Comparative Biochemistry and Physiology C-toxicology & Pharmacology最新文献_第9页

Morphological, behavioral, and molecular neurotoxicity of octocrylene in zebrafish larvae 八烯烯对斑马鱼幼体的形态学、行为学和分子神经毒性。

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 : 2025-09-13 DOI: 10.1016/j.cbpc.2025.110355

Sihan Hou , Daoyuan Qin , Daoxi Lei , Qin Wang

Octocrylene (OC), a prevalent ultraviolet (UV) filter in sunscreens, is frequently detected in soils, sediments, aquatic systems, and food chains, making it an emerging contaminant. Although evidence suggests OC impairs zebrafish larval development, its neurotoxic effects remain incompletely understood. In this study, zebrafish embryos were exposed to OC (0–30 μM) to assess impacts on early neurodevelopment. The results showed that exposure to 30 μM OC reduced the hatching rate of zebrafish and decreased their heart rate at 48 hpf. OC concentrations above 10 μM increased the body length of zebrafish larvae. Moreover, OC exposure significantly reduced various types of neural cells, including neural stem cells, neural progenitor cells, neurons, and glial cells, and led to behavioral abnormalities. Mechanistically, transcriptomic profiling revealed that the differentially expressed genes were mainly enriched in the process of activating apoptosis. Concentration-dependent increases in acridine orange (AO) and reactive oxygen species (ROS) staining confirmed apoptosis in brain tissues. Further analysis suggested that OC-induced neurotoxicity may be mediated by dysregulation of the MDM2-p53 signaling axis. These findings elucidate previously unrecognized mechanisms of OC neurotoxicity, providing critical insights for environmental risk assessment of UV filters.

八烯（OC）是防晒霜中普遍存在的紫外线（UV）过滤器，在土壤、沉积物、水生系统和食物链中经常被检测到，使其成为一种新兴污染物。尽管有证据表明OC会损害斑马鱼幼虫的发育，但其神经毒性作用仍不完全清楚。在本研究中，斑马鱼胚胎暴露于OC（0-30 μM）以评估其对早期神经发育的影响。结果表明，暴露于30 μ OC可降低斑马鱼的孵化率，并降低48 hpf时的心率。10 μM以上的OC浓度使斑马鱼幼鱼体长增加。此外，OC暴露显著减少了各种类型的神经细胞，包括神经干细胞、神经祖细胞、神经元和神经胶质细胞，并导致行为异常。机制上，转录组学分析显示，差异表达基因主要富集在激活凋亡的过程中。吖啶橙（AO）和活性氧（ROS）染色的浓度依赖性增加证实了脑组织的凋亡。进一步分析表明，oc诱导的神经毒性可能是由MDM2-p53信号轴的失调介导的。这些发现阐明了以前未被认识的OC神经毒性机制，为紫外线过滤器的环境风险评估提供了重要见解。

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引用次数: 0

Inhibitory effects of isobavachalcone against Tetrahymena thermophila: Mechanistic insights 异巴伐恰尔酮对嗜热四膜虫的抑制作用：机理研究。

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 : 2025-09-13 DOI: 10.1016/j.cbpc.2025.110352

Hongming Tang , Juan Liu , Dong Sheng , Xu Ren , Qinghua Yu , Zhixin Guo , Yunpeng Wu , Yuxiao Liu , Yuehan Xiao , Wei Wang , Shigen Ye , Weijia Zhou

Isobavachalcone (IBC), a bioactive flavonoid derived from Psoralea corylifolia, exhibits potent anti-ciliate activity, but its underlying mechanism remains unclear. Utilizing Tetrahymena thermophila as a model organism, we demonstrated that IBC induces dose-dependent mortality (12 h-IC₅₀: 1.39 mg/L) and inhibits growth. Mechanistically, IBC triggers oxidative stress by elevating reactive oxygen species (ROS) and disrupting antioxidant enzymes, including superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione (GSH). This disruption leads to membrane damage, as evidenced by lactate dehydrogenase (LDH) leakage and ATPase inhibition, as well as mitochondrial dysfunction. Microscopic examination and staining confirmed that cell death occurs via necrotic cell death rather than apoptosis. Transcriptome analysis revealed key pathways, including peroxisome-mediated oxidation, glutathione metabolism, and ATP-binding cassette (ABC) transporters, further supporting the role of IBC in oxidative and structural disruption. These findings elucidate the anti-ciliate mechanism of IBC, providing valuable insights for developing targeted anti-parasitic agents.

