Pub Date : 2025-10-31DOI: 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.
{"title":"PFAS-induced immunotoxicity in freshwater fish of inland China: mechanisms and ecological risks","authors":"Helei Cai , Qizhuan Lin , Changyong Gong , Fan Yu , Libo Jin , Renyi Peng","doi":"10.1016/j.cbpc.2025.110382","DOIUrl":"10.1016/j.cbpc.2025.110382","url":null,"abstract":"<div><div><em>Per</em>-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.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110382"},"PeriodicalIF":4.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145430167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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}
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.
{"title":"Detoxification metabolic pathways and hepatotoxicity mechanisms of B[a]P in reproductive clam Ruditapes philippinarum","authors":"Yueyao Zhou, Zhiheng He, Qiuhong Xu, Songhui Xie, Pengfei Li, Qiaoqiao Wang, Jingjing Miao, Luqing Pan","doi":"10.1016/j.cbpc.2025.110378","DOIUrl":"10.1016/j.cbpc.2025.110378","url":null,"abstract":"<div><div>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[<em>a</em>]P in the clam <em>Ruditapes philippinarum</em> and identified the hepatotoxicity mechanism of B[<em>a</em>]P using technical approaches such as transcriptomics, computer simulation and experimental validation. We found that the <em>AhR</em> signaling pathway and <em>CYP450</em> family (<em>CYP1A1</em>, <em>CYP2B1</em>, <em>CYP3A4</em>) and <em>FMO</em> in the digestive gland of clam play important roles in the detoxification metabolism of B[<em>a</em>]P, but the performance varied between male and female clams. <em>SOD1</em> 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[<em>a</em>]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.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110378"},"PeriodicalIF":4.3,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145367745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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}
Pub Date : 2025-10-20DOI: 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.
{"title":"Combined effects of cadmium and antibiotics on the immune defense system of the wolf spider Pardosa pseudoannulata","authors":"Juan Wang , Yingying Lu , Xinyi Wu , Xinru Zhang , Qu Cai , Chenbo Huang , Zhi Wang","doi":"10.1016/j.cbpc.2025.110376","DOIUrl":"10.1016/j.cbpc.2025.110376","url":null,"abstract":"<div><div>This study investigated the compound stresses of cadmium (Cd) and antibiotics on the immune defense system of wolf spiders, <em>Pardosa pseudoannulata</em>, 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.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110376"},"PeriodicalIF":4.3,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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}
Pub Date : 2025-10-19DOI: 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.
{"title":"Bromoacetic acid and dibromoacetic acid induce cardiotoxicity in larval zebrafish by triggering oxidative stress","authors":"Xiaoyu Mao , Dashuang Mo , Mengzhu Lv","doi":"10.1016/j.cbpc.2025.110377","DOIUrl":"10.1016/j.cbpc.2025.110377","url":null,"abstract":"<div><div>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 <em>in vivo</em> organ-specific toxicity of BAAs remains poorly understood. In this study, zebrafish (<em>Danio rerio</em>) 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 <em>N</em>-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.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110377"},"PeriodicalIF":4.3,"publicationDate":"2025-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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}
Pub Date : 2025-10-18DOI: 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.
{"title":"Enantioselective toxicity of 3,4-methylenedioxypyrovalerone in Daphnia magna: Assessment of morphophysiological, behavioural, biochemical and reproductive responses","authors":"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","doi":"10.1016/j.cbpc.2025.110375","DOIUrl":"10.1016/j.cbpc.2025.110375","url":null,"abstract":"<div><div>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 <em>Daphnia magna</em> using two approaches: (<em>i</em>) an 8-day sub-chronic assay focused on early development stages; and (<em>ii</em>) the standard 21-day reproduction assay. The sub-chronic assay tested two environmental concentrations (0.10 and 1.0 μg L<sup>−1</sup>), for both racemate or individual enantiomers, and a higher sublethal concentration of 10 μg L<sup>−1</sup> 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<sup>−1</sup>, and evaluated survival, body size, and reproductive effects.</div><div>Sub-chronic exposure to 10 μg L<sup>−1</sup> (<em>R</em>,<em>S</em>)-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<sup>−1</sup> of (<em>R</em>)-MDPV whereas the heart size decreased with 0.10 and 1.0 μg L<sup>−1</sup> of (<em>S</em>)-MDPV. Enantioselective effects were observed in swimming behaviour: (<em>S</em>)-MDPV increased speed and (<em>R</em>)-MDPV increased active time. No effects were observed in biochemical (except in reactive oxygen species for (<em>S</em>)-MDPV) and early reproductive parameters. The reproduction assay revealed enhanced growth in all MDPV forms (except at 0.56 μg L<sup>−1</sup>). A nonsignificant reduction in survival to the higher concentrations of (<em>R</em>)-MDPV was accompanied by reduced reproductive output (at 1.00 and 1.79 μg L<sup>−1</sup>) and intrinsic rate of population increase (at 1.79 μg L<sup>−1</sup>). Our findings suggest that, in general, (<em>S</em>)-MDPV triggers more severe sub-chronic effects, whereas (<em>R</em>)-MDPV is associated with harmful effects for longer time exposure.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110375"},"PeriodicalIF":4.3,"publicationDate":"2025-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145336519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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}
Pub Date : 2025-10-14DOI: 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.
{"title":"Neurodevelopmental toxicity induced by iron oxide nanoparticles: Insights from chick and zebrafish embryonic models","authors":"Bi-Xia Huang , Tao Zhang , Qing-Bin Dong , Peng-Xing Lin , Yi Zhou , Xin-Shuo Chen","doi":"10.1016/j.cbpc.2025.110372","DOIUrl":"10.1016/j.cbpc.2025.110372","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110372"},"PeriodicalIF":4.3,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145298873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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}
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。
{"title":"Attenuation of rotenone-induced neurodegeneration by Bacillus coagulans supplementation in zebrafish","authors":"Monalisa Rout , Shakti Ketan Prusty , Sonali Sahoo , Prerana Sarangi , Anshuman Rath , Durga Madhab Kar","doi":"10.1016/j.cbpc.2025.110374","DOIUrl":"10.1016/j.cbpc.2025.110374","url":null,"abstract":"<div><div>The relatable therapeutic properties of the selected probiotic (PBT) <em>Bacillus coagulans</em> 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 (<em>Danio rerio</em>) model. However, our research has been performed for 28 consecutive days using zebrafish (<em>n</em> = 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.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110374"},"PeriodicalIF":4.3,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145307149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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}
Pub Date : 2025-10-13DOI: 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.
{"title":"Fish cancer and its assistance to human cancer research: A fresh perspective","authors":"Hao Dan , Wentong Wang , Xuhong Chen , Mariam N. Goda , Mohamed S. Kisha , Quanquan Cao","doi":"10.1016/j.cbpc.2025.110369","DOIUrl":"10.1016/j.cbpc.2025.110369","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110369"},"PeriodicalIF":4.3,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145298867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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}
Pub Date : 2025-10-12DOI: 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.
{"title":"Selenium ameliorates fumonisin B1-induced mitochondrial dysfunction and barrier impairment in porcine intestinal epithelial cells","authors":"Changyu Cao , Weifeng Ni , Nixin Chen , Runxi Xian , Yang Liu , Xinran Li","doi":"10.1016/j.cbpc.2025.110370","DOIUrl":"10.1016/j.cbpc.2025.110370","url":null,"abstract":"<div><div>This study reveals for the first time that selenium (Se) antagonizes Fumonisin B<sub>1</sub> (FB<sub>1</sub>)-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 FB<sub>1</sub>-induced intestinal epithelium injury, and underlying role of Se in FB<sub>1</sub>-induced intestinal epithelium cell damage remains unclear. Our study was aimed to investigate the role of Se in FB<sub>1</sub>-induced intestinal epithelium cell damage and underlying possibly mechanism, investigated whether Se could alleviate intestinal epithelium injury, and mitochondrial dysfunction by FB<sub>1</sub> in IPEC-J2. The results indicated that Se alleviated the FB<sub>1</sub>-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 FB<sub>1</sub>-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 FB<sub>1</sub>-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 FB<sub>1</sub>-induced intestinal epithelial cell damage.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110370"},"PeriodicalIF":4.3,"publicationDate":"2025-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145291466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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}
Pub Date : 2025-10-11DOI: 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.
{"title":"Astaxanthin mitigates dibutyl phthalate-induced thyroid hormone disruption in zebrafish larvae via multi-target regulation","authors":"Shunyan Yu , Jing Gao , Yongpan Wang , Hao Ji , Weiqiang Huang","doi":"10.1016/j.cbpc.2025.110371","DOIUrl":"10.1016/j.cbpc.2025.110371","url":null,"abstract":"<div><div>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 <em>dio2</em>, <em>tg</em>, <em>crhβ</em>, and <em>tsh</em>. 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.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110371"},"PeriodicalIF":4.3,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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}