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PFAS-induced immunotoxicity in freshwater fish of inland China: mechanisms and ecological risks pfas诱导的中国内陆淡水鱼免疫毒性:机制和生态风险。
IF 4.3 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-10-31 DOI: 10.1016/j.cbpc.2025.110382
Helei Cai , Qizhuan Lin , Changyong Gong , Fan Yu , Libo Jin , Renyi Peng
Per-and polyfluoroalkyl substances (PFAS) are widely distributed across freshwater systems in mainland China, with concentrations showing marked spatial heterogeneity—particularly in eastern regions with intensive industrial activity. Fish not only play a vital ecological role but also serve as an important source of protein for humans. Due to the biomagnification factors (BMF > 1) of PFAS in the food chain, the risk of exposure increases for high-trophic-level fish, other predators, and ultimately humans. Co-exposure with other environmental pollutants further amplifies PFAS-induced immunotoxic effects. The immunotoxicity of PFAS is influenced by carbon chain length and functional groups, with long-chain PFAS and sulfonic acid groups generally exhibiting stronger immunotoxic effects in fish. These compounds significantly suppress both innate and adaptive immune responses by interfering with Toll-like receptor signaling pathways, inducing oxidative stress, and impairing immune cell function. Although current technologies are available for PFAS removal, they still face considerable limitations and challenges. This review summarizes the characteristics and spatial distribution of PFAS contamination in mainland China's aquatic environments and focuses on the mechanisms of PFAS-induced immunotoxicity in fish. It offers valuable insights for future research into the synergistic/antagonistic and time-dependent effects of combined PFAS and multi-pollutant exposure. Moreover, it provides important references for the development of mitigation technologies targeting PFAS-related ecotoxicity in aquatic food chains and for informing relevant policy formulation.
全氟烷基和多氟烷基物质(PFAS)广泛分布在中国大陆的淡水系统中,其浓度表现出明显的空间异质性,特别是在工业活动密集的东部地区。鱼类不仅扮演着重要的生态角色,也是人类重要的蛋白质来源。由于食物链中PFAS的生物放大因子(BMF > 1),高营养水平鱼类、其他捕食者以及最终人类的暴露风险增加。与其他环境污染物的共暴露进一步放大了pfas诱导的免疫毒性作用。PFAS的免疫毒性受碳链长度和官能团的影响,其中长链PFAS和磺酸基团对鱼类的免疫毒性一般较强。这些化合物通过干扰toll样受体信号通路、诱导氧化应激和损害免疫细胞功能,显著抑制先天和适应性免疫反应。尽管目前的技术可用于去除PFAS,但它们仍然面临相当大的局限性和挑战。本文综述了中国大陆水生环境中PFAS污染的特征和空间分布,重点探讨了PFAS诱导鱼类免疫毒性的机制。它为未来研究PFAS和多污染物联合暴露的协同/拮抗效应和时间依赖性提供了有价值的见解。此外,它还为开发针对水生食物链中pfas相关生态毒性的缓解技术和制定相关政策提供了重要参考。
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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 Pub 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
Combined effects of cadmium and antibiotics on the immune defense system of the wolf spider Pardosa pseudoannulata 镉和抗生素对假环狼蛛免疫防御系统的联合影响。
IF 4.3 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-10-20 DOI: 10.1016/j.cbpc.2025.110376
Juan Wang , Yingying Lu , Xinyi Wu , Xinru Zhang , Qu Cai , Chenbo Huang , Zhi Wang
This study investigated the compound stresses of cadmium (Cd) and antibiotics on the immune defense system of wolf spiders, Pardosa pseudoannulata, which is a vital predator for pest control in the paddy ecosystem. Overall, the synergistic effect of Cd and antibiotics on the inhibition of immune response was identified in spiderlings, which manifested by decreased resistance to a pathogen, reduced concentration of immune effectors, and altered concentrations of antioxidants. Similarly, changes in the relative abundances of several antimicrobial peptides, such as lycosins, lycotoxins, and pardosins, were consistent with the change of immune effectors. Specific responsive genes of compound stresses suggested a broader disturbance in the immune system, like the antioxidase system, phenoloxidase, and lysosome, as well as changes in the developmental events like the biosynthesis of molting and juvenile hormones in spiderlings, which were acknowledged as potential contributors to the combined exposure toxicity. Another group of genes involved in ribosome, energy metabolism, and phagosome can act as co-damage markers in response to alone or combined exposures of Cd and antibiotics. These results expanded the insights into the ecotoxicology assessment of combined pollutants in the paddy field.
