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}
Pub Date : 2025-10-11DOI: 10.1016/j.cbpc.2025.110373
Hanwen Hu , Jin Chen , Xin Wang , Mingxue Gong , Wenzhuo Li , Yiming Liu , Hongbiao Li , Ming Huang , Anfei Liu , Zhenzhong Liu
Trimethyltin chloride (TMT), a toxic byproduct of organotin manufacturing, is an emerging environmental contaminant linked to developmental cardiotoxicity. However, its pathogenic mechanism remains undefined. Here, using zebrafish embryos, we show that TMT exposure induced dose-dependent cardiac malformations, increasing pericardial area by 44.9 % and decreasing heart rate by 16.8 % at 5 μM (both P < 0.001), accompanied by excessive ROS (+48.5 %, P < 0.001) and mitochondrial ROS (+82.8 %, P < 0.001) generation. Co-treatment with resveratrol (RSV) or the ROS inhibitor N-acetylcysteine (NAC) reduced TMT-induced cardiac defects and suppressed ROS and mitochondrial ROS overproduction (all P < 0.05). RSV or NAC also mitigated DNA damage, mitochondrial injury, and apoptosis in the heart. Mechanistically, TMT inhibited the Wnt/β-catenin signaling pathway (−61.7 % β-catenin, P < 0.001), an effect attenuated by RSV or NAC. Inhibition of apoptosis with Ac-DEVD-CHO or activation of Wnt/β-catenin signaling with CHIR likewise alleviated TMT-induced cardiac malformations. These results indicate that TMT disrupts heart development through ROS-mediated suppression of Wnt/β-catenin signaling, leading to mitochondrial damage, DNA damage, and apoptosis. Furthermore, RSV, a dietary antioxidant, provides significant protection against TMT-induced cardiac developmental toxicity. This study identifies potential molecular targets for preventing and treating embryonic heart injury caused by environmental toxicants.
{"title":"Resveratrol attenuates trimethyltin chloride-induced cardiac defects via the ROS/Wnt/β-catenin pathway","authors":"Hanwen Hu , Jin Chen , Xin Wang , Mingxue Gong , Wenzhuo Li , Yiming Liu , Hongbiao Li , Ming Huang , Anfei Liu , Zhenzhong Liu","doi":"10.1016/j.cbpc.2025.110373","DOIUrl":"10.1016/j.cbpc.2025.110373","url":null,"abstract":"<div><div>Trimethyltin chloride (TMT), a toxic byproduct of organotin manufacturing, is an emerging environmental contaminant linked to developmental cardiotoxicity. However, its pathogenic mechanism remains undefined. Here, using zebrafish embryos, we show that TMT exposure induced dose-dependent cardiac malformations, increasing pericardial area by 44.9 % and decreasing heart rate by 16.8 % at 5 μM (both <em>P</em> < 0.001), accompanied by excessive ROS (+48.5 %, <em>P</em> < 0.001) and mitochondrial ROS (+82.8 %, <em>P</em> < 0.001) generation. Co-treatment with resveratrol (RSV) or the ROS inhibitor <em>N</em>-acetylcysteine (NAC) reduced TMT-induced cardiac defects and suppressed ROS and mitochondrial ROS overproduction (all <em>P</em> < 0.05). RSV or NAC also mitigated DNA damage, mitochondrial injury, and apoptosis in the heart. Mechanistically, TMT inhibited the Wnt/β-catenin signaling pathway (−61.7 % β-catenin, <em>P</em> < 0.001), an effect attenuated by RSV or NAC. Inhibition of apoptosis with Ac-DEVD-CHO or activation of Wnt/β-catenin signaling with CHIR likewise alleviated TMT-induced cardiac malformations. These results indicate that TMT disrupts heart development through ROS-mediated suppression of Wnt/β-catenin signaling, leading to mitochondrial damage, DNA damage, and apoptosis. Furthermore, RSV, a dietary antioxidant, provides significant protection against TMT-induced cardiac developmental toxicity. This study identifies potential molecular targets for preventing and treating embryonic heart injury caused by environmental toxicants.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110373"},"PeriodicalIF":4.3,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285727","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 : 2025-10-10DOI: 10.1016/j.cbpc.2025.110368
Bence Ivánovics , Gyöngyi Gazsi , Zoltán K. Varga , Ádám Staszny , Eszter Váradi , Zsófia Varga , András Ács , Márta Tóth , Apolka Domokos , Márta Reining , Erna Vásárhelyi , Szilárd Póliska , Róbert Kovács , Ferenc Baska , Zoltán Filep , Attila Bácsi , Julianna Kobolák , Béla Urbányi , István Szabó , Tamás Müller , Zsolt Czimmerer
The emergence and spread of vector-borne diseases necessitate the increased use of insecticides, such as carbamates, raising concerns about their potential toxicological risks to non-target organisms, including humans. Bendiocarb, frequently applied in indoor spraying operations and detected in maternal and fetal circulation, warrants particular attention for its developmental toxicity. This study aimed to assess transcriptional and phenotypic effects of sublethal bendiocarb exposure at concentrations of 0.035, 0.2, 0.4, 0.75, and 1.5 mg/L, using zebrafish embryos, a vertebrate model for developmental toxicity testing. Our analyses revealed acetylcholinesterase inhibition-associated morphological and behavioral abnormalities, including reduced locomotor activity in response to both visual and tactile stimuli, as well as impaired non-associative learning. Transcriptomic analysis indicated activation of muscle, immune, and metabolic pathways, while neurodevelopmental, phototransduction, and cell proliferation processes were suppressed. Consistent with these molecular findings, structural damage was observed in the retina, skeletal muscle, and notochord. Furthermore, bendiocarb exposure disrupted neutrophil granulocyte distribution and impaired inflammatory responses. Altogether, our results provide new insights into the embryotoxic effects of bendiocarb, highlighting its potential to disrupt early vertebrate development. These findings provide mechanistic insight that may support more informed evaluations of potential public health risks associated with developmental exposure to carbamates.
{"title":"Carbamate insecticide bendiocarb induces complex embryotoxic effects, including morphological, behavioral, transcriptional, and immunological alterations in zebrafish","authors":"Bence Ivánovics , Gyöngyi Gazsi , Zoltán K. Varga , Ádám Staszny , Eszter Váradi , Zsófia Varga , András Ács , Márta Tóth , Apolka Domokos , Márta Reining , Erna Vásárhelyi , Szilárd Póliska , Róbert Kovács , Ferenc Baska , Zoltán Filep , Attila Bácsi , Julianna Kobolák , Béla Urbányi , István Szabó , Tamás Müller , Zsolt Czimmerer","doi":"10.1016/j.cbpc.2025.110368","DOIUrl":"10.1016/j.cbpc.2025.110368","url":null,"abstract":"<div><div>The emergence and spread of vector-borne diseases necessitate the increased use of insecticides, such as carbamates, raising concerns about their potential toxicological risks to non-target organisms, including humans. Bendiocarb, frequently applied in indoor spraying operations and detected in maternal and fetal circulation, warrants particular attention for its developmental toxicity. This study aimed to assess transcriptional and phenotypic effects of sublethal bendiocarb exposure at concentrations of 0.035, 0.2, 0.4, 0.75, and 1.5 mg/L, using zebrafish embryos, a vertebrate model for developmental toxicity testing. Our analyses revealed acetylcholinesterase inhibition-associated morphological and behavioral abnormalities, including reduced locomotor activity in response to both visual and tactile stimuli, as well as impaired non-associative learning. Transcriptomic analysis indicated activation of muscle, immune, and metabolic pathways, while neurodevelopmental, phototransduction, and cell proliferation processes were suppressed. Consistent with these molecular findings, structural damage was observed in the retina, skeletal muscle, and notochord. Furthermore, bendiocarb exposure disrupted neutrophil granulocyte distribution and impaired inflammatory responses. Altogether, our results provide new insights into the embryotoxic effects of bendiocarb, highlighting its potential to disrupt early vertebrate development. These findings provide mechanistic insight that may support more informed evaluations of potential public health risks associated with developmental exposure to carbamates.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110368"},"PeriodicalIF":4.3,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274062","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 : 2025-10-02DOI: 10.1016/j.cbpc.2025.110366
Lihua Qi , Chengang Hua , Zongqi Ye , Xu Shen , Yuefeng Cai , Xin Shen
Cypermethrin, highly toxic to aquatic life, impacts Ruditapes philippinarum (A. Adams & Reeve, 1850), an economically valuable species. Thus, studying its toxicity mechanism to R. philippinarum is crucial. In this research, R. philippinarum was exposed to 5000 ng/L cypermethrin and sampled on days 0, 1, 3, 6, 10, 15, and 21 to assess enzymatic activities and conduct transcriptome sequencing. The enzymatic activity results showed that cypermethrin could increase the activity of the ethoxyresorufin-O-deethylase (EROD), turn on the antioxidant defenses, cause an initial increase in total antioxidant capacity (T-AOC) and then a decrease, increase the activities of antioxidant enzymes catalase (CAT) and glutathione peroxidase (GPx), and inhibit superoxide dismutase (SOD). Furthermore, the contents of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) increased in the body at 10, 15, and 21 days of exposure. Transcriptome sequencing was carried out to analyze the responses of cypermethrin stress for 1 day and 21 days. Differentially expressed genes (DEGs) were linked to detoxification metabolism and oxidative stress, according to Gene Ontology (GO) enrichment analysis. In addition, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis demonstrated that cypermethrin had toxic effects through key factors affecting detoxification metabolism, oxidative stress, immune response, and apoptosis-related pathways. This study gives insights into the harmful mechanism of cypermethrin stress on R. philippinarum, as well as a theoretical basis for assessing the ecological danger of cypermethrin in Chinese coastal waters.
{"title":"Effects of cypermethrin on the clams Ruditapes philippinarum (A. Adams & Reeve, 1850)","authors":"Lihua Qi , Chengang Hua , Zongqi Ye , Xu Shen , Yuefeng Cai , Xin Shen","doi":"10.1016/j.cbpc.2025.110366","DOIUrl":"10.1016/j.cbpc.2025.110366","url":null,"abstract":"<div><div>Cypermethrin, highly toxic to aquatic life, impacts <em>Ruditapes philippinarum</em> (A. Adams & Reeve, 1850), an economically valuable species. Thus, studying its toxicity mechanism to <em>R. philippinarum</em> is crucial. In this research, <em>R. philippinarum</em> was exposed to 5000 ng/L cypermethrin and sampled on days 0, 1, 3, 6, 10, 15, and 21 to assess enzymatic activities and conduct transcriptome sequencing. The enzymatic activity results showed that cypermethrin could increase the activity of the ethoxyresorufin-O-deethylase (EROD), turn on the antioxidant defenses, cause an initial increase in total antioxidant capacity (T-AOC) and then a decrease, increase the activities of antioxidant enzymes catalase (CAT) and glutathione peroxidase (GPx), and inhibit superoxide dismutase (SOD). Furthermore, the contents of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) increased in the body at 10, 15, and 21 days of exposure. Transcriptome sequencing was carried out to analyze the responses of cypermethrin stress for 1 day and 21 days. Differentially expressed genes (DEGs) were linked to detoxification metabolism and oxidative stress, according to Gene Ontology (GO) enrichment analysis. In addition, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis demonstrated that cypermethrin had toxic effects through key factors affecting detoxification metabolism, oxidative stress, immune response, and apoptosis-related pathways. This study gives insights into the harmful mechanism of cypermethrin stress on <em>R. philippinarum</em>, as well as a theoretical basis for assessing the ecological danger of cypermethrin in Chinese coastal waters.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110366"},"PeriodicalIF":4.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145228469","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 : 2025-10-02DOI: 10.1016/j.cbpc.2025.110367
Fan-Bin Kong , Yong-Po Lv , Bai-Zhong Zhang , Meng-Yuan Zhang , Ling-Ling Cui , Ren-Jie Li , Dong-Mei Chen , Yu-Yang Peng , Run-Qiang Liu
The fall armyworm Spodoptera frugiperda (Smith) can damage many crops distributed worldwide, and chemical insecticide application is the main control strategy. However, the frequent application of insecticides can lead to severe insecticide resistance in S. frugiperda. Glutathione S-transferases (GSTs) play a critical role in insecticide resistance in pests. In this study, it was found that the expression of SfGSTs3 was significantly up-regulated after exposure to chlorantraniliprole. After injection of dsSfGSTs3, the susceptibility of chlorantraniliprole was improved, and microRNA-23a binding on 3’UTR of SfGSTs3 was found. Luciferase reporter assays revealed that the effects of miR-23a on SfGSTs3 expression were suppressed via this binding site in S. frugiperda. Injection of the miR-23a agomir significantly reduced SfGSTs3 expression, together with increased chlorantraniliprole susceptibility. In contrast, injection of the miR-23a antagomir significantly improved SfGSTs3 expression and thus decreased chlorantraniliprole susceptibility in the larvae of S. frugiperda. These findings provide a theoretical foundation for better understanding the posttranscriptional regulation of SfGSTs3 and can be used to further study the mechanism by which miRNAs regulate insecticide susceptibility in pests.
{"title":"miR-23a modulates chlorantraniliprole susceptibility by targeting SfGSTs3 in Spodoptera frugiperda (Smith)","authors":"Fan-Bin Kong , Yong-Po Lv , Bai-Zhong Zhang , Meng-Yuan Zhang , Ling-Ling Cui , Ren-Jie Li , Dong-Mei Chen , Yu-Yang Peng , Run-Qiang Liu","doi":"10.1016/j.cbpc.2025.110367","DOIUrl":"10.1016/j.cbpc.2025.110367","url":null,"abstract":"<div><div>The fall armyworm <em>Spodoptera frugiperda</em> (Smith) can damage many crops distributed worldwide, and chemical insecticide application is the main control strategy. However, the frequent application of insecticides can lead to severe insecticide resistance in <em>S. frugiperda</em>. Glutathione S-transferases (GSTs) play a critical role in insecticide resistance in pests. In this study, it was found that the expression of SfGSTs3 was significantly up-regulated after exposure to chlorantraniliprole. After injection of dsSfGSTs3, the susceptibility of chlorantraniliprole was improved, and microRNA-23a binding on 3’UTR of SfGSTs3 was found. Luciferase reporter assays revealed that the effects of miR-23a on <em>SfGSTs3</em> expression were suppressed via this binding site in <em>S. frugiperda</em>. Injection of the miR-23a agomir significantly reduced <em>SfGSTs3</em> expression, together with increased chlorantraniliprole susceptibility. In contrast, injection of the miR-23a antagomir significantly improved <em>SfGSTs3</em> expression and thus decreased chlorantraniliprole susceptibility in the larvae of <em>S. frugiperda</em>. These findings provide a theoretical foundation for better understanding the posttranscriptional regulation of <em>SfGSTs3</em> and can be used to further study the mechanism by which miRNAs regulate insecticide susceptibility in pests.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110367"},"PeriodicalIF":4.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145228452","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}
Bisphenol A (BPA), a widespread environmental pollutant, is known for its endocrine-disrupting and pro-oxidant effects, posing serious risks to aquatic organisms. This study evaluated the impact of BPA on biochemical markers in the digestive gland of the freshwater mussel Unio ravoisieri, and assessed the potential protective role of selenium (Se), a trace element with antioxidant properties. Under laboratory conditions, mussels were exposed for 14 days to two BPA concentrations (C1 = 10 μg/L and C2 = 100 μg/L), either alone or combined with 100 μg/L Se. The enzymatic activity of acetylcholinesterase (AChE), catalase (CAT), and glutathione S-transferase (GST), along with the levels of malondialdehyde (MDA), reduced glutathione (GSH), and hydrogen peroxide (H₂O₂), were quantified as indicators of neurotoxicity and oxidative stress. BPA exposure led to a significant dose-dependent inhibition of AChE activity, indicating neurotoxicity, while GST activity increased, suggesting an upregulated detoxification response. An increase in CAT activity was observed at the lower BPA dose, while inhibition occurred at the higher dose. Importantly, BPA significantly GSH levels, indicating oxidative stress and impaired antioxidant and detoxification defenses. Additionally, BPA exposure at both 10 μg/L and 100 μg/L significantly elevated MDA and H₂O₂ levels, with a more pronounced increase observed at the higher dose (100 μg/L), confirming enhanced lipid peroxidation and reactive oxygen species (ROS). Notably, Se co-treatment mitigated these adverse effects by partially restoring AChE and CAT activities, normalizing GST responses, preserving GSH content, and reducing oxidative damage. These findings demonstrate the intertwined oxidative and detoxification responses of U. ravoisieri to BPA exposure and underscore the protective role of Se in counteracting BPA-induced toxicity. This study reinforces the utility of biochemical biomarkers in environmental monitoring and supports the potential use of Se in pollution mitigation strategies.
{"title":"Effects of bisphenol A on freshwater mussels: Insights into the protective mechanisms of selenium","authors":"Oumaima Abidi , Abdelhafidh Khazri , Rihab Belgacem , Tamara García-Barrera , Ezzeddine Mahmoudi , Mohamed Dellali","doi":"10.1016/j.cbpc.2025.110362","DOIUrl":"10.1016/j.cbpc.2025.110362","url":null,"abstract":"<div><div>Bisphenol A (BPA), a widespread environmental pollutant, is known for its endocrine-disrupting and pro-oxidant effects, posing serious risks to aquatic organisms. This study evaluated the impact of BPA on biochemical markers in the digestive gland of the freshwater mussel <em>Unio ravoisieri</em>, and assessed the potential protective role of selenium (Se), a trace element with antioxidant properties. Under laboratory conditions, mussels were exposed for 14 days to two BPA concentrations (C<sub>1</sub> = 10 μg/L and C<sub>2</sub> = 100 μg/L), either alone or combined with 100 μg/L Se. The enzymatic activity of acetylcholinesterase (AChE), catalase (CAT), and glutathione S-transferase (GST), along with the levels of malondialdehyde (MDA), reduced glutathione (GSH), and hydrogen peroxide (H₂O₂), were quantified as indicators of neurotoxicity and oxidative stress. BPA exposure led to a significant dose-dependent inhibition of AChE activity, indicating neurotoxicity, while GST activity increased, suggesting an upregulated detoxification response. An increase in CAT activity was observed at the lower BPA dose, while inhibition occurred at the higher dose. Importantly, BPA significantly GSH levels, indicating oxidative stress and impaired antioxidant and detoxification defenses. Additionally, BPA exposure at both 10 μg/L and 100 μg/L significantly elevated MDA and H₂O₂ levels, with a more pronounced increase observed at the higher dose (100 μg/L), confirming enhanced lipid peroxidation and reactive oxygen species (ROS). Notably, Se co-treatment mitigated these adverse effects by partially restoring AChE and CAT activities, normalizing GST responses, preserving GSH content, and reducing oxidative damage. These findings demonstrate the intertwined oxidative and detoxification responses of <em>U. ravoisieri</em> to BPA exposure and underscore the protective role of Se in counteracting BPA-induced toxicity. This study reinforces the utility of biochemical biomarkers in environmental monitoring and supports the potential use of Se in pollution mitigation strategies.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110362"},"PeriodicalIF":4.3,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145155991","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 : 2025-09-23DOI: 10.1016/j.cbpc.2025.110365
Yue Li , Zihao Jiang , Zhuoshuo Zhou , Naitian Zhang , Ximing Cui , Xiaoyan Yu , Yanli Zhao , Zhong Wang , Jinlian Li , Dongmei Wu
Atractylenolides (I, II, and III), active sesquiterpene lactones from Atractylodes macrocephala Koidz, exhibit diverse pharmacological activities but have been reported to impair drug-metabolizing enzymes and hepatocellular function. However, a comprehensive safety assessment of these compounds remains lacking. In this study, we investigated the developmental toxicity profile of Atractylenolides (I, II, and III) in zebrafish embryos, with a particular focus on hepatotoxicity and its underlying mechanisms. Exposure to Atractylenolides (I, II, and III) resulted in concentration-dependent mortality, with 96-h median lethal concentrations (LC₅₀) of 81.64 μM, 138.40 μM, and 151.90 μM, respectively. Atractylenolides (I, II) induced multiple developmental abnormalities, among which Atractylenolide-I uniquely led to neuronal developmental arrest and diminished locomotor activity. Importantly, Atractylenolides (I, II) exhibited marked hepatotoxicity, evidenced by liver shrinkage, reduced liver-specific fluorescence intensity, and elevated levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). In contrast, exposure to Atractylenolide-III did not induce significant toxic effects. Network toxicology analysis revealed that cytochrome P450 (CYP450) metabolism and apoptosis were closely associated with Atractylenolides (I, II) induced hepatotoxicity. qRT-PCR analysis revealed that Atractylenolides (I, II) suppressed mRNA expression of key drug-metabolizing genes, including cyp3c1 and cyp3a65. Simultaneously, Atractylenolides (I, II) downregulated genes associated with cell proliferation (top2α, uhrf1). Co-treatment with the hepatoprotective agent silybin partially reversed the liver injury and the alterations in drug metabolism gene expression induced by Atractylenolides (I, II). Collectively, our results provide important insights into the safety evaluation of Atractylenolides (I, II, and III).
{"title":"Differential toxic phenotypes and liver injury induced by Atractylenolides (I, II, and III): Insights from zebrafish (Danio rerio) models and network toxicology","authors":"Yue Li , Zihao Jiang , Zhuoshuo Zhou , Naitian Zhang , Ximing Cui , Xiaoyan Yu , Yanli Zhao , Zhong Wang , Jinlian Li , Dongmei Wu","doi":"10.1016/j.cbpc.2025.110365","DOIUrl":"10.1016/j.cbpc.2025.110365","url":null,"abstract":"<div><div>Atractylenolides (I, II, and III), active sesquiterpene lactones from <em>Atractylodes macrocephala</em> Koidz, exhibit diverse pharmacological activities but have been reported to impair drug-metabolizing enzymes and hepatocellular function. However, a comprehensive safety assessment of these compounds remains lacking. In this study, we investigated the developmental toxicity profile of Atractylenolides (I, II, and III) in zebrafish embryos, with a particular focus on hepatotoxicity and its underlying mechanisms. Exposure to Atractylenolides (I, II, and III) resulted in concentration-dependent mortality, with 96-h median lethal concentrations (LC₅₀) of 81.64 μM, 138.40 μM, and 151.90 μM, respectively. Atractylenolides (I, II) induced multiple developmental abnormalities, among which Atractylenolide-I uniquely led to neuronal developmental arrest and diminished locomotor activity. Importantly, Atractylenolides (I, II) exhibited marked hepatotoxicity, evidenced by liver shrinkage, reduced liver-specific fluorescence intensity, and elevated levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). In contrast, exposure to Atractylenolide-III did not induce significant toxic effects. Network toxicology analysis revealed that cytochrome P450 (CYP450) metabolism and apoptosis were closely associated with Atractylenolides (I, II) induced hepatotoxicity. qRT-PCR analysis revealed that Atractylenolides (I, II) suppressed mRNA expression of key drug-metabolizing genes, including <em>cyp3c1</em> and <em>cyp3a65</em>. Simultaneously, Atractylenolides (I, II) downregulated genes associated with cell proliferation (<em>top2α</em>, <em>uhrf1</em>). Co-treatment with the hepatoprotective agent silybin partially reversed the liver injury and the alterations in drug metabolism gene expression induced by Atractylenolides (I, II). Collectively, our results provide important insights into the safety evaluation of Atractylenolides (I, II, and III).</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110365"},"PeriodicalIF":4.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148195","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}
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