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The association between exposure to polycyclic aromatic hydrocarbons and the risk of premature rupture of membranes 暴露于多环芳烃与膜过早破裂风险之间的关系。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-20 DOI: 10.1016/j.ecoenv.2026.119844
Kui Xie , Haixia Tian , Xinyi Xiao , Linfei Wu , Cheng Chen , Shimin Xiong , Lulu Dai , Xingyan Liu , Rong Zeng , Yan Xie , Yijun Liu , Xubo Shen , Zuqiang Wu , Yuanzhong Zhou

Background

Premature rupture of membranes (PROM) remains a significant clinical challenge. It has substantial socioeconomic impacts. Despite the known toxicity of polycyclic aromatic hydrocarbons (PAH), there is limited epidemiological evidence on their association with PROM in pregnant populations.

Methods

Our investigation addressed this gap. We analyzed 1717 late-pregnancy women from the Zunyi Birth Cohort, quantifying urinary PAH metabolites as exposure biomarkers. We used logistic regression and restricted cubic spline (RCS) models to examine the individual and nonlinear associations between PAH and PROM. Bayesian kernel machine regression (BKMR) was also used for the mixed association.

Results

Logistic regression revealed that the third tertiles of 2-OHFlu, 9-OHFlu, 2-OHPhe, 3-OHPhe, and 9-OHPhe were associated with 1.58-fold (95 % CI: 1.03–2.47), 2.02-fold (95 % CI: 1.3–3.2), 1.83-fold (95 % CI: 1.23–2.75), 1.52-fold (95 % CI: 1.01–2.32), 2.1-fold (95 % CI: 1.38–3.24) higher PROM risks, respectively. RCS regression showed the nonlinear associations between 2-OHFlu (P-nonlinear = 0.040), 9-OHFlu (P-nonlinear = 0.027), and 3-OHPhe (P-nonlinear = 0.020) and the risk of PROM. BKMR further revealed an increasing trend in PROM risk associated with PAH mixture exposure.

Conclusions

This study provides epidemiological evidence that exposure to PAH during late gestation may increase susceptibility to PROM. These findings offer empirical reference evidence for implementing targeted environmental interventions in prenatal care.
背景:胎膜早破(PROM)仍然是一个重大的临床挑战。它具有重大的社会经济影响。尽管已知多环芳烃(PAH)的毒性,但关于其与怀孕人群中胎膜早破之间关系的流行病学证据有限。方法:我们的调查解决了这一差距。我们分析了来自遵义出生队列的1717名晚期妊娠妇女,量化了尿中多环芳烃代谢物作为暴露生物标志物。我们使用逻辑回归和限制三次样条(RCS)模型来检验多环芳烃和PROM之间的个体和非线性关联。贝叶斯核机回归(BKMR)也用于混合关联。结果:Logistic回归显示,2-OHFlu、9-OHFlu、2-OHPhe、3-OHPhe和9-OHPhe的三分位数分别与1.58倍(95 % CI: 1.03-2.47)、2.02倍(95 % CI: 1.3-3.2)、1.83倍(95 % CI: 1.23-2.75)、1.52倍(95 % CI: 1.01-2.32)、2.1倍(95 % CI: 1.38-3.24)的PROM高风险相关。RCS回归显示,2-OHFlu (p -非线性= 0.040)、9-OHFlu (p -非线性= 0.027)和3-OHPhe (p -非线性= 0.020)与早PROM风险呈非线性相关。BKMR进一步揭示了与多环芳烃混合物暴露相关的PROM风险增加趋势。结论:本研究为妊娠后期暴露于多环芳烃可能增加胎膜早破的易感性提供了流行病学证据。这些发现为在产前护理中实施有针对性的环境干预提供了经验参考证据。
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引用次数: 0
AATE-UNet automated assessment of inflammatory response in zebrafish larvae exposed to environmental risks ate - unet对暴露于环境风险的斑马鱼幼虫炎症反应的自动评估。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-26 DOI: 10.1016/j.ecoenv.2026.119939
Jiaqi Yang , Lulu Xu , Zhenglin Chen , Tingqiao Ye , Yungui Li , Min Dai , Pei Yang , Peiwu Qin
In the evaluation of drugs/cosmetics toxicology/efficacy on livings, rapid assessment of inflammatory responses in zebrafish models is critical but hindered by labor-intensive manual neutrophil counting. To be addressed, this study developed the innovative AATE-UNet, a deep learning model that automates high-throughput image analysis for precise inflammation quantification. In result, this UNet-based architecture processes lateral zebrafish images to segment complex anatomical regions (yolk sac, spinal cord) and quantify neutrophils with 90 % accuracy (<10 % error versus manual counts), while slashing processing time from ∼1 h to < 5 min per sample. The advancement eliminates subjective variability and workflow bottlenecks inherent to manual methods. As a supplement, qPCR analysis revealed pollutant-driven dysregulation of inflammatory cytokines (e.g. IL-1β, IL-6, IL-10, and TNF-α), bridging cellular neutrophil dynamics with molecular pathways. Moreover, the AATE-UNet model was packaged as a user-friendly executable file (.exe), facilitating application in standard fluorescence imaging systems by enabling use on computers with compatible hardware without the need for specialized software or training. By correlating neutrophil thresholds with pollutant concentrations, our framework establishes actionable metrics for toxicity evaluation while offering a scalable solution to accelerate environmental risk assessments. Consequently, this study provides a reliable method effectively enables objective morphometric analysis of zebrafish larvae to evaluate the inflammatory responses of environmental exposures.
在评估药物/化妆品毒理学/对生物的功效时,快速评估斑马鱼模型的炎症反应是至关重要的,但由于人工中性粒细胞计数的劳动密集型而受到阻碍。为了解决这个问题,本研究开发了创新的ate - unet,这是一种深度学习模型,可自动进行高通量图像分析,以精确量化炎症。因此,这种基于unet的架构处理斑马鱼侧面图像,以分割复杂的解剖区域(卵黄囊,脊髓)并定量中性粒细胞,准确率为90% % (
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引用次数: 0
Perfluorooctane sulfonate induces joint inflammation to trigger osteoarthritis through the YAP1/IκBα signaling pathway 全氟辛烷磺酸通过YAP1/ i - κ b α信号通路诱导关节炎症引发骨关节炎。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-03-02 DOI: 10.1016/j.ecoenv.2026.119961
Huiying Guo , Jieruo Li , Guiwang Shen , Zifeng Wu , Hengyu Liao , Zhiyu Huang , Xiaofei Zheng , Zhengang Zha , Jinshao Ye , Jie Yang
Perfluoroalkyl and polyfluoroalkyl substances (PFASs) are persistent pollutants that have been linked to chronic inflammation. Epidemiologic studies have indicated that PFAS exposure is associated with an increased prevalence of osteoarthritis (OA). We previously hypothesized that inflammation may facilitate the penetration of perfluorooctane sulfonate (PFOS) across the joint barrier; however, the potential impact of PFASs on OA progression remains unclear. Herein, we revealed that exposure to PFOS induced joint inflammation, contributing to the development of OA in vivo; PFOS decreased the expression of YAP1 and IκBα, causing inflammation of the synovium and cartilage. The regulation of OA by PFOS is conserved in human synovicytes, synovial explants, and mice. Our findings clarify the hazards and potential mechanisms of PFOS towards joint inflammation and highlight YAP1/IκBα as a potential therapeutic target for OA.
全氟烷基和多氟烷基物质(PFASs)是与慢性炎症有关的持久性污染物。流行病学研究表明,PFAS暴露与骨关节炎(OA)患病率增加有关。我们先前假设炎症可能促进全氟辛烷磺酸(PFOS)穿过关节屏障;然而,PFASs对OA进展的潜在影响尚不清楚。在此,我们揭示了暴露于全氟辛烷磺酸诱导关节炎症,促进体内OA的发展;PFOS降低YAP1和IκBα的表达,引起滑膜和软骨的炎症。全氟辛烷磺酸对OA的调节在人滑膜细胞、滑膜外植体和小鼠中是保守的。我们的研究结果阐明了PFOS对关节炎症的危害和潜在机制,并强调了YAP1/ i - κ b α是OA的潜在治疗靶点。
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引用次数: 0
Genome-wide screen identifies genes conferring sensitivity to the pollutant bisphenol A in Saccharomyces cerevisiae 全基因组筛选鉴定了酿酒酵母对污染物双酚A敏感的基因。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-28 DOI: 10.1016/j.ecoenv.2026.119883
Luqian Sun , Leilei Ni , Keliang Lyu, Jianing Xian, Xiaolin Liu, Jiyang Li, Jie Sun, Peng Xiong, Xue Wang
Bisphenol A (BPA), a widely used industrial and agricultural chemical, is a pervasive environmental pollutant with documented harmful effects on ecosystems. Though BPA is known to adversely affect plants, animals, and microorganisms, the precise molecular mechanisms underlying its toxicity remain poorly understood. To address this gap, we investigated the cellular response to BPA using the unicellular eukaryotic model organism Saccharomyces cerevisiae. A genome-wide screen of the diploid single-gene deletion library (comprising 4741 non-essential gene deletion mutants) identified 108 strains exhibiting hypersensitivity to BPA. Functional categorization revealed that the corresponding genes are primarily involved in metabolism, cell cycle regulation, transcription, cellular transport, protein synthesis, and modification. Further analysis via high-performance liquid chromatography demonstrated that 34 of the sensitive mutants accumulated significantly higher intracellular levels of BPA compared to the wild-type strain. Our findings may provide systematic insights into the genetic determinants of BPA sensitivity in yeast and highlight various cellular pathways implicated in its toxic mechanism.
双酚A (BPA)是一种广泛使用的工业和农业化学品,是一种普遍存在的环境污染物,对生态系统产生了有害影响。虽然已知双酚a对植物、动物和微生物有不良影响,但其毒性背后的确切分子机制仍然知之甚少。为了解决这一空白,我们使用单细胞真核模式生物酿酒酵母研究了细胞对BPA的反应。二倍体单基因缺失文库(包括4741个非必需基因缺失突变体)的全基因组筛选鉴定出108株对BPA过敏的菌株。功能分类表明,相应的基因主要参与代谢、细胞周期调节、转录、细胞转运、蛋白质合成和修饰。通过高效液相色谱进一步分析表明,34个敏感突变体的细胞内BPA水平明显高于野生型菌株。我们的发现可能为酵母中BPA敏感性的遗传决定因素提供了系统的见解,并突出了涉及其毒性机制的各种细胞途径。
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引用次数: 0
Chain-length matters: How benzylalkyldimethylammonium quaternary disinfectants disrupt gonadal steroidogenesis via 3β-hydroxysteroid dehydrogenase inhibition 链长问题:苯烷基二甲基铵季铵盐消毒剂如何通过抑制3β-羟基类固醇脱氢酶破坏性腺类固醇生成。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-27 DOI: 10.1016/j.ecoenv.2026.119960
Mengyao Yin , Jingyun Yan , Cong Chen , Zhixiang Mao , Qianyu Wang , Huitao Li , Linxin Li , Ren-shan Ge , Jing Cheng
Benzylalkyldimethylammonium (BAC) quaternary disinfectants are extensively used as antimicrobial agents. However, the specific BACs responsible for inhibition and their structure-activity relationship (SAR) for human 3β-hydroxysteroid dehydrogenase 2 (3β-HSD2) and its homolog rat 3β-HSD1, the critical enzyme in gonadal steroidogenesis, remain poorly understood. This study evaluated nine BACs for their inhibitory effects on human 3β-HSD2 and rat 3β-HSD1, determining potency (IC50), inhibition kinetics, cellular impact, and binding interactions via molecular docking and 3D-QSAR. Inhibitory potency (IC50) revealed C18 (11.84 μM) > C16 (15.51 μM) > C14 (25.25 μM) > C12 (30.63 μM) > C10 (56.86 μM) > C1-C8 BACs (no inhibition at 100 μM) against human 3β-HSD2 and C18 (8.23 μM) > C16 (10.74 μM) > C14 (12.21 μM) > C12 (14.38 μM) > C10 (26.62 μM) > C1-C8 BACs (no inhibition at 100 μM) against rat 3β-HSD1. Both enzymes exhibited mixed-type inhibition. Cellular suppression showed that C14, C16, and C18 BACs inhibited progesterone synthesis in human KGN granulosa tumor cells at ≥ 5 μM. Docking and SAR revealed binding at the NAD+ /steroid site via hydrogen bonding, hydrophobic, and van der Waals interactions. Lipophilicity (LogP), steric bulk, Fsp3, and flexibility correlated positively with potency, indicating that longer alkyl chains (≤C18) enhance inhibition. 3D-QSAR confirmed the importance of hydrophobic regions in binding affinity due to long alkyl chain. In conclusion, BACs inhibit gonadal 3β-HSD activity in a chain-length-dependent manner (C10-C18), with lipophilicity as a key determinant. These findings suggest that BAC disinfectants may act as potential endocrine disruptors by interfering with steroidogenesis.
苄基烷基二甲基铵(BAC)季铵盐是一种广泛使用的抗菌药物。然而,对人类3β-羟基类固醇脱氢酶2 (3β-HSD2)及其同源物大鼠3β-HSD1(性腺类固醇生成的关键酶)的抑制作用及其结构-活性关系(SAR)的特异性BACs仍知之甚少。本研究评估了9种BACs对人3β-HSD2和大鼠3β-HSD1的抑制作用,确定了效价(IC50)、抑制动力学、细胞影响以及通过分子对接和3D-QSAR进行的结合相互作用。抑制能力(IC50)显示使用C18(11.84 μM) > C16(15.51 μM) > 碳(25.25 μM) > C12(30.63 μM) > C10(56.86 μM) > C1-C8•巴(没有抑制100μM)对人类3β-HSD2和C18(8.23 μM) > C16(10.74 μM) > 碳(12.21 μM) > C12(14.38 μM) > C10(26.62 μM) > C1-C8•巴(没有抑制100μM)对大鼠3β-HSD1。两种酶均表现出混合型抑制作用。细胞抑制显示,C14、C16和C18 BACs抑制≥ 5 μM的人KGN颗粒肿瘤细胞的孕酮合成。对接和SAR显示NAD+ /类固醇位点通过氢键、疏水和范德华相互作用结合。亲脂性(LogP)、立体体积、Fsp3和柔韧性与效价呈正相关,表明较长的烷基链(≤C18)增强了抑制作用。3D-QSAR证实了由于长烷基链,疏水区域在结合亲和力中的重要性。综上所述,BACs以链长依赖的方式(C10-C18)抑制性腺3β-HSD活性,亲脂性是关键决定因素。这些发现表明BAC消毒剂可能通过干扰类固醇生成而成为潜在的内分泌干扰物。
{"title":"Chain-length matters: How benzylalkyldimethylammonium quaternary disinfectants disrupt gonadal steroidogenesis via 3β-hydroxysteroid dehydrogenase inhibition","authors":"Mengyao Yin ,&nbsp;Jingyun Yan ,&nbsp;Cong Chen ,&nbsp;Zhixiang Mao ,&nbsp;Qianyu Wang ,&nbsp;Huitao Li ,&nbsp;Linxin Li ,&nbsp;Ren-shan Ge ,&nbsp;Jing Cheng","doi":"10.1016/j.ecoenv.2026.119960","DOIUrl":"10.1016/j.ecoenv.2026.119960","url":null,"abstract":"<div><div>Benzylalkyldimethylammonium (BAC) quaternary disinfectants are extensively used as antimicrobial agents. However, the specific BACs responsible for inhibition and their structure-activity relationship (SAR) for human 3β-hydroxysteroid dehydrogenase 2 (3β-HSD2) and its homolog rat 3β-HSD1, the critical enzyme in gonadal steroidogenesis, remain poorly understood. This study evaluated nine BACs for their inhibitory effects on human 3β-HSD2 and rat 3β-HSD1, determining potency (IC<sub>50</sub>), inhibition kinetics, cellular impact, and binding interactions via molecular docking and 3D-QSAR. Inhibitory potency (IC<sub>50</sub>) revealed C18 (11.84 μM) &gt; C16 (15.51 μM) &gt; C14 (25.25 μM) &gt; C12 (30.63 μM) &gt; C10 (56.86 μM) &gt; C1-C8 BACs (no inhibition at 100 μM) against human 3β-HSD2 and C18 (8.23 μM) &gt; C16 (10.74 μM) &gt; C14 (12.21 μM) &gt; C12 (14.38 μM) &gt; C10 (26.62 μM) &gt; C1-C8 BACs (no inhibition at 100 μM) against rat 3β-HSD1. Both enzymes exhibited mixed-type inhibition. Cellular suppression showed that C14, C16, and C18 BACs inhibited progesterone synthesis in human KGN granulosa tumor cells at ≥ 5 μM. Docking and SAR revealed binding at the NAD+ /steroid site via hydrogen bonding, hydrophobic, and van der Waals interactions. Lipophilicity (LogP), steric bulk, Fsp3, and flexibility correlated positively with potency, indicating that longer alkyl chains (≤C18) enhance inhibition. 3D-QSAR confirmed the importance of hydrophobic regions in binding affinity due to long alkyl chain. In conclusion, BACs inhibit gonadal 3β-HSD activity in a chain-length-dependent manner (C10-C18), with lipophilicity as a key determinant. These findings suggest that BAC disinfectants may act as potential endocrine disruptors by interfering with steroidogenesis.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"312 ","pages":"Article 119960"},"PeriodicalIF":6.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321065","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}
引用次数: 0
Distribution and characterization of microplastics in Narmada River: Insights from differently impacted anthropogenic zones of upper and middle basin in Central India 纳尔马达河中微塑料的分布和特征:来自印度中部上游和中部盆地不同受影响人为带的见解。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-27 DOI: 10.1016/j.ecoenv.2026.119964
Dinesh Parida , Konica Katare , Kanika Kiran , Regina Nogueira , Florian Bittner , Pia Ansahl , Robin-Macmahon Bähre , Hans-Josef Endres , Kiran Bala
The Narmada River is a vital water source for irrigation, drinking, and hydroelectric projects in India. It passes through rural, agricultural, semi urban, and tourist intensive areas, making it vulnerable to anthropogenic pressure. We proposed that the abundance of microplastics (MP) and the diversity of polymers vary across these anthropogenically disturbed regions, with tourist and semi-urban contributing more than rural agriculture regions. To test this, we assessed the upper and middle river basin (in surface water and sediments). Morphological characterisation (shape, size, colour) was performed using a stereomicroscope and particle size analyser, while chemical composition was determined by ATR-FTIR and µFTIR. The average concentration of MPs is 4738 ± 5303 particles/m³ in surface water and 290071 ± 199929 particles/m³ in sediments, respectively. Nineteen distinct polymers including hazardous polymers like polyurethane and poly vinyl chloride were identified revealing complex chemical footprint. In surface water, polypropylene, polyethylene, and polyethylