potential neurodegenerative effects. The myelin sheath plays a crucial role in maintaining the health of the nervous system, whereas demyelination contributes to the onset of brain diseases. This study investigated the effect of DEHP on the neurological development with special reference to endoplasmic reticulum (ER) stress, inflammation, and concurrently with demyelination and cellular apoptotic development in zebrafish larvae. Results indicated that DEHP exposure can lead to demyelination through ER stress and inflammation, as evident from the decreased expression of myelin basic protein (Mbp) in both the brain and spinal cord of zebrafish larvae analyzed through immunofluorescent assay. The mRNA expression of axon marker nfl significantly increased, while tuba1a was decreased with DEHP exposure. Western blotting analysis revealed that ER stress markers such as phosphorylated inositol-requiring enzyme 1 alpha (p-Ire1α), activating transcription factor 4 (Atf4), binding immunoglobulin protein (Bip), phosphorylated e-IF2 alpha (p-eIF2α), CCAAT/enhancer-binding protein homologous protein (Chop), and inflammatory markers (nuclear factor kappa B subunit p65; Nf-κb p65), ionized calcium-binding adaptor molecule 1 (Iba1), and glial fibrillary acid protein (Gfap), were significantly upregulated on exposure to DEHP. Scototaxis, a behavioral assay, showed an altered anxiety-like behaviour in DEHP-treated larvae. Oxidative stress markers, such as superoxide dismutase (SOD), catalase, and monoamine oxidase (MAO) were also elevated. Apoptotic cells were observed in DEHP-treated zebrafish larvae in acridine orange staining. Overall, the DEHP exposure to zebrafish larvae caused myelin sheath degeneration and axonal dysfunction due to the generation of ER stress and inflammation.

邻苯二甲酸二乙基己酯（DEHP）是一种内分泌干扰物，具有神经毒性和潜在的神经退行性作用。髓鞘在维持神经系统健康方面起着至关重要的作用，而脱髓鞘则会导致脑部疾病的发生。本研究探讨了DEHP对斑马鱼幼体神经发育的影响，特别是内质网应激、炎症以及同时发生的脱髓鞘和细胞凋亡发育。结果表明，DEHP暴露可通过内质网应激和炎症导致脱髓鞘脱髓鞘，免疫荧光分析显示斑马鱼幼鱼脑和脊髓中髓鞘碱性蛋白（Mbp）表达降低。DEHP暴露后，轴突标记物nfl mRNA表达显著升高，tuba1a mRNA表达降低。内质网应激标志物如肌醇要求酶1 α (Ire1)、激活转录因子4 （Atf4）、结合免疫球蛋白蛋白（Bip）、磷酸化e-IF2 α （p-eIF2α)、CCAAT/增强子结合蛋白同源蛋白（Chop）、炎症标志物（核因子κ B亚基p65； Nf-κb p65）、离子钙结合接头分子1 （Iba1）和胶质原纤维酸蛋白（Gfap））在DEHP暴露时显著上调。在dehp处理的幼虫中，行为性测定也发生了变化。氧化应激标志物如超氧化物歧化酶（SOD）、过氧化氢酶和单胺氧化酶（MAO）也升高。用吖啶橙染色观察dehp处理的斑马鱼幼虫细胞凋亡。总体而言，DEHP暴露于斑马鱼幼虫后，由于内质网应激和炎症的产生，导致髓鞘变性和轴突功能障碍。

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引用次数: 0

Synergistic effects of high temperature and hypoxia on energy metabolism and physiological homeostasis in the Chinese mitten crab (Eriocheir sinensis) 高温和缺氧对中华绒螯蟹能量代谢和生理稳态的协同作用

IF 4.3 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2026-03-01 Epub Date: 2025-12-16 DOI: 10.1016/j.cbpc.2025.110436

Cong Zhang , Dunqian Deng , Huixia Feng , Su Jiang , Zihao Song , Kai Zhang , Longlong Fu , Shaowu Yin