研究了镉(Cd)和抗生素复合胁迫对稻田生态系统中重要害虫捕食者假环狼蛛(Pardosa pseudoannulata)免疫防御系统的影响。总之,Cd和抗生素在抑制蜘蛛免疫应答方面具有协同作用,表现为对病原体的抵抗力降低,免疫效应物浓度降低,抗氧化剂浓度改变。同样,一些抗菌肽,如lycoins、lycotoxins和pardosin的相对丰度的变化与免疫效应物的变化是一致的。复合应激的特异性应答基因提示免疫系统受到更广泛的干扰,如抗氧化酶系统、酚氧化酶和溶酶体,以及发育事件的变化,如蜘蛛蜕皮和幼崽激素的生物合成,这些都被认为是联合暴露毒性的潜在贡献者。另一组涉及核糖体、能量代谢和吞噬体的基因可以作为单独或联合暴露于Cd和抗生素的共同损伤标记物。这些结果扩大了对稻田复合污染物生态毒理学评价的认识。
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引用次数: 0
Bromoacetic acid and dibromoacetic acid induce cardiotoxicity in larval zebrafish by triggering oxidative stress 溴乙酸和二溴乙酸通过引发氧化应激诱导斑马鱼幼体心脏毒性。
IF 4.3 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-10-19 DOI: 10.1016/j.cbpc.2025.110377
Xiaoyu Mao , Dashuang Mo , Mengzhu Lv
Disinfection by-products are widespread contaminants formed during water disinfection processes, with bromoacetic acids (BAAs), including bromoacetic acid (BAA) and dibromoacetic acid (DBAA), frequently detected in swimming pools, spas, and tap water. Although their environmental occurrence is well documented, the in vivo organ-specific toxicity of BAAs remains poorly understood. In this study, zebrafish (Danio rerio) were employed to investigate the developmental and cardiotoxic effects of BAA and DBAA, individually and in combination. Exposure to BAA or combined BAA/DBAA significantly increased mortality and reduced hatching rates, whereas DBAA alone showed no significant effect on hatching. Both compounds induced morphological abnormalities, including reduced body length, swim bladder defects, and pericardial edema. Cardiac assessments revealed enlarged pericardial areas, decreased heart rates, and downregulation of key cardiac developmental genes. BAAs also elevated reactive oxygen species (ROS) levels in the heart, upregulated ROS-generating genes, and suppressed antioxidant genes. Furthermore, BAAs reduced cardiomyocyte proliferation, increased γH2AX-positive cells, and upregulated apoptosis-related genes, indicating DNA damage and apoptosis. Co-treatment with the antioxidant N-acetylcysteine mitigated pericardial edema and reduced γH2AX-positive cells, confirming a central role of oxidative stress in BAAs-induced cardiotoxicity. These findings demonstrate that BAA and DBAA impair zebrafish heart development through oxidative stress–mediated disruption of cell proliferation and promotion of apoptosis. This study highlights the need for further evaluation of BAA and DBAA toxicity to better understand their potential health risks in humans.
