Ecotoxicology and Environmental Safety最新文献

{"title":"Combined exposure of copper and iron induces nerve damage in Caenorhabditis elegans through ROS-induced autophagy/mitophagy.","authors":"Zijia Wang, Ruo Zhang, Kejia Liu, Xianghe Zhou, Wei Shi, Lu Lu, Qian Zhou, Feng Xiaorui, Yuepu Pu, Lihong Yin, Ying Zhang","doi":"10.1016/j.ecoenv.2026.121030","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2026.121030","url":null,"abstract":"<p><p>Copper (Cu) and iron (Fe) are essential trace elements that become biotoxic in excess. Their widespread coexistence in the environment poses a significant risk of co-exposure to human populations. This study aimed to elucidate the combined toxic effects and underlying mechanisms of Cu and Fe using Caenorhabditis elegans as a model organism. Our results demonstrated that combined exposure to Cu and Fe synergistically inhibited motor behaviors, including head thrashes and body bends, to a greater extent than individual metal exposures. Furthermore, this co-exposure exacerbated the degeneration of both dopaminergic (DAergic) and GABAergic neurons, revealing a potent synergistic neurotoxic effect. Mechanistic investigations indicated that the combined exposure group exhibited a significant increase in both cellular and mitochondrial reactive oxygen species (ROS), pointing to severe oxidative stress as a primary driver of toxicity. This oxidative stress led to profound mitochondrial damage, characterized by a reduced mitochondrial membrane potential and ultrastructural defects, such as rupture and cristae loss, as observed via transmission electron microscopy. Consequently, pathways for mitochondrial quality control and cellular clearance were activated, evidenced by the upregulation of PINK-1 (mitophagy), HSP-6 (mitochondrial stress), LGG-1 (autophagy), and the transcription factor HLH-30. Validation experiments using the antioxidant N-acetylcysteine (NAC) confirmed this mechanism. While NAC treatment effectively rescued neurodegeneration and motor deficits, it only partially mitigated the molecular damage in the co-exposure group, underscoring the severity of the synergistic interaction. In conclusion, our findings demonstrate that Cu and Fe co-exposure induces synergistic neurotoxicity mediated primarily by an oxidative stress-driven autophagy/mitophagy pathway.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"326 ","pages":"121030"},"PeriodicalIF":6.6,"publicationDate":"2026-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149369764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}

{"title":"Composition-driven fibrogenic potential of environmental particles: Complementary roles of iron-mediated redox activity and silica-associated TGF-β adsorption.","authors":"Yingying Sun, Qiang Jia, Siqi Sun, Cunxiang Bo, Yu Zhang, Huan Liang, Ben Cummings, T David Waite","doi":"10.1016/j.ecoenv.2026.121019","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2026.121019","url":null,"abstract":"<p><p>Respirable mineral particles are compositionally heterogeneous environmental stressors increasingly linked to pulmonary fibrosis, yet how coexisting reactive mineral phases regulate early profibrotic signalling remains unclear. In this study, the fibrogenic potential of respirable mineral particles with distinct silica and iron mineralogy was evaluated using alveolar macrophages (AMs), fibroblasts (FBs), A549 epithelial cells, and a Sprague-Dawley rat model, focusing on transforming growth factor-β (TGF-β)-associated signalling. At equivalent particle burdens, silica-bearing particles promoted profibrotic responses partly by enhancing TGF-β adsorption and associated fibroblast activation, leading to stronger α-smooth muscle actin (α-SMA) expression in FBs. In parallel, bioavailable iron (BAI) released from reduced iron-bearing phases induced stronger early reactive oxygen species (ROS) generation in AMs, enhanced CD206-associated responses among surviving AMs, and increased TGF-β production, indicating macrophage-mediated amplification of fibrogenic signalling. Under a focused high-dose in vivo challenge using a single selected BAI-rich particle sample (PM 2), the PM 2-silica mixture exhibited significantly greater collagen deposition than either individual particle group at day 42, providing supportive tissue-level evidence for a composition-associated mixed-particle response. These findings support an adverse outcome pathway relevant framework in which silica and BAI regulate distinct but complementary early events converging on pulmonary fibrosis.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"326 ","pages":"121019"},"PeriodicalIF":6.6,"publicationDate":"2026-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149369765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}