High temperature and hypoxia are critical environmental stressors affecting the intensive aquaculture of the Chinese mitten crab (Eriocheir sinensis). This study aimed to investigate the differential physiological response mechanisms of juvenile crabs under single stress and combined stress. The results revealed that combined high-temperature and hypoxia stress exerted a significant synergistic negative effect on juvenile crabs compared to single stressors. Under combined stress, mitochondrial structural damage is observed in gill tissues, accompanied by markedly reduced activities of cytochrome c oxidase and cytochrome c, indicating impairment of the aerobic respiratory pathway. In response, the hepatopancreas undergoes reconstruction of energy metabolism patterns, characterized by a significant decrease in glycogen content, along with elevated levels of glucose, pyruvate, and lactate in the hemolymph. In addition, the activities of hexokinase and pyruvate kinase in the hepatopancreas increased, while succinate dehydrogenase activity decreased. Concurrently, the function of the antioxidant system is dysregulated, with decreases in total antioxidant capacity and glutathione levels, and the expression of antioxidant-related genes shows a similar trend. In addition, the expression levels of immune- and apoptosis-related genes were significantly up-regulated. These results indicate that combined stress leads to systemic energy metabolism disorder, exacerbated oxidative stress, pro-inflammatory response and apoptosis, and functional organ damage. The results underscore that combined environmental stressors can induce nonlinear and more severe physiological damage.

高温和缺氧是影响中华绒螯蟹集约化养殖的重要环境胁迫因素。本研究旨在探讨蟹幼鱼在单一胁迫和复合胁迫下的生理反应机制差异。结果表明，与单一应激源相比，高温低氧复合应激对蟹幼鱼具有显著的协同负作用。在联合应激下，鳃组织线粒体结构损伤，细胞色素c氧化酶和细胞色素c活性明显降低，表明有氧呼吸通路受损。作为回应，肝胰脏经历能量代谢模式的重建，其特征是糖原含量显著降低，同时血淋巴中葡萄糖、丙酮酸和乳酸水平升高。肝胰脏己糖激酶和丙酮酸激酶活性升高，琥珀酸脱氢酶活性降低。同时，抗氧化系统功能失调，总抗氧化能力和谷胱甘肽水平下降，抗氧化相关基因表达也呈现类似趋势。此外，免疫和凋亡相关基因的表达水平显著上调。上述结果提示，复合应激导致全身能量代谢紊乱，氧化应激加剧，促炎反应和细胞凋亡加剧，功能器官受损。结果表明，复合环境应激可引起非线性且更为严重的生理损伤。

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引用次数: 0

Triclosan induces spermatogenic damage via the oxidative stress-P53-apoptosis pathway in zebrafish 三氯生通过氧化应激- p53 -凋亡通路诱导斑马鱼生精损伤。

IF 4.3 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2026-02-01 Epub Date: 2025-10-31 DOI: 10.1016/j.cbpc.2025.110379

Fan Wang, Yiran Liu, Huiwen Yang, Ying Zhang, Fei Liu

Triclosan (TCS), a widely used antimicrobial agent, has been identified as a reproductive endocrine disruptor. However, the mechanisms underlying TCS-induced gonadal damage remain incompletely understood. In this study, zebrafish were chronically exposed to TCS from 4 h post-fertilization (hpf) to 120 days post-fertilization (dpf). A comprehensive analysis was conducted, including assessment of testicular cell apoptosis in adult fish, evaluation of apoptosis-related genes and proteins in both adult testes and 50-day-old juveniles, and transcriptome sequencing. The results showed that TCS exposure downregulated mRNA expression of oxidative stress-related and anti-apoptotic genes, while upregulating pro-apoptotic gene expression along with P53 and Caspase 3 protein levels, ultimately leading to a significant increase in testicular apoptotic cells. Transcriptome sequencing analysis revealed enrichment of the P53 signaling pathway, apoptosis pathway, response to oxidative stress biological process. These findings indicate that postembryonic exposure to TCS causes gonadal damage primarily by inducing oxidative stress, which increases P53 expression, subsequently regulating pro-apoptotic gene expression and suppressing anti-apoptotic proteins, thereby activating the mitochondrial apoptosis pathway and death receptor pathway, potentially affecting growth, development, and reproductive toxicity. This study systematically elucidates the molecular mechanism by which TCS induces reproductive toxicity through the oxidative stress-P53 axis, which triggers both the mitochondrial and death receptor apoptotic pathways. Our findings provide important experimental evidence and a theoretical reference for the scientific assessment of TCS-related reproductive health risks.