消毒副产物是水消毒过程中形成的广泛污染物,其中溴乙酸(BAAs),包括溴乙酸(BAA)和二溴乙酸(DBAA),经常在游泳池、水疗中心和自来水中检测到。尽管它们在环境中的发生已被充分记录,但对BAAs的体内器官特异性毒性仍知之甚少。本研究以斑马鱼(Danio rerio)为研究对象,分别研究BAA和DBAA对发育和心脏毒性的影响。暴露于BAA或BAA/DBAA联合暴露显著增加了死亡率,降低了孵化率,而单独暴露于DBAA对孵化没有显著影响。这两种化合物都会引起形态异常,包括体长缩短、膀胱缺损和心包水肿。心脏评估显示心包面积扩大,心率降低,心脏关键发育基因下调。BAAs还会升高心脏中的活性氧(ROS)水平,上调ROS生成基因,抑制抗氧化基因。此外,BAAs降低心肌细胞增殖,增加γ - h2ax阳性细胞,上调凋亡相关基因,提示DNA损伤和凋亡。与抗氧化剂n -乙酰半胱氨酸共同治疗可减轻心包水肿并减少γ - h2ax阳性细胞,证实氧化应激在baas诱导的心脏毒性中起核心作用。这些发现表明,BAA和DBAA通过氧化应激介导的细胞增殖破坏和促进细胞凋亡来损害斑马鱼心脏发育。这项研究强调需要进一步评估BAA和DBAA的毒性,以更好地了解它们对人类的潜在健康风险。
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引用次数: 0
Enantioselective toxicity of 3,4-methylenedioxypyrovalerone in Daphnia magna: Assessment of morphophysiological, behavioural, biochemical and reproductive responses 3,4-亚甲基二氧基丙烯酮对大水蚤的对映选择性毒性:形态、生理、行为、生化和生殖反应的评估。
IF 4.3 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-10-18 DOI: 10.1016/j.cbpc.2025.110375
Ariana Pérez-Pereira , Ana R. Carvalho , Pedro A. Costa , Bruno B. Castro , João S. Carrola , Virgínia M.F. Gonçalves , Ana R.L. Ribeiro , Ana Sofia Almeida , Carla Fernandes , Maria E. Tiritan , Cláudia Ribeiro
The enantioselective toxicity of 3,4-methylenedioxypyrovalerone (MDPV) remains unexplored in freshwater organisms. This study investigated the effects of MDPV racemate and its enantiomers in Daphnia magna using two approaches: (i) an 8-day sub-chronic assay focused on early development stages; and (ii) the standard 21-day reproduction assay. The sub-chronic assay tested two environmental concentrations (0.10 and 1.0 μg L−1), for both racemate or individual enantiomers, and a higher sublethal concentration of 10 μg L−1 for the racemate. Survival, morphophysiological, behavioural, reproductive, and biochemical responses were evaluated. The reproduction assay tested concentrations from 0.10 to 1.79 μg L−1, and evaluated survival, body size, and reproductive effects.
Sub-chronic exposure to 10 μg L−1 (R,S)-MDPV decreased survival. MDPV racemate and its enantiomers changed morphophysiological parameters, except for body growth. In juveniles, the heart area increased with 0.10 μg L−1 of (R)-MDPV whereas the heart size decreased with 0.10 and 1.0 μg L−1 of (S)-MDPV. Enantioselective effects were observed in swimming behaviour: (S)-MDPV increased speed and (R)-MDPV increased active time. No effects were observed in biochemical (except in reactive oxygen species for (S)-MDPV) and early reproductive parameters. The reproduction assay revealed enhanced growth in all MDPV forms (except at 0.56 μg L−1). A nonsignificant reduction in survival to the higher concentrations of (R)-MDPV was accompanied by reduced reproductive output (at 1.00 and 1.79 μg L−1) and intrinsic rate of population increase (at 1.79 μg L−1). Our findings suggest that, in general, (S)-MDPV triggers more severe sub-chronic effects, whereas (R)-MDPV is associated with harmful effects for longer time exposure.