{"title":"Early-life cigarette smoke exposure predisposes to COPD by suppressing the HAS2-TGF-B1-MAPK axis in lung fibroblasts","authors":"Yaowei Fang,&nbsp;Ken Lin,&nbsp;Longjuan Zhang,&nbsp;Xuefeng Wu,&nbsp;Yao Xu,&nbsp;Ahammad Ebraheem Sultan,&nbsp;Fanyu Jiao,&nbsp;Xiangyu Yang,&nbsp;Jia Fang","doi":"10.1016/j.ecoenv.2026.120964","DOIUrl":"10.1016/j.ecoenv.2026.120964","url":null,"abstract":"<div><div>Early‑life exposure to environmental tobacco smoke (ETS) increases the risk of developing chronic obstructive pulmonary disease (COPD) in adulthood, but the underlying mechanisms remain poorly understood. Using comparative cigarette smoke (CS) exposure in neonatal and adult mice, we show that early‑life CS produces fundamentally different pathology from adult exposure. Transcriptomic and protein analyses reveal that neonatal CS exposure suppresses the transforming growth factor-β1 (TGF-β1)–mitogen-activated protein kinase (MAPK) axis, with decreased expression of fibroblast markers but not epithelial markers, identifying fibroblasts as the primary targets. In vitro, cigarette smoke extract directly downregulates Platelet-Derived Growth Factor Receptor Alpha（PDGFRα）, Fibronectin 1 (FN1), Collagen Type I (COL1), and Alpha-Smooth Muscle Actin (α-SMA) in lung fibroblasts, effects that are dose‑dependently rescued by exogenous TGF-β1. Mechanistically, the HAS2-TGF-β1-MAPK signaling axis regulates fibrosis through a uniquely inflammation-driven mechanism. Together, these findings establish that early-life CS exposure causes irreversible alveolar simplification by suppressing the TGF-β1-MAPK axis in lung fibroblasts, linking childhood ETS exposure to COPD susceptibility and identifying Hyaluronan Synthase 2（HAS2）, a marker of myofibroblasts, as a potential therapeutic target.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"326 ","pages":"Article 120964"},"PeriodicalIF":6.6,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149306994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of GSK3β as a molecular target of Alternaria mycotoxin-induced reproductive toxicity using integrated network toxicology and surface plasmon resonance (SPR) validation","authors":"Miao Yang,&nbsp;Yuwei Qiang,&nbsp;Jing Wu,&nbsp;Jinping Li,&nbsp;Xiuming Mei,&nbsp;Hanxu Ji,&nbsp;Xiaoxiao Wu,&nbsp;Diyao Jiang,&nbsp;Jingjing Xu,&nbsp;Yufeng Li,&nbsp;Chi Zhang","doi":"10.1016/j.ecoenv.2026.120999","DOIUrl":"10.1016/j.ecoenv.2026.120999","url":null,"abstract":"<div><div><em>Alternaria</em> mycotoxins are emerging foodborne contaminants associated with reproductive toxicity, yet the molecular mechanisms remain poorly understood. In this study, we integrated network toxicology, molecular docking, and surface plasmon resonance (SPR) to identify potential molecular targets of reproductive toxicity induced by two <em>Alternaria</em> mycotoxins, alternariol (AOH) and alternariol monomethyl ether (AME). The CCK-8 assay revealed that both toxins induced time- and dose-dependent cytotoxicity in TM3 mouse Leydig cells and HTR-8/SVneo human trophoblast cells. Network toxicology identified 76 overlapping targets associated with mycotoxin-induced reproductive toxicity. Enrichment analysis revealed that these targets were significantly enriched in pathways related to cancer and viral infection. A protein–protein interaction network was constructed and analyzed in Cytoscape. Based on this network, the robust rank aggregation method was employed to prioritize ten core targets: CASP3, DNMT1, ABL1, ESR1, RELA, CDK2, GSK3β, CDK4, CHEK1, and SRC. Molecular docking showed favorable binding between AOH/AME and these targets, with GSK3β displaying the lowest binding energy scores for both toxins. Subsequently, SPR analysis confirmed direct molecular interactions between GSK3β and both AOH and AME, with dissociation constants in the micromolar range. This study provides experimental evidence of direct binding of AOH/AME to GSK3β, suggesting that GSK3β is a candidate molecular target mediating the reproductive toxicity induced by <em>Alternaria</em> mycotoxins and providing a mechanistic basis for future risk assessment.