三氯生（TCS）是一种广泛使用的抗菌剂，已被确定为生殖内分泌干扰物。然而，tcs诱导性腺损伤的机制仍不完全清楚。在本研究中，斑马鱼从受精后4 h （hpf）到受精后120 d （dpf）长期暴露于TCS。我们进行了全面的分析，包括评估成鱼睾丸细胞凋亡，评估成鱼睾丸和50日龄幼鱼中凋亡相关基因和蛋白，以及转录组测序。结果表明，TCS暴露可下调氧化应激相关基因和抗凋亡基因的mRNA表达，上调促凋亡基因的表达以及P53和Caspase 3蛋白水平，最终导致睾丸凋亡细胞显著增加。转录组测序分析显示P53信号通路、凋亡通路富集，响应氧化应激的生物过程。这些研究结果表明，胚胎后暴露于TCS主要通过诱导氧化应激导致性腺损伤，氧化应激增加P53表达，随后调节促凋亡基因表达，抑制抗凋亡蛋白，从而激活线粒体凋亡途径和死亡受体途径，可能影响生长发育和生殖毒性。本研究系统阐明了TCS通过氧化应激- p53轴诱导生殖毒性的分子机制，该轴触发线粒体和死亡受体凋亡途径。本研究结果为科学评估tcs相关生殖健康风险提供了重要的实验依据和理论参考。

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引用次数: 0

Detoxification metabolic pathways and hepatotoxicity mechanisms of B[a]P in reproductive clam Ruditapes philippinarum B[a]P在繁殖蛤体内的解毒代谢途径及肝毒性机制

IF 4.3 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2026-02-01 Epub Date: 2025-10-22 DOI: 10.1016/j.cbpc.2025.110378

Yueyao Zhou, Zhiheng He, Qiuhong Xu, Songhui Xie, Pengfei Li, Qiaoqiao Wang, Jingjing Miao, Luqing Pan

The liver is a major organ of digestion and detoxification metabolism in animals, and the occurrence of most liver diseases is closely associated with environmental pollution. Besides, liver is a non-reproductive primary target organ regulated by sex steroid hormone signaling. In this study, we elucidated the detoxification metabolism pathways of B[a]P in the clam Ruditapes philippinarum and identified the hepatotoxicity mechanism of B[a]P using technical approaches such as transcriptomics, computer simulation and experimental validation. We found that the AhR signaling pathway and CYP450 family (CYP1A1, CYP2B1, CYP3A4) and FMO in the digestive gland of clam play important roles in the detoxification metabolism of B[a]P, but the performance varied between male and female clams. SOD1 and CAT, GPX, PRDX play antioxidant function but PRDX pathway did not function in females. The level of detoxification metabolism in reproductive clams under B[a]P stress was female < male, oxidative stress was female > male, and oxidative damage was female < male. Cell death (apoptosis, pyroptosis and ferroptosis) was aggravated in the digestive gland of both males and females, with a reduced level of hepatic function health and an increase in the level of inflammatory factors, but males presented a more pronounced tendency toward hepatic fibrosis. In summary, the results of this study enrich the research perspectives on the metabolic pathways of POPs in aquatic invertebrates and lay the foundation for the study of POPs-induced hepatotoxicity, which is of great significance for the conservation of marine biological resources and the monitoring of POPs pollution.

肝脏是动物消化和解毒代谢的主要器官，大多数肝脏疾病的发生与环境污染密切相关。此外，肝脏是受性类固醇激素信号调控的非生殖性主要靶器官。本研究通过转录组学、计算机模拟和实验验证等技术手段，阐明了B[a]P在菲律宾蛤（Ruditapes philippinarum）中的解毒代谢途径，并确定了B[a]P的肝毒性机制。我们发现，蛤蜊消化腺中的AhR信号通路、CYP450家族（CYP1A1、CYP2B1、CYP3A4）和FMO在B[a]P的解毒代谢中发挥重要作用，但雌雄蛤蜊的表现不同。SOD1和CAT、GPX、PRDX具有抗氧化作用，而PRDX通路在雌性中不起作用。生殖蛤在B[a]P胁迫下解毒代谢水平为雌性<雄性，氧化应激为雌性>雄性，氧化损伤为雌性<雄性。男性和女性消化腺细胞死亡（凋亡、焦亡和铁亡）加重，肝功能健康水平降低，炎症因子水平升高，但男性肝纤维化倾向更明显。综上所述，本研究结果丰富了POPs在水生无脊椎动物体内代谢途径的研究视角，为POPs致肝毒性研究奠定了基础，对海洋生物资源保护和POPs污染监测具有重要意义。