异巴瓦恰尔酮（IBC）是一种从补骨脂中提取的具有生物活性的类黄酮，具有很强的抗纤毛虫活性，但其作用机制尚不清楚。利用嗜热四膜虫作为模式生物，我们证明了IBC诱导剂量依赖性死亡（12 h-IC50: 1.39 mg/L）并抑制生长。在机制上，IBC通过升高活性氧（ROS）和破坏抗氧化酶（包括超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）和谷胱甘肽（GSH））触发氧化应激。这种破坏导致膜损伤，如乳酸脱氢酶（LDH）渗漏和atp酶抑制，以及线粒体功能障碍。显微镜检查和染色证实细胞死亡是通过坏死细胞死亡而不是凋亡发生的。转录组分析揭示了关键途径，包括过氧化物酶体介导的氧化、谷胱甘肽代谢和atp结合盒（ABC）转运蛋白，进一步支持IBC在氧化和结构破坏中的作用。这些发现阐明了IBC的抗纤毛虫机制，为开发靶向抗寄生虫药物提供了有价值的见解。

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引用次数: 0

Unveiling excessive feed-sources copper-induced ileitis in chickens: Insights into tight junction damage and ROS/NLRP3/pyroptosis axis 揭示过量饲料来源铜诱导的鸡回肠炎：对紧密连接损伤和ROS/NLRP3/焦亡轴的见解。

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 : 2025-09-13 DOI: 10.1016/j.cbpc.2025.110357

Boran Zhou , Yufei Cao , Yingxue Zhang, Mingwei Xing, Yu Wang

Copper, widely used as a growth promoter and antibacterial agent, is commonly added to livestock and poultry feed. However, this widespread use leads to its accumulation in the animals' bodies, resulting in intestinal toxicity. The specific mechanisms of copper-induced ileitis in broilers remain unclear. In this study, broilers were fed diets containing 0, 100, or 300 mg/kg CuSO₄ over a five-week period. Results showed that the high‑copper group (300 mg/kg) exhibited significant suppression of antioxidant defenses, including reduced heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), total superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels, while catalase (CAT) activity was paradoxically elevated. Notably, NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome complex activation (NLRP3, apoptosis-associated speck-like protein containing a CARD [ASC], Caspase-1) and upregulated pyroptosis markers (Caspase-1, interleukin-1β [IL-1β]) indicated reactive oxygen species (ROS)–NLRP3 axis involvement. Concurrently, pro-inflammatory mediators (interleukin-7 [IL-7], interleukin-17 [IL-17], inducible nitric oxide synthase [iNOS], tumor necrosis factor-α [TNF-α]) were dysregulated, accompanied by diminished expression of tight junction proteins (zonula occludens-1 [ZO-1], Claudin-3, Occludin) and inhibition of the Wnt/β-catenin pathway. These findings demonstrate that copper-induced intestinal inflammation and pyroptosis are driven by ROS–NLRP3 axis activation, while simultaneously compromising mucosal barrier integrity. This study elucidates critical mechanisms of copper toxicity in broilers and highlights risks associated with excessive copper exposure.

铜被广泛用作生长促进剂和抗菌剂，通常添加到畜禽饲料中。然而，这种广泛使用导致其在动物体内积累，导致肠道毒性。铜诱发肉鸡回肠炎的具体机制尚不清楚。在本研究中，肉鸡在5周内分别饲喂含有0、100或300 mg/kg硫酸铜的饲粮。结果表明，高铜组（300 mg/kg）显著抑制了抗氧化防御，包括血红素氧化酶-1 （HO-1）、NAD(P)H醌脱氢酶1 （NQO1）、总超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）水平降低，而过氧化氢酶（CAT）活性却升高。值得注意的是，nod样受体家族pyrin结构域包含3 （NLRP3）炎性体复合物激活（NLRP3，凋亡相关斑点样蛋白含有CARD [ASC]， Caspase-1）和上调的焦亡标志物（Caspase-1，白细胞介素-1β [IL-1β]）表明活性氧(ROS)-NLRP3轴参与。同时，促炎介质（白细胞介素-7 [IL-7]、白细胞介素-17 [IL-17]、诱导型一氧化氮合酶[iNOS]、肿瘤坏死因子-α [TNF-α]）出现异常，并伴有紧密连接蛋白（闭塞带-1 [ZO-1]、Claudin-3、Occludin）表达减少，Wnt/β-catenin通路受到抑制。这些发现表明，铜诱导的肠道炎症和焦亡是由ROS-NLRP3轴激活驱动的，同时损害了粘膜屏障的完整性。本研究阐明了肉仔鸡铜中毒的关键机制，并强调了过量铜暴露的相关风险。

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引用次数: 0

Toxic effects of polystyrene and polyethylene microplastics on the zebrafish cardiovascular system and their differential mechanisms 聚苯乙烯和聚乙烯微塑料对斑马鱼心血管系统的毒性作用及其差异机制。

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 : 2025-09-12 DOI: 10.1016/j.cbpc.2025.110353

Qingzheng Liu , Feifei Yan , Haoran Liu , Jing Zhang , Jidong Zhang

This study investigated the toxic effects of polystyrene (PS) and polyethylene (PE) microplastics on the cardiovascular systems of zebrafish, as well as the differences in their mechanisms. Using a larval zebrafish (Danio rerio) model, we systematically evaluate the effects of the two microplastics on growth and development, oxidative stress, myocardial cell number and structure, histopathological changes, cell apoptosis, and gene expression via physiological parameter measurements, histopathological analysis, and molecular biological techniques. The experimental results showed that PS exerted a more significant inhibitory effect on body weight, whereas PE had a more marked inhibitory effect on body length. Both substances caused a dose-dependent decrease in heart rate, induced oxidative stress, aggravated myocardial damage and fibrosis and activated inflammatory responses. Additionally, PS and PE microplastics exhibit differences in their toxic mechanisms. PS enhances toxicity primarily through the adsorption capacity of its rigid benzene ring structures. While PE, due to its strong hydrophobicity, tends to accumulate more readily in myocardial tissue and exacerbate cell apoptosis via physical damage pathways. This study is the first to compare the differential mechanisms of cardiovascular toxicity between PS and PE microplastics in zebrafish, providing scientific evidence for environmental risk assessment and human health protection related to microplastics.

本研究探讨了聚苯乙烯（PS）和聚乙烯（PE）微塑料对斑马鱼心血管系统的毒性作用及其机制的差异。以斑马鱼（Danio rerio）幼体为研究对象，通过生理参数测量、组织病理学分析和分子生物学技术，系统评价了两种微塑料对斑马鱼生长发育、氧化应激、心肌细胞数量和结构、组织病理学改变、细胞凋亡和基因表达的影响。实验结果表明，PS对体重的抑制作用更为显著，而PE对体长的抑制作用更为显著。两种物质均引起剂量依赖性心率降低，诱导氧化应激，加重心肌损伤和纤维化，并激活炎症反应。此外，PS和PE微塑料在毒性机制上也存在差异。PS增强毒性主要是通过其刚性苯环结构的吸附能力。而PE由于其较强的疏水性，更容易在心肌组织中积累，通过物理损伤途径加剧细胞凋亡。本研究首次比较了PS和PE微塑料对斑马鱼心血管毒性的差异机制，为微塑料相关的环境风险评估和人类健康保护提供科学依据。

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引用次数: 0

Pyridaben-induced biochemical and molecular stress in Daphnia magna 吡嘧虫酯诱导的水蚤生化和分子应激。

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 : 2025-09-08 DOI: 10.1016/j.cbpc.2025.110350