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"326 ","pages":"Article 120999"},"PeriodicalIF":6.6,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149307119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of prenatal PM1, PM2.5, and PM10 exposure with early childhood hemoglobin levels and anemia: Identification of susceptibility windows","authors":"Yibing Zhu,&nbsp;Xinru Zhao,&nbsp;Yudiyang Ma,&nbsp;Ning Chen,&nbsp;Rui Tang,&nbsp;Wenpu Shao,&nbsp;Bin Sun,&nbsp;Haibo Li,&nbsp;Ziyi Zhou,&nbsp;Meiyan Zhu,&nbsp;Haoran Xu,&nbsp;Yaohua Tian,&nbsp;Jianying Yan","doi":"10.1016/j.ecoenv.2026.120980","DOIUrl":"10.1016/j.ecoenv.2026.120980","url":null,"abstract":"<div><div>The effects of exposure to particulate matter (PM) during different gestational periods on childhood anemia remain unexplored. This study included 1235 mother-offspring pairs derived from the pediatric subcohort of the Fujian Birth Cohort Study. Maternal exposure to PM₁, PM_2.5, and PM₁₀ was estimated using the ChinaHighAirPollutants dataset for four periods: the entire pregnancy and each of the three trimesters. We employed linear and logistic regression models to assess the effects of PM exposure on hemoglobin levels and anemia incidence, respectively. Additionally, distributed lag models were performed to detect the sensitive windows. PM exposure was associated with reductions in hemoglobin levels throughout the entire pregnancy, particularly during the first and second trimesters. During the entire pregnancy, each 1 μg/m³ increment in PM₁, PM_2.5, and PM₁₀ exposure was linked to a decrease in hemoglobin levels of 1.02 (95% CI: −1.52, −0.53), 0.87 (95% CI: −1.28, −0.46), and 0.37 (95% CI: −0.56, −0.19), respectively. Regarding anemia risk, in the first trimester, each unit increase in PM₁, PM_2.5, and PM₁₀ increased the odds of developing anemia with ORs of 1.23, 1.16, and 1.09. DLMs showed that the sensitive window for PM exposure was early-mid pregnancy for hemoglobin levels but was limited to the first trimester for anemia risk.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"326 ","pages":"Article 120980"},"PeriodicalIF":6.6,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149284428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of heat wave combined with sublethal doses of thiamethoxam on oviposition performance and gut microbial community of Bombus terrestris","authors":"Xi Xu,&nbsp;Shuang Wang,&nbsp;Yunfei Xue,&nbsp;Shaozi Xu,&nbsp;Rujie He,&nbsp;Dan Yue,&nbsp;Danyin Zhou,&nbsp;Kun Dong,&nbsp;Yakai Tian","doi":"10.1016/j.ecoenv.2026.121013","DOIUrl":"10.1016/j.ecoenv.2026.121013","url":null,"abstract":"<div><div>Climate warming has increased the frequency and intensity of extreme heat events, while neonicotinoid insecticides such as thiamethoxam are widely applied in agroecosystems. These two stressors frequently co-occur, yet their combined effects on pollinator health remain poorly understood. Here, we aimed to investigate the individual and interactive impacts of sublethal thiamethoxam and heat stress on bumblebee microcolonies. We examined the median lethal concentration (LC₅₀), food intake, survival rate, oviposition performance, biochemical activity, gene expression, and gut microbiota in <em>Bombus terrestris</em> microcolonies. The findings revealed that thiamethoxam and heat stress, alone and in combination, exerted effects on bumblebees across different dimensions. Heat stress markedly weakened worker tolerance to thiamethoxam: the LC₅₀ at 32 °C was 0.69 times and 0.52 times that at 26 °C at the 24 h and 48 h time points, respectively. Food intake declined significantly under all three exposure scenarios, whereas survival remained unaffected. The combined treatment significantly altered egg size and <em>VgR</em> expression. Heat stress offset the thiamethoxam-induced decline in SOD and GSH, but MDA remained elevated, indicating that maintained antioxidant markers did not restore protection against lipid peroxidation. Neither thiamethoxam nor heat stress, whether applied singly or in combination, significantly changed the alpha diversity indices of the gut microbiota; however, the microbial community composition underwent marked restructuring. The heat stress alone group yielded the highest number of unique ASVs. Thiamethoxam treatment noticeably shifted the gut microbial community profile, and the combined treatment produced a shift similar to that of thiamethoxam alone but with additional synergistic modulation. LEfSe analysis identified distinct sets of differentially abundant bacterial taxa across the treatment groups, confirming substantial community restructuring; the heat stress alone group harbored the largest number of significantly discriminant taxa. Overall, heat stress synergistically amplifies the sublethal toxicity of thiamethoxam in bumblebees, altering egg traits and reproductive gene expression and reshaping the gut microbiota, which underscores the urgency of incorporating temperature scenarios into pesticide risk assessment and pollinator conservation strategies.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"326 ","pages":"Article 121013"},"PeriodicalIF":6.6,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149316662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated multi-omics and experimental evidence implicate DVL3-associated Wnt/β-catenin signaling in PFHxS-related colorectal cancer progression","authors":"Ke Xu,&nbsp;Qiong Teng,&nbsp;Gang Yu,&nbsp;Wanjing Chen","doi":"10.1016/j.ecoenv.2026.121006","DOIUrl":"10.1016/j.ecoenv.2026.121006","url":null,"abstract":"<div><div>Perfluorohexanesulfonic acid (PFHxS) is a persistent per- and polyfluoroalkyl substance (PFAS) widely detected in human biospecimens, yet its relationship with colorectal cancer (CRC) progression remains poorly defined. We integrated network toxicology, bulk transcriptomics, machine-learning-based prognostic modeling, single-cell and spatial transcriptomics, and functional experiments to characterize PFHxS-associated molecular features in CRC. Intersecting PFHxS-related targets with CRC-associated genes identified 707 shared targets, of which 203 core nodes were retained after protein–protein interaction and topological filtering. A 14-gene gradient boosting machine signature stratified overall survival in TCGA and two external cohorts and remained independently prognostic after adjustment for clinical covariates. Single-cell analysis and SHAP-based model attribution prioritized DVL3 for experimental investigation. Chronic PFHxS exposure increased DVL3 abundance and malignant phenotypes in CRC models. DVL3 knockdown attenuated PFHxS-associated clonogenic and invasive phenotypes and reduced Wnt/β-catenin transcriptional activity and downstream target-gene expression, with key findings reproduced in CT26 cells. Continuous in vivo PFHxS exposure increased xenograft tumor burden and relative Ki-67-positive cell counts, with stronger DVL3 staining in representative tumor sections. Collectively, these findings link PFHxS exposure to aggressive CRC phenotypes and support DVL3 as a functional contributor to Wnt/β-catenin transcriptional responses.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"326 ","pages":"Article 121006"},"PeriodicalIF":6.6,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149306993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure to environmental phenols and growth indicators in adolescents: Epidemiological analysis and mechanistic exploration","authors":"Shuqin Tang,&nbsp;Aiqin Qiu,&nbsp;Long Zhang,&nbsp;Fengjiang Sun,&nbsp;Da Chen","doi":"10.1016/j.ecoenv.2026.121027","DOIUrl":"10.1016/j.ecoenv.2026.121027","url":null,"abstract":"<div><div>Environmental phenols, a typical group of endocrine-disrupting chemicals (EDCs), are widely used in consumer and personal care products. Although gestational exposure to environmental phenols has been linked to growth indicators in offspring, little is known about their effects on adolescence. We examined the associations between environmental phenols and anthropometric indicators in 2218 adolescents aged 12<strong>–</strong>19 from the National Health and Nutrition Examination Survey 2005<strong>–</strong>2016. Multivariable linear regression and quantile-based g-computation assessed individual and mixture associations, respectively. Exploratory mediation analysis evaluated bone mineral density (BMD) in a subsample, and network toxicology identified candidate pathways. We found that higher urinary concentrations of bisphenol A (BPA), methylparaben, and propylparaben were significantly associated with lower body mass index (BMI), BMI z-score, weight, and arm circumference. Methylparaben and propylparaben were also inversely associated with waist circumference and waist circumference/height ratio. Mixture analysis revealed the joint effects of environmental phenol mixture on reduced BMI, weight, and arm circumference. Mediation analysis suggested that BMD partly mediated the BPA<strong>–</strong>weight association. Network toxicology analysis identified significant enrichment in thyroid hormone, PI3K/AKT, and MAPK signaling pathways. These findings suggest negative associations between selected urinary phenols and adolescent growth indicators, and highlight adolescence as a potentially sensitive window for environmental chemical exposure, with possible involvement of bone metabolism and endocrine-related signaling pathways.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"326 ","pages":"Article 121027"},"PeriodicalIF":6.6,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149340107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acetyl tributyl citrate induces neuronal ferroptosis through ATM-associated disruption of iron and redox homeostasis","authors":"Xiao-Ting Luo,&nbsp;Yan Li,&nbsp;Li-Ming Xu,&nbsp;Hui-Rong Hu,&nbsp;Zhen-Dong Sun,&nbsp;Li-Hong Zhang","doi":"10.1016/j.ecoenv.2026.121021","DOIUrl":"10.1016/j.ecoenv.2026.121021","url":null,"abstract":"<div><h3>Background</h3><div>Acetyl tributyl citrate (ATBC) is widely used as a non-phthalate plasticizer, raising concerns about its potential health effects. Although emerging evidence suggests that ATBC may adversely affect the nervous system, the underlying mechanisms remain poorly understood. Given the critical role of ferroptosis in neuronal injury, this study investigated whether ferroptosis contributes to ATBC-induced neuronal injury and explored the potential involvement of ataxia-telangiectasia mutated (ATM) in this process.