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引用次数: 0

The marine water flea Diaphanosoma celebensis as an emerging model for ocean health research: A review 海洋水蚤：海洋健康研究的新模式综述。

IF 4.3 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2026-02-01 Epub Date: 2025-11-20 DOI: 10.1016/j.cbpc.2025.110400

Duck-Hyun Kim , Jin-Sol Lee , Min-Sub Kim , Zhou Yang , Atsushi Hagiwara , Jae-Seong Lee

Diaphanosoma celebensis, a marine water flea, has gained recognition as a valuable model organism in marine ecotoxicology, ecophysiology, and epigenetics. This review highlights the significance of D. celebensis in environmental research, emphasizing its high-quality genomic and transcriptomic resources, adaptability to environmental stressors, and sensitivity to pollutants. The species' utility in studying molecular responses to contaminants such as microplastics, heavy metals, and endocrine disruptors is underscored by its ability to provide insights into detoxification pathways, stress response mechanisms, and epigenetic modifications. Diaphanosoma celebensis serves as a critical tool for advancing our understanding of the ecological impacts of pollution and the adaptive capacities of marine invertebrates. This review synthesizes existing research, explores the species' strengths as a research model, and identifies future research directions. All evidence suggests D. celebensis can complement traditional freshwater models and enhance our capacity to monitor and protect marine health.

海洋水蚤（Diaphanosoma celebensis）在海洋生态毒理学、生态生理学和表观遗传学等领域已被公认为有价值的模式生物。本文重点介绍了紫菜在环境研究中的重要意义，强调了其高质量的基因组和转录组资源，对环境胁迫的适应性和对污染物的敏感性。该物种在研究微塑料、重金属和内分泌干扰物等污染物的分子反应方面的效用被强调为其提供解毒途径、应激反应机制和表观遗传修饰的能力。对于提高我们对污染的生态影响和海洋无脊椎动物的适应能力的理解，彩螺是一个重要的工具。本文在综合现有研究成果的基础上，探讨了该物种作为研究模式的优势，并对未来的研究方向进行了展望。所有证据都表明，D. celebensis可以补充传统的淡水模型，并增强我们监测和保护海洋健康的能力。

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引用次数: 0

Rare earth element lanthanum induces inflammatory response in zebrafish through TLR4/NF-κB signaling pathway 稀土元素镧通过TLR4/NF-κB信号通路诱导斑马鱼炎症反应。

IF 4.3 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2026-02-01 Epub Date: 2025-11-20 DOI: 10.1016/j.cbpc.2025.110391

Xinhao Ye , Shiyi Duan , Hao Wang , Shimei Xiao , Mijia Li , Wei Yuan , Yan Zhao , Yiyue Zhang , Keyuan Zhong

The inflammatory response is a core protective physiological process against stimuli like infection or injury, and can be initiated by autoimmune disorders. It is primarily characterized by neutrophil-dominated leukocytosis and may lead to multiple organ dysfunction in severe cases. Environmental factors play an important role in the inflammatory response. Rare earth elements are not essential elements for living organisms. However, owing to large-scale mining and use, their concentrations in the environment have increased. Thus, rare earth elements are now considered emerging environmental pollutants, and the risks that rare earth elements pose to human health need further investigation. In this study, zebrafish were used as experimental animals, and zebrafish embryos were exposed to the different concentrations of lanthanum chloride (0, 5, 15, and 25 mg/L) to analyze its effect on embryo development and immune system. The number and distribution of zebrafish neutrophils as well as changes in oxidative stress and the expression of genes related to inflammation were analyzed. The results indicated that lanthanum chloride exposure reduced the heart rate, shortened the body length, and increased the yolk area of zebrafish embryos. In addition, exposure to lanthanum chloride caused the diffusion of neutrophils, leading to inflammation in zebrafish. Concurrently, the exposure led to the accumulation of reactive oxygen species in zebrafish, which subsequently resulted in the upregulation of malondialdehyde, catalase, and superoxide dismutase levels. Further experiments revealed that exposure to lanthanum chloride led to the upregulation of several inflammation-related genes, such as il-6, il-8, il-10, and cxcl-c1c, as well as certain TLR4/NF-κB signaling-related genes, including tlr4, myd88, nf-κb p65, il-1β, and tnf-α. The TLR4/NF-κB signaling pathway inhibitor andrographolide can alleviate the inflammatory response induced by lanthanum chloride exposure. In conclusion, lanthanum chloride induced inflammation in zebrafish by activating the TLR4/NF-κB signaling pathway. The study results can provide a reference for evaluating the health risks of rare earth elements in humans.

炎症反应是针对感染或损伤等刺激的核心保护性生理过程，可由自身免疫性疾病引发。它主要以中性粒细胞为主的白细胞增多为特征，严重者可导致多器官功能障碍。环境因素在炎症反应中起重要作用。稀土元素不是生物体的必需元素。但是，由于大规模开采和使用，它们在环境中的浓度有所增加。因此，稀土元素现在被认为是新兴的环境污染物，稀土元素对人类健康构成的风险需要进一步调查。本研究以斑马鱼为实验动物，将斑马鱼胚胎暴露于不同浓度的氯化镧（0、5、15和25 mg/L）中，分析其对胚胎发育和免疫系统的影响。分析斑马鱼中性粒细胞的数量和分布，以及氧化应激和炎症相关基因的表达变化。结果表明，氯化镧使斑马鱼胚胎心率降低，体长缩短，卵黄面积增大。此外，暴露于氯化镧引起中性粒细胞的扩散，导致斑马鱼炎症。同时，暴露导致斑马鱼体内活性氧积累，进而导致丙二醛、过氧化氢酶和超氧化物歧化酶水平上调。进一步的实验表明，暴露于氯化镧会导致几种炎症相关基因，如IL-6、IL-8、IL-10和cxcl-c1c，以及某些TLR4/NF-κB信号相关基因，包括TLR4、MyD88、NF-κB P65、IL-1β和TNF-α的上调。TLR4/NF-κB信号通路抑制剂穿心莲内酯可减轻氯化镧暴露引起的炎症反应。综上所述，氯化镧通过激活TLR4/NF-κB信号通路诱导斑马鱼炎症。研究结果可为评价稀土元素对人体的健康风险提供参考。

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引用次数: 0

Behavioral and biochemical effects of benzophenone-3 ingestion in dusky damselfish Stegastes fuscus 食入二苯甲酮-3对暗鲷的行为和生化影响。

IF 4.3 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2026-02-01 Epub Date: 2025-10-31 DOI: 10.1016/j.cbpc.2025.110386

Jéssica Ferreira de Souza , Mayara Moura Silveira , Ana Luisa Pires Moreira , Juliana Alves Costa Ribeiro Souza , Rafael Xavier Martins , Davi Farias , Francisco Carlos da Silva Junior , Ana Carolina Luchiari

Oxybenzone (also known as benzophenone-3 or BP-3) is an organic ultraviolet (UV) filter commonly used in personal care products. BP-3 has been detected in various aquatic environments and is a major concern in reef areas due to their biological richness and vital role in marine ecosystems. This research focused on investigating the effects of BP-3 exposure in dusky damselfish Stegastes fuscus, an endemic species of the Brazilian coast, analyzing behavioral responses, enzymatic biomarkers on encephalon and liver (catalase (CAT), glutathione S-transferase (GST), acetylcholinesterase (AChE), and lactate dehydrogenase (LDH)), and general health indicators (growth rate and hepatosomatic index). Adults of S. fuscus were fed a diet containing BP-3 at concentrations of 10 μg/g food and 20 μg/g food for 44 days, with behavioral tests starting after 30 days of exposure. Light-dark preference, novel tank and aggressiveness tests were conducted. Our results showed that BP-3 exposure decreased health indicators and altered fish behavior, decreasing risk-perception and locomotion, although agonistic behavior remained unaffected. Enzymatic assays revealed changes that varied depending on the tissue analyzed. These findings highlight the potential of BP-3 to impair behavioral and physiological processes in reef fish, emphasizing the need for regulations on UV filters to protect marine ecosystems and reef life.