3,4-亚甲基二氧基戊烷酮(MDPV)在淡水生物中的对映选择性毒性尚未研究。本研究通过两种方法研究了MDPV外消旋体及其对映异构体对大水蚤的影响:(i)一项为期8天的亚慢性实验,重点关注水蚤的早期发育阶段;(ii)标准的21天繁殖试验。亚慢性试验测试了两种环境浓度(0.10和1.0 μg L-1),对外消旋体或单个对映体,并在更高的亚致死浓度(10 μg L-1)下测试了外消旋体。评估生存、形态生理、行为、生殖和生化反应。繁殖试验测试浓度为0.10至1.79 μg L-1,并评估存活率、体型和繁殖效果。亚慢性暴露于10 μg L-1 (R,S)-MDPV降低了生存率。MDPV外消旋体及其对映体除了对机体生长有影响外,还能改变机体的形态生理参数。(R)-MDPV的心脏面积增加0.10 μg L-1, (S)-MDPV的心脏大小减少0.10和1.0 μg L-1。在游泳行为中观察到对映体选择效应:(S)-MDPV增加速度,(R)-MDPV增加活动时间。生物化学(除(S)-MDPV的活性氧外)和早期生殖参数未见影响。繁殖试验显示,所有MDPV形式的生长都增强了(0.56 μg L-1除外)。在(R)-MDPV浓度较高的情况下,存活率不显著降低,同时生殖产量降低(分别为1.00和1.79 μg L-1),种群内在增长率降低(1.79 μg L-1)。我们的研究结果表明,一般来说,(S)-MDPV引发更严重的亚慢性效应,而(R)-MDPV与长时间暴露的有害效应有关。
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引用次数: 0
Neurodevelopmental toxicity induced by iron oxide nanoparticles: Insights from chick and zebrafish embryonic models 氧化铁纳米颗粒诱导的神经发育毒性:来自小鸡和斑马鱼胚胎模型的见解。
IF 4.3 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-10-14 DOI: 10.1016/j.cbpc.2025.110372
Bi-Xia Huang , Tao Zhang , Qing-Bin Dong , Peng-Xing Lin , Yi Zhou , Xin-Shuo Chen
Iron oxide nanoparticles (IONPs) are widely applied in biomedicine and industry, yet their impact on early nervous system formation is poorly understood. Here, we assessed IONP toxicity using cultured chick embryo fibroblasts, fertilized chicken eggs, and zebrafish embryos. In vitro exposure reduced fibroblast viability, elevated lipid peroxidation, and boosted reactive oxygen species levels. The injection of IONPs in chick embryo caused growth delays, smaller brain size, neuroepithelial thickening, and marked loss of neural stem and progenitor cells. At the molecular level, IONPs reduced PI3K and mTOR activity, increased apoptotic markers, and induced ferroptosis hallmarks, including mitochondrial membrane potential loss, ATP depletion, elevated mitochondrial ROS, and downregulation of xCT and GPX4. In zebrafish, IONPs triggered early developmental defects, microcephaly, and yolk malabsorption, alongside redox imbalance and dysregulation of ferroptosis-related genes. Together, these data show that IONPs impair neural proliferation, promote multiple forms of cell death, and disrupt redox equilibrium through ferroptotic mechanisms, highlighting the need for careful safety evaluation before their widespread use.