</div></div><div><h3>Methods</h3><div>Network toxicology was first employed to identify potential targets linking ATBC exposure, neuronal injury, and ferroptosis, followed by protein–protein interaction analysis, functional enrichment, and molecular docking. The predicted mechanisms were subsequently evaluated in ATBC-exposed HT22 cells through ferroptosis-related molecular, oxidative, and ultrastructural assessments, with ATM silencing used to examine its regulatory role. An ATBC-exposed mouse model was further employed to validate ferroptosis-related alterations in hippocampal tissue.</div></div><div><h3>Results</h3><div>Network analysis identified ATM as a central candidate target, while molecular docking and molecular dynamics simulation predicted a potential ATBC–ATM interaction. ATBC exposure reduced HT22 cell viability, increased ATM, TFRC, Keap1 and PTGS2 expression, decreased SLC7A11, SLC40A1, NRF2 and GPX4 expression, disrupted iron and redox homeostasis, and induced ferroptosis-associated mitochondrial alterations. ATM knockdown partially reversed these changes. Consistently, ATBC exposure induced similar molecular, redox, and mitochondrial alterations in the mouse hippocampus.</div></div><div><h3>Conclusions</h3><div>These findings support the involvement of ferroptosis in ATBC-induced hippocampal neuronal injury and suggest ATM as an important mediator of this process. This study provides mechanistic insight into the potential neurological effects of ATBC and identifies ATM-associated ferroptosis as a potential mechanism underlying ATBC-induced neuronal injury.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"326 ","pages":"Article 121021"},"PeriodicalIF":6.6,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149357011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential regulation of conjugative transfer and OMV-mediated ARG delivery by iprovalicarb and cycluron: Implications for pathway-specific risk assessment","authors":"Shaqiu Zhang,&nbsp;Yan Fan,&nbsp;Peijie He,&nbsp;Qianlong Li,&nbsp;Mingshu Wang,&nbsp;Renyong Jia,&nbsp;Shun Chen,&nbsp;Mafeng Liu,&nbsp;Dekang Zhu,&nbsp;Xinxin Zhao,&nbsp;Ying Wu,&nbsp;Qiao Yang,&nbsp;Juan Huang,&nbsp;Xumin Ou,&nbsp;Di Sun,&nbsp;Bin Tian,&nbsp;Yu He,&nbsp;Zhen Wu,&nbsp;Anchun Cheng","doi":"10.1016/j.ecoenv.2026.120972","DOIUrl":"10.1016/j.ecoenv.2026.120972","url":null,"abstract":"<div><div>Horizontal gene transfer (HGT) is a major driver of the rapid dissemination of antibiotic resistance genes (ARGs) among bacteria. Non-antibiotic compounds can promote plasmid-mediated conjugative transfer. In waterfowl farming, waterfowl frequently move among water, soil, and feces, which serve as reservoirs for pesticides and ARGs and thus potential hotspots for ARG spread. However, whether outer membrane vesicles (OMVs), an emerging ARG transmission pathway, are regulated by pesticides and respond in a manner consistent with conjugation is unclear. In this study, two pesticides detected in waterfowl farm environments, iprovalicarb and cycluron were selected to investigate their effects on conjugative transfer and OMV-mediated ARG dissemination. Both pesticides significantly promoted RP4 plasmid conjugation frequency at sub-inhibitory concentrations. This effect was associated with elevated bacterial reactive oxygen species (ROS), increased membrane permeability and fluidity, enhanced interbacterial contact, and altered energy metabolism. However, their effects on the OMV pathway diverged: iprovalicarb increased OMV production and vesicle size and was associated with more <em>bla</em>-positive colonies after OMV exposure, whereas cycluron inhibited OMV production. This decoupling suggests that pesticides can differentially regulate conjugative and OMV-mediated ARG transfer. However, the <em>bla</em> gene was not stably inherited in recipient bacteria. Overall, these findings highlight the need to evaluate these two pathways separately when assessing the risk of antimicrobial resistance.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"326 ","pages":"Article 120972"},"PeriodicalIF":6.6,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149284399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}