氧苯酮（也称为二苯甲酮-3或BP-3）是一种有机紫外线（UV）过滤器，通常用于个人护理产品。BP-3已在各种水生环境中被检测到，由于其丰富的生物多样性和在海洋生态系统中的重要作用，它是珊瑚礁地区的主要关注点。本研究旨在研究BP-3暴露对巴西海岸特有物种褐豆鲷的影响，分析其行为反应、脑和肝脏酶生物标志物（过氧化氢酶（CAT）、谷胱甘肽s -转移酶（GST）、乙酰胆碱酯酶（AChE）和乳酸脱氢酶（LDH））以及一般健康指标（生长速度和肝体指数）。以10 μg和20 μg/g的BP-3为饵料饲喂褐曲虫成虫44 天，暴露30 天后开始行为测试。进行了光暗偏好、新槽和侵袭性试验。我们的研究结果表明，BP-3暴露降低了鱼的健康指标，改变了鱼的行为，降低了风险感知和运动，尽管激动行为不受影响。酶分析揭示了不同组织的变化。这些发现强调了BP-3对珊瑚鱼行为和生理过程的潜在影响，强调了对紫外线过滤器进行监管以保护海洋生态系统和珊瑚礁生物的必要性。

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引用次数: 0

Polystyrene microplastics and nanoplastics induce neurotoxicity in zebrafish via oxidative stress and neurotransmitter disruption 聚苯乙烯微塑料和纳米塑料通过氧化应激和神经递质破坏诱导斑马鱼神经毒性。

IF 4.3 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2026-02-01 Epub Date: 2025-11-19 DOI: 10.1016/j.cbpc.2025.110397

Jiejie Li , Yingjie Chen , Yuequn Chen , Han Xie , Ganglong Wu , Yiming Zhang , Kusheng Wu

The widespread use of plastic products has led to the global accumulation of microplastics (MPs) and nanoplastics (NPs) in aquatic and terrestrial environments, posing significant risks to ecosystems and human health. This study investigated the neurodevelopmental toxicity of polystyrene MPs (PS-MPs, 5 μm) and NPs (PS-NPs, 60 nm) in zebrafish (Danio rerio) and explored the underlying mechanisms. Zebrafish embryos were exposed to 0.05–50 mg/L PS-MPs/PS-NPs from 2 hour post-fertilization (hpf) to 7 days post-fertilization (dpf). Morphological, behavioral, and molecular endpoints were analyzed. Exposure to polystyrene MPs and NPs (PS-MNPs) induced dose-dependent developmental malformations, including spinal curvature, pericardial edema, and abnormal body pigmentation, accompanied by increased heart rate and body length. Behavioral assays revealed reduced spontaneous tail-coiling in embryos and hyperactive swimming in larvae, particularly under light stimulation. Mechanistic studies showed PS-MNPs disrupted neurotransmitter homeostasis (reduced dopamine, acetylcholine, GABA, and serotonin levels) and altered neurodevelopment-related gene expression (e.g., mbpa, ache, gfap). Oxidative stress was evident via elevated reactive oxygen species (ROS) and upregulated antioxidant genes (sod1, cat) in PS-NP-exposed larvae. These findings demonstrate that PS-MNPs induce neurodevelopmental toxicity in zebrafish through oxidative stress and neurotransmitter system dysfunction, highlighting the potential risks of plastic pollution to aquatic organisms and human health via trophic transfer.