Gülüzar Atli , Yusuf Sevgiler , Serdar Kilercioglu

Pyridaben (PDB) is a widely used acaricide in agriculture, classified as highly toxic to aquatic life (H400, H410; USEPA) because it inhibits mitochondrial complex I. This study aimed to evaluate the subacute toxicity of PDB (0.20–0.80 TU for 48 h) in the model organism Daphnia magna using an integrated molecular and biochemical multi-biomarker approach. To the best of our knowledge, this is the first comprehensive study to integrate molecular and biochemical markers related to oxidative stress and osmoregulation in assessing subacute PDB toxicity in D. magna using the Integrated Biomarker Response index (IBR). PDB exposure altered antioxidant system dynamics, with decreased SOD and GPX activities, increased CAT and GST activities, and elevated GSH and TBARS levels. The increase in Ca²⁺-ATPase activity was positively correlated with antioxidant enzymes, suggesting an adaptive osmoregulatory response to oxidative stress. Reduced total protein levels were negatively correlated with most of the biomarkers. At the molecular level, while the expression of oxidative stress-related genes decreased, miR-153 was significantly upregulated, showing a negative correlation with these genes but a positive correlation with other biomarker levels. The results revealed significant and interrelated alterations at both biochemical and molecular levels, and IBR analysis demonstrated that responses were notably triggered at 0.35 TU, with maximal effects observed at concentrations of 0.50 TU and above. These findings provide new insights into the ecological risk of PDB, supporting the use of multi-biomarker approaches for environmental monitoring, as well as elucidating molecular pathways underlying the adaptive responses of aquatic organisms to stress.

嘧达宾（Pyridaben， PDB）是一种广泛应用于农业的杀螨剂，因其抑制线粒体复合体i而被列为对水生生物的高毒性（H400, H410； USEPA）。本研究旨在利用综合分子和生化多生物标志物方法评估PDB （0.20-0.80 TU / 48 h）对模式生物大水蚤的亚急性毒性。据我们所知，这是第一个综合氧化应激和渗透调节相关的分子和生化标志物，利用综合生物标志物反应指数（IBR）评估D. magna亚急性PDB毒性的综合研究。PDB暴露改变了抗氧化系统动力学，SOD和GPX活性降低，CAT和GST活性增加，GSH和TBARS水平升高。Ca2+- atp酶活性的增加与抗氧化酶正相关，提示对氧化应激的适应性渗透调节反应。总蛋白水平的降低与大多数生物标志物呈负相关。在分子水平上，miR-153在氧化应激相关基因表达降低的同时显著上调，与这些基因呈负相关，而与其他生物标志物水平呈正相关。结果显示，在生化和分子水平上发生了显著且相互关联的变化，IBR分析表明，在0.35 TU时引起的反应明显，在0.50 TU及以上浓度时观察到的效果最大。这些发现为PDB的生态风险提供了新的见解，支持使用多生物标志物方法进行环境监测，并阐明了水生生物对胁迫的适应性反应的分子途径。

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引用次数: 0

Significantly enhanced effects of heavy metals on the toxicity, bioconcentration and biomagnification under combined exposure 在复合暴露下，重金属对毒性、生物浓度和生物放大的影响显著增强

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 : 2025-09-08 DOI: 10.1016/j.cbpc.2025.110346

Qian Cheng , Jin Zhang , Bi-ya Dai , Xin-yue Wang , Guang-zhen Ji , Yuan-fan Zhao

Heavy metal (HM) co-contamination is prevalent in the aquatic ecosystems and often induces complex combined effects such as synergism or antagonism, bioconcentration and biomagnification on the food-chain organisms, which is threatening the survival of living creatures and even to human health. However, the combined effects of HMs under combined exposure on the aquatic food chains still remain poorly understood. Therefore, toxic responses, bioconcentration and biomagnification of four typical HMs, lead (Pb), cadmium (Cd), nickel (Ni) and zinc (Zn), were systematically investigated under different combined exposure conditions. Results demonstrated that combined toxicity significantly exceeded single-metal effects and increased with component number, following the order: quaternary > ternary > binary > single. The CdNi combination exhibited the strongest toxicity at 96 h (pEC₅₀ = 4.15), confirming significant synergistic. Further analysis of the reactive oxygen species (ROS) production, membrane integrity, and chlorophyll a and b contents demonstrated that HM interactions disrupt redox balance and photosynthetic function, amplifying toxicity. Under the combined exposure, HMs were readily bioconcentrated in Chlorella pyrenoidosa and transferred to Daphnia magna. Notably, Cd showed clear biomagnification under single-metal exposure. As the number and complexity of metal components increased, biomagnification factor values for both Cd and Ni further increased. Cd and Ni exhibited stronger trophic magnification effects, indicating that Cd and Ni may be the key drivers of combined toxicity and biomagnification. All the findings in this study will provide the basic reference for the ecological risk assessment of compound contamination of multiple HMs.

重金属共污染在水生生态系统中普遍存在，并对食物链生物产生协同或拮抗、生物浓缩和生物放大等复杂的综合效应，威胁着生物的生存乃至人类的健康。然而，在综合暴露下，HMs对水生食物链的综合影响仍然知之甚少。因此，系统地研究了铅（Pb）、镉（Cd）、镍（Ni）和锌（Zn）四种典型HMs在不同组合暴露条件下的毒性反应、生物浓度和生物放大效应。结果表明，联合毒性明显超过单一金属效应，并随成分数的增加而增加，其顺序为：四元>；三元>；二元>；单一。CdNi组合在96 h时毒性最强（pEC50 = 4.15），证实了显著的协同作用。对活性氧（ROS）生成、膜完整性和叶绿素a和b含量的进一步分析表明，HM相互作用破坏了氧化还原平衡和光合功能，放大了毒性。在联合暴露下，HMs很容易在核核小球藻中被生物浓缩，并转移到大水蚤中。值得注意的是，Cd在单金属暴露下表现出明显的生物放大。随着金属组分数量和复杂性的增加，Cd和Ni的生物放大因子值进一步增加。Cd和Ni表现出较强的营养放大效应，表明Cd和Ni可能是联合毒性和生物放大的关键驱动因素。本研究结果将为多种卫生管理物质复合污染的生态风险评价提供基础参考。

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引用次数: 0

Low-level tetrabromobisphenol A (TBBPA) exposure disrupts early embryonic architecture: molecular impacts on dorsoventral patterning 低水平四溴双酚a （TBBPA）暴露破坏早期胚胎结构：对背腹模式的分子影响。

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 : 2025-09-06 DOI: 10.1016/j.cbpc.2025.110348

Kanchaka Senarath Pathirajage , Rosemaria Serradimigni , Copeland R. Johnson , Sunil Sharma , Christopher Chouinard , Subham Dasgupta

Tetrabromobisphenol A (TBBPA), a widely used flame retardant in textiles and electronics, poses toxicological risks through both environmental and indoor exposures. Biomonitoring studies have detected significant TBBPA levels in prenatal environments, including cord blood, raising concerns about developmental impacts. Using zebrafish as a model, this study addresses critical gaps in understanding how developmental TBBPA exposures perturb regulatory pathways that govern dorsoventral patterning. Embryos were exposed at 0.75- or 6-h post-fertilization (hpf) and phenotyped at 24 hpf, with tissue uptake quantified by LC-MS. At 24 hpf, embryos exhibited concentration-dependent ventralization characterized by loss of dorsal structures. Whole-mount immunohistochemistry revealed concentration-dependent alterations in dorsoventral, cell adhesion, and germ layer markers, indicating disruptions in cell migration and germ layer integrity. At later stages, even nontoxic exposures led to craniofacial and hematopoietic defects, linking early molecular perturbations to downstream developmental abnormalities. Although the phenotypes strongly resembled BMP pathway overactivation, co-exposure with the BMP inhibitor dorsomorphin failed to rescue the defects, suggesting involvement of alternative mechanisms. Collectively, these findings demonstrate that TBBPA disrupts proteins critical for cell migration, fate specification, and germ layer formation at environmentally relevant concentrations, fundamentally altering embryonic physiology prior to organogenesis and inducing systemic changes in tissue development.

四溴双酚A （TBBPA）是一种广泛用于纺织品和电子产品的阻燃剂，通过环境和室内暴露都会产生毒性风险。生物监测研究已经在产前环境中检测到显著的TBBPA水平，包括脐带血，这引起了对发育影响的关注。使用斑马鱼作为模型，本研究解决了理解发育中的TBBPA暴露如何干扰控制背腹模式的调节途径的关键空白。胚胎在受精后0.75或6小时（hpf）暴露，在24 hpf时表型，用LC-MS定量组织摄取。在24 hpf时，胚胎表现出浓度依赖性腹化，其特征是背部结构的丧失。全挂载免疫组织化学显示背腹侧、细胞粘附和胚层标记物的浓度依赖性改变，表明细胞迁移和胚层完整性受到破坏。在后期，即使是无毒暴露也会导致颅面和造血缺陷，将早期分子扰动与下游发育异常联系起来。尽管表型与BMP通路过度激活非常相似，但与BMP抑制剂dorsomorphin共同暴露未能挽救这些缺陷，这表明涉及其他机制。总的来说，这些发现表明，TBBPA在环境相关浓度下会破坏对细胞迁移、命运规范和胚层形成至关重要的蛋白质，从根本上改变器官发生前的胚胎生理学，并诱导组织发育的系统性变化。

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引用次数: 0

Artificial light at night disrupts fertility in Drosophila melanogaster 夜间的人造光会干扰果蝇的生育能力。

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 : 2025-09-06 DOI: 10.1016/j.cbpc.2025.110349

Margherita Martelli , Raffaella Lazzarini , Francesco Piva , Gianmaria Salvio , Alessandro Ciarloni , Lory Santarelli , Massimo Bracci

Artificial light at night (ALAN) can disrupt numerous biological processes, and is increasingly studied in animal models. Here, we evaluated the impact of red and blue ALAN on Drosophila melanogaster, focusing on fertility, development, circadian rhythms, and gene expression. All results were compared to those of a control group maintained under a 12 h white light/12 h dark cycle.

Red ALAN exposure increased the number of eggs laid but reduced the hatching rate and shortened the larval period. Conversely, blue ALAN led to fewer eggs laid, fewer emerging adults, and lower hatching success. Significant alterations in circadian rhythm and the sleep–wake cycle were observed in flies exposed to both red and blue ALAN, including a reduction in mean locomotor activity over 24 h and during the daytime period, increased sleep duration during the day, and reduced sleep duration at night. Effects were more pronounced under blue ALAN, which disrupted circadian rhythm by eliminating morning and evening activity peaks and increasing nocturnal activity. Gene expression analyses revealed that red ALAN upregulated ecdysone-induced protein 74EF (E74) and the ecdysone receptor (EcR) expression in adults, while juvenile hormone binding protein 1 (Jhbp1) was elevated under both light conditions. In larvae, both ALAN spectra increased expression of E74 and Jhbp1.

These findings demonstrate that red and blue ALAN can significantly disrupt fertility and development in Drosophila melanogaster. Given the rising prevalence of light pollution and night-shift work, further studies are needed to investigate ALAN-related reproductive impairments in other animals, including vertebrates and humans.

夜间人造光（ALAN）可以破坏许多生物过程，并且越来越多地在动物模型中进行研究。在这里，我们评估了红色和蓝色ALAN对黑腹果蝇的影响，重点是生育力、发育、昼夜节律和基因表达。所有结果都与对照组在12 h白光/12 h暗循环下的结果进行了比较。赤色艾伦暴露增加了产卵数，但降低了孵化率，缩短了幼虫期。相反，蓝色ALAN导致产卵量减少，成虫数量减少，孵化成功率降低。在暴露于红色和蓝色ALAN的果蝇中，观察到昼夜节律和睡眠-觉醒周期的显著变化，包括24 h和白天平均运动活动减少，白天睡眠时间增加，夜间睡眠时间减少。蓝色ALAN的效果更明显，它通过消除早晚活动高峰和增加夜间活动来扰乱昼夜节律。基因表达分析显示，红色ALAN上调蜕皮激素诱导蛋白74EF （E74）和蜕皮激素受体（EcR）的表达，而幼体激素结合蛋白1 （Jhbp1）在两种光照条件下均升高。在幼虫中，ALAN光谱均增加了E74和Jhbp1的表达。这些发现表明，红色和蓝色ALAN可以显著破坏果蝇的生育和发育。鉴于光污染和夜班工作的日益普遍，需要进一步研究包括脊椎动物和人类在内的其他动物与alan相关的生殖障碍。