氧化铁纳米颗粒(Iron oxide nanoparticles, IONPs)广泛应用于生物医学和工业领域,但其对早期神经系统形成的影响尚不清楚。在这里,我们用培养的鸡胚成纤维细胞、受精卵和斑马鱼胚胎来评估IONP的毒性。体外暴露降低成纤维细胞活力,提高脂质过氧化和促进活性氧水平。在鸡胚中注射IONPs导致发育迟缓、脑体积减小、神经上皮增厚、神经干细胞和祖细胞明显缺失。在分子水平上,IONPs降低PI3K和mTOR活性,增加凋亡标志物,诱导铁下垂标志,包括线粒体膜电位损失、ATP消耗、线粒体ROS升高以及xCT和GPX4的下调。在斑马鱼中,IONPs引发了早期发育缺陷、小头畸形和蛋黄吸收不良,以及氧化还原失衡和铁中毒相关基因的失调。综上所述,这些数据表明,IONPs会损害神经细胞增殖,促进多种形式的细胞死亡,并通过趋铁机制破坏氧化还原平衡,因此在广泛使用IONPs之前,需要进行仔细的安全性评估。
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引用次数: 0
Attenuation of rotenone-induced neurodegeneration by Bacillus coagulans supplementation in zebrafish 添加凝固芽孢杆菌对斑马鱼鱼藤酮诱导的神经变性的抑制作用。
IF 4.3 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-10-14 DOI: 10.1016/j.cbpc.2025.110374
Monalisa Rout , Shakti Ketan Prusty , Sonali Sahoo , Prerana Sarangi , Anshuman Rath , Durga Madhab Kar
The relatable therapeutic properties of the selected probiotic (PBT) Bacillus coagulans could make this supplement a potential entity to cease the progression of Parkinson's disease (PD). Yet no studies have been carried out to explore the anti-PD activity of this chosen probiotic using the zebrafish (Danio rerio) model. However, our research has been performed for 28 consecutive days using zebrafish (n = 12) for each group: control (CNT), rotenone (ROT), and groups administered rotenone along with L-dopa, ROT with PBT, PBT along with L-dopa, and ROT. Following 28 days of treatment, behavioral responses were recorded via novel tank test (NTT) and light-dark test (LDT). Antioxidant biomarkers were estimated along with dopamine (DA) level, aggregated alpha-synuclein (α-syn) level, monoamine oxidase-B (MAO-B) activity, acetylcholine esterase (AChE) activity, and nitrite level using brain homogenates. Resulting data indicated that PBT alone and in combination with L-dopa attenuated the ROT-induced behavioral alterations and rescued the altered biomarker activity involved in PD pathophysiology. Furthermore, our observed data from brain histology demarcates towards remarkable prevention of neuronal damage in PBT and PBT + L-dopa-treated zebrafish brains. Collectively, the gross outcome of our study delineates the idea that chronic exposure to ROT is associated with aggressive neurobehavioral transformation, neuroinflammation, and neurodegeneration in the zebrafish brain that was rescued using PBT supplement pending further clinical studies.
所选益生菌(PBT)凝固芽孢杆菌的相关治疗特性可能使这种补充剂成为阻止帕金森病(PD)进展的潜在实体。然而,目前还没有研究利用斑马鱼(Danio rerio)模型来探索所选益生菌的抗pd活性。然而,我们用斑马鱼(n = 12)对每组进行了连续28天的研究:对照组(CNT)、鱼藤酮(ROT)和鱼藤酮与左旋多巴、ROT与PBT、PBT与左旋多巴和ROT。在28 天的治疗后,通过新型罐试验(NTT)和光暗试验(LDT)记录了行为反应。利用脑匀浆测定抗氧化生物标志物与多巴胺(DA)水平、聚集α-突触核蛋白(α-syn)水平、单胺氧化酶- b (MAO-B)活性、乙酰胆碱酯酶(AChE)活性和亚硝酸盐水平。结果表明,PBT单独或联合左旋多巴可减轻rot诱导的行为改变,并恢复PD病理生理中改变的生物标志物活性。此外,我们观察到的脑组织组织学数据表明,PBT和PBT + 左旋多巴处理的斑马鱼大脑对神经元损伤有显著的预防作用。总的来说,我们研究的总体结果描述了这样一种观点,即慢性暴露于ROT与斑马鱼大脑中的侵袭性神经行为转变、神经炎症和神经变性有关,这些斑马鱼使用PBT补充剂进行拯救,有待进一步的临床研究。
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引用次数: 0
Fish cancer and its assistance to human cancer research: A fresh perspective 鱼类癌症及其对人类癌症研究的帮助:一个新的视角。
IF 4.3 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-10-13 DOI: 10.1016/j.cbpc.2025.110369
Hao Dan , Wentong Wang , Xuhong Chen , Mariam N. Goda , Mohamed S. Kisha , Quanquan Cao
Cancer is a complex disease affecting various species, including fish, which have emerged as valuable models for studying cancer mechanisms. Recent studies highlight the similarities and differences between fish and mammalian tumors, offering insights for novel human cancer therapies. Fish models, particularly zebrafish, replicate key cancer phenotypes and molecular pathways seen in humans, making them powerful tools for cancer research. This review explores the transition from fish to human cancer studies, focusing on the molecular basis, diagnosis, and treatment of fish cancer. Key findings include the role of blood vessel formation in fish tumors and the application of zebrafish tumor models to understand human cancer. These studies provide new perspectives and technologies for human cancer research, though challenges remain in fully leveraging fish models for future therapeutic advancements.
癌症是一种影响各种物种的复杂疾病,包括鱼类,它们已成为研究癌症机制的有价值的模型。最近的研究强调了鱼类和哺乳动物肿瘤之间的异同,为新的人类癌症治疗提供了见解。鱼类模型,特别是斑马鱼,复制了在人类中看到的关键癌症表型和分子途径,使它们成为癌症研究的有力工具。本文综述了从鱼类到人类癌症研究的转变,重点介绍了鱼类癌症的分子基础、诊断和治疗。主要发现包括血管形成在鱼类肿瘤中的作用,以及应用斑马鱼肿瘤模型来了解人类癌症。这些研究为人类癌症研究提供了新的视角和技术,尽管在充分利用鱼类模型促进未来治疗进展方面仍存在挑战。
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引用次数: 0
Selenium ameliorates fumonisin B1-induced mitochondrial dysfunction and barrier impairment in porcine intestinal epithelial cells 硒改善伏马菌素b1诱导的猪肠上皮细胞线粒体功能障碍和屏障损伤。
IF 4.3 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-10-12 DOI: 10.1016/j.cbpc.2025.110370
Changyu Cao , Weifeng Ni , Nixin Chen , Runxi Xian , Yang Liu , Xinran Li
This study reveals for the first time that selenium (Se) antagonizes Fumonisin B1 (FB1)-induced damage in porcine intestinal epithelial cells (IPEC-J2) by modulating mitochondrial biogenesis and dynamics. Fumonisins (FBs) are mycotoxins that are widely distributed in crops and feed, and ingestion of FBs-contaminated crops is harmful to animal health especially in intestine. Se has a protective effect on mycotoxin-induced tissue and cell toxicity. Nevertheless, whether Se can antagonize FB1-induced intestinal epithelium injury, and underlying role of Se in FB1-induced intestinal epithelium cell damage remains unclear. Our study was aimed to investigate the role of Se in FB1-induced intestinal epithelium cell damage and underlying possibly mechanism, investigated whether Se could alleviate intestinal epithelium injury, and mitochondrial dysfunction by FB1 in IPEC-J2. The results indicated that Se alleviated the FB1-induced abnormal intestinal barrier function, the disturbance of reactive oxygen species (ROS), increased mitochondrial membrane potential (MMP), mitochondrial DNA (mtDNA), and mRNA expression of genes related to mitochondrial function. These showed Se alleviated FB1-induced abnormal intestinal barrier function might related with the destroyed mitochondrial homestasis. We concluded that Se enhances mitochondrial function by regulating mitochondrial biogenesis and dynamics to antagonize FB1-reduced the damage to the intestinal epithelial barrier and protect intestinal barrier integrity. Overall, our study provides promising insights into the protective role of Se in FB1-induced intestinal epithelial cell damage.
本研究首次揭示了硒通过调节线粒体生物发生和动力学来拮抗fb1诱导的猪肠上皮细胞损伤。伏马菌素是一种广泛存在于作物和饲料中的真菌毒素,食用受伏马菌素污染的作物对动物健康有害,尤其是肠道。硒(Se)对真菌毒素诱导的组织和细胞毒性具有保护作用。然而,硒是否能拮抗fb1诱导的肠上皮细胞损伤,以及硒在fb1诱导的肠上皮细胞损伤中的潜在作用尚不清楚。本研究旨在探讨硒在FB1诱导的猪肠上皮细胞损伤中的作用及其可能机制,探讨硒是否能减轻FB1对猪肠上皮细胞的损伤和线粒体功能障碍(IPEC-J2)。结果表明,硒减轻了fb1诱导的肠道屏障功能异常、活性氧(ROS)紊乱、线粒体膜电位(MMP)升高、线粒体DNA (mtDNA)升高以及线粒体功能相关基因mRNA表达。提示硒减轻fb1诱导的肠屏障功能异常可能与线粒体稳态破坏有关。综上所述,硒通过调节线粒体生物发生和动力学来增强线粒体功能,从而拮抗fb1,减少对肠上皮屏障的损伤,保护肠屏障的完整性。总之,我们的研究为硒在fb1诱导的肠上皮细胞损伤中的保护作用提供了有希望的见解。
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引用次数: 0
Astaxanthin mitigates dibutyl phthalate-induced thyroid hormone disruption in zebrafish larvae via multi-target regulation 虾青素通过多靶点调节减轻邻苯二甲酸二丁酯诱导的斑马鱼幼体甲状腺激素紊乱。
IF 4.3 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-10-11 DOI: 10.1016/j.cbpc.2025.110371
Shunyan Yu , Jing Gao , Yongpan Wang , Hao Ji , Weiqiang Huang
Dibutyl phthalate (DBP), a ubiquitous environmental contaminant, has been shown to induce developmental toxicity and thyroid hormone disruption in aquatic organisms. In this study, we evaluated the protective effects of the natural astaxanthin (AST) against DBP-induced toxicity in early-life stage zebrafish. Exposure to DBP (0.1–1 mg/L) significantly impaired embryonic development, reduced body length and weight, and disrupted thyroid hormone homeostasis by decreasing T4 and increasing T3 levels. These effects were accompanied by oxidative stress, inflammation, and dysregulated expression of key genes along the hypothalamic-pituitary-thyroid (HPT) axis, including dio2, tg, crhβ, and tsh. AST supplementation dose-dependently alleviated these developmental and thyroid hormone disruption, restored redox balance and anti-inflammatory responses, and normalized HPT axis gene expression. Molecular docking identified strong binding affinities between AST and core regulatory targets (HSP90AB1, HIF1A, MTOR, NFKB1), demonstrating its multi-target mechanism involving oxidative stress mitigation, metabolic regulation, and immune modulation. These findings provide new insight into AST's protective role against endocrine-disrupting pollutants and suggest its potential application in aquatic toxicology and human health.
邻苯二甲酸二丁酯(DBP)是一种普遍存在的环境污染物,已被证明可引起水生生物的发育毒性和甲状腺激素紊乱。在这项研究中,我们评估了天然虾青素(AST)对dbp诱导的早期斑马鱼毒性的保护作用。暴露于DBP(0.1-1 mg/L)显著影响胚胎发育,降低体长和体重,并通过降低T4和增加T3水平扰乱甲状腺激素稳态。这些影响伴随着氧化应激、炎症和沿下丘脑-垂体-甲状腺(HPT)轴的关键基因表达失调,包括dio2、tg、crhβ和tsh。补充AST可以剂量依赖性地缓解这些发育和甲状腺激素紊乱,恢复氧化还原平衡和抗炎反应,并使HPT轴基因表达正常化。分子对接发现AST与核心调控靶点(HSP90AB1、HIF1A、MTOR、NFKB1)之间具有很强的结合亲和性,证明其多靶点机制涉及氧化应激缓解、代谢调节和免疫调节。这些发现为AST对内分泌干扰污染物的保护作用提供了新的认识,并提示其在水生毒理学和人类健康方面的潜在应用。
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Comparative Biochemistry and Physiology C-toxicology & Pharmacology
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