塑料产品的广泛使用导致全球水生和陆地环境中微塑料（MPs）和纳米塑料（NPs）的积累，对生态系统和人类健康构成重大风险。本研究研究了聚苯乙烯MPs （PS-MPs, 5 μm）和NPs （PS-NPs, 60 nm）对斑马鱼的神经发育毒性，并探讨了其机制。斑马鱼胚胎在受精后2 小时（hpf）至7 天（dpf）暴露于0.05-50 mg/L的PS-MPs/PS-NPs中。形态学、行为学和分子终点分析。暴露于聚苯乙烯MPs和NPs （PS-MNPs）会引起剂量依赖性发育畸形，包括脊柱弯曲、心包水肿和异常的身体色素沉着，并伴有心率和体长增加。行为分析显示，在光刺激下，胚胎自发尾卷减少，幼虫过度活跃游泳。机制研究表明，PS-MNPs破坏神经递质稳态（降低多巴胺、乙酰胆碱、GABA和血清素水平），并改变神经发育相关基因表达（如mbpa、ache、gfap）。在ps - np暴露的幼虫中，氧化应激通过活性氧（ROS）的升高和抗氧化基因（sod1, cat）的上调而明显。这些研究结果表明，PS-MNPs通过氧化应激和神经递质系统功能障碍诱导斑马鱼神经发育毒性，突出了塑料污染通过营养转移对水生生物和人类健康的潜在风险。

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引用次数: 0

Phenol exposure promotes tumor-related signaling and blood vessel formation through the extracellular signal-regulated kinase/p38/hypoxia-inducible factor-1α pathway in cellular and zebrafish models 在细胞和斑马鱼模型中，苯酚暴露通过细胞外信号调节激酶/p38/缺氧诱导因子-1α途径促进肿瘤相关信号传导和血管形成。

IF 4.3 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2026-02-01 Epub Date: 2025-11-19 DOI: 10.1016/j.cbpc.2025.110396

Chung-Yu Lin , Wangta Liu , Pei-Hsuan Chen , Chia C. Wang , Che-Hsin Lee

Phenol is a common aquatic contaminant originating from industrial discharge, plastics, and personal care products, and is frequently detected due to its high solubility and environmental persistence. Although its acute toxicity is well documented, the effects of phenol at environmentally relevant concentrations on cellular mechanisms linked to tumor progression remain underexplored. In this study, we investigated the impact of phenol exposure (0–125 μM) on cancer-related cellular behaviors using B16F10 melanoma and LL2 lung carcinoma cells, as well as zebrafish xenograft models, which serve as an integrated aquatic toxicology platform. Phenol exposure activated extracellular signal-regulated kinase (ERK) and p38 pathways, upregulated hypoxia-inducible factor 1α (HIF-1α), increased vascular endothelial growth factor (VEGF) expression, and induced epithelial–mesenchymal transition (EMT). These molecular events collectively enhanced tumor cell migration and angiogenesis both in vitro and in vivo. Our findings provide mechanistic evidence that environmentally relevant phenol exposure can modulate conserved stress and signaling pathways associated with tumor-related phenotypes. This work underscores the importance of combining molecular biomarkers with aquatic vertebrate models to assess the ecological and toxicological risks of persistent organic pollutants such as phenol.

苯酚是一种常见的水生污染物，源于工业排放、塑料和个人护理产品，由于其高溶解度和环境持久性，经常被检测到。尽管其急性毒性已被充分证明，但环境相关浓度下苯酚对肿瘤进展相关细胞机制的影响仍未得到充分研究。在这项研究中，我们研究了苯酚暴露（0-125 μM）对癌症相关细胞行为的影响，使用B16F10黑色素瘤和LL2肺癌细胞以及斑马鱼异种移植模型，作为综合水生毒理学平台。苯酚暴露激活细胞外信号调节激酶（ERK）和p38通路，上调缺氧诱导因子1α (HIF-1α)，增加血管内皮生长因子（VEGF）表达，诱导上皮-间质转化（EMT）。这些分子事件共同增强了肿瘤细胞在体内和体外的迁移和血管生成。我们的研究结果提供了机制证据，表明环境相关的苯酚暴露可以调节与肿瘤相关表型相关的保守应激和信号通路。这项工作强调了将分子生物标志物与水生脊椎动物模型结合起来评估持久性有机污染物（如苯酚）的生态和毒理学风险的重要性。

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引用次数: 0