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引用次数: 0

Fisetin modulates fluoride induced osteochondral toxicity in zebrafish larvae 非西汀调节氟诱导的斑马鱼幼鱼骨软骨毒性。

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 : 2025-09-06 DOI: 10.1016/j.cbpc.2025.110351

Harsheema Ottappilakkil , Grace Helena Yesudas , Theeksha Sreedharan , Ekambaram Perumal

Excessive fluoride (F⁻) exposure, particularly during early development, poses a significant risk to skeletal integrity by disrupting bone homeostasis through oxidative stress and altered mineralization. While F⁻ induced oxidative stress is well documented, studies investigating the role of natural antioxidants in mitigating F⁻ induced osteochondral toxicity remain limited. Hence, the present study investigated the osteomodulatory effect of fisetin (Fis) against F⁻ toxicity in zebrafish larvae. Fis (15 μM) was exposed to zebrafish larvae at 3 days post fertilization (dpf) for 24 h, followed by 72 h exposure to 25 ppm sodium fluoride (NaF). F⁻ accumulation, oxidant (ROS, LPO, NO, PCC) and antioxidant (SOD, CAT, GSH) levels, cartilage (alcian blue staining), skeletal (alizarin red staining, hydroxyproline content, ALP activity) markers, and expression of osteochondral genes (sox9b, runx2b, ocn, osx, col1a1, alp, rankl, and opg) were assessed in control and treated larvae. F⁻ exposure significantly elevated oxidative stress, disrupted craniofacial cartilage morphology, and induced premature ossification, alongside altered expression of osteogenic and resorptive markers. Remarkably, Fis pretreatment effectively reduced F⁻ accumulation, restored redox homeostasis, preserved cartilage architecture, and normalized mineral deposition. Gene expression analysis further confirmed that Fis modulated key regulators of osteogenesis, chondrogenesis, and bone resorption, underscoring its osteoprotective role. Collectively, these findings demonstrate that Fis confers protection against F⁻ induced osteochondral toxicity by attenuating oxidative stress, supporting bone matrix development, and regulating genes essential for bone homeostasis.

过量的氟化物（F-）暴露，特别是在发育早期，通过氧化应激和矿化改变破坏骨骼稳态，对骨骼完整性构成重大风险。虽然F诱导的氧化应激有很好的文献记载，但关于天然抗氧化剂在减轻F诱导的骨软骨毒性中的作用的研究仍然有限。因此，本研究探讨了非西汀（Fis）对斑马鱼幼鱼F-毒性的骨调节作用。Fis（15 μM）在受精后3 天（dpf）暴露于斑马鱼幼虫24 h，然后暴露于25 ppm氟化钠（NaF） 72 h。测定F-积累、氧化剂（ROS、LPO、NO、PCC）和抗氧化剂（SOD、CAT、GSH）水平、软骨（alcian blue染色）、骨骼（茜素红染色、羟脯氨酸含量、ALP活性）标志物和骨软骨基因（sox9b、runx2b、ocn、osx、col1a1、ALP、rankl和opg）表达。氟暴露显著增加氧化应激，破坏颅面软骨形态，诱导过早骨化，同时改变成骨和吸收标志物的表达。值得注意的是，Fis预处理有效地减少了F-积累，恢复了氧化还原稳态，保存了软骨结构，并使矿物质沉积正常化。基因表达分析进一步证实Fis调节成骨、软骨形成和骨吸收的关键调控因子，强调其骨保护作用。总的来说，这些发现表明，Fis通过减轻氧化应激、支持骨基质发育和调节骨骼稳态所必需的基因，对F诱导的骨软骨毒性具有保护作用。

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引用次数: 0

Effects of short-term exposure to environmentally relevant pesticides mixture on morphological alterations, oxidative-nitrative stress biomarkers, cellular apoptosis, and antioxidant expression in kidneys of goldfish 短期暴露于环境相关农药混合物对金鱼肾脏形态改变、氧化-硝化应激生物标志物、细胞凋亡和抗氧化剂表达的影响

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 : 2025-09-01 DOI: 10.1016/j.cbpc.2025.110337

Esmirna Cantu , Md Saydur Rahman

Chemical stressors are pervasive, affecting both terrestrial and aquatic environments. The continual influx of these toxins is damaging ecosystems and the organisms that inhabit them. The abundance of environmental toxins makes aquatic habitats inhospitable for aquatic life. These chemical stressors consistently disrupt the life processes of aquatic organisms, particularly their physiological functions. This study examined on the effects of environmentally relevant pesticides mixture (low-dose and high-dose: S-metolachlor: 2.4 go/L, 12 μg/L; linuron: 2.0 μg/L, 10 μg/L; isoproturon: 1.2 μg/L, 6.0 μg/L; tebucanozole: 1.2 μg/L, 6.0 μg/L; aclonifen: 0.8 μg/L, 4.0 μg/L; atrazine: 0.4 μg/L, 2.0 μg/L; pendimethalin: 0.4 μg/L, 2.0 μg/L, and azinphos-methyl: 0.8 μg/L, 4.0 μg/L) on tissue morphology, cellular apoptosis, and nitrotyrosine protein (NTP), dinitrophenyl protein (DNP), renin, superoxide dismutase (SOD), and catalase (CAT) expression in the kidneys of goldfish (Carassius auratus) exposed for one week under controlled laboratory conditions. Histopathological analysis revealed severe tissue damage in the kidneys, while silver staining identified melano-macrophage centers, and immunohistochemistry and real-time PCR shed light on the expression of molecular biomarkers in these tissues. Exposure to pesticide mixtures caused fish to exhibit glomerular shrinkage, enlargement of Bowman's space, and degradation of glomerular cells. Moreover, the expression of renin, DNP, NTP, SOD, and apoptotic nuclei increased in kidney tissues, while CAT expression decreased. Overall, our findings indicate that exposure of goldfish to an environmentally relevant pesticide mixture leads to increased cellular damage and altered osmoregulatory and antioxidant enzyme expressions, which may impair physiological functions, including growth, reproduction, and development in teleost fish.

化学压力源无处不在，影响着陆地和水生环境。这些毒素的不断涌入正在破坏生态系统和栖息在其中的生物。丰富的环境毒素使水生生物的栖息地不适宜生存。这些化学应激源不断破坏水生生物的生命过程，特别是它们的生理功能。这项研究检查了相关环保农药混合物的影响(低剂量和高剂量:S-metolachlor: 2.4 / L, 12 μg / L;利谷隆: 2.0μg / L, 10 μg / L; isoproturon: 1.2μg / L, 6.0μg / L; tebucanozole: 1.2μg / L, 6.0μg / L; aclonifen: 0.8μg / L, 4.0μg / L;莠去津: 0.4μg / L, 2.0μg / L;在实验室条件下，二甲萘：0.4 μg/L, 2.0 μg/L，甲基氮磷：0.8 μg/L, 4.0 μg/L，对鲫鱼（Carassius auratus）肾脏组织形态、细胞凋亡及硝基酪氨酸蛋白（NTP）、二硝基苯蛋白（DNP）、肾素、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）表达的影响。组织病理学分析显示肾脏严重的组织损伤，而银染色鉴定了黑素巨噬细胞中心，免疫组织化学和实时PCR揭示了这些组织中分子生物标志物的表达。暴露于农药混合物中使鱼表现出肾小球收缩、鲍曼间隙增大和肾小球细胞降解。肾组织中肾素、DNP、NTP、SOD、凋亡核表达升高，CAT表达降低。总的来说，我们的研究结果表明，金鱼暴露于与环境相关的农药混合物中会导致细胞损伤增加，渗透调节和抗氧化酶表达改变，这可能会损害硬骨鱼的生理功能，包括生长、繁殖和发育。

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引用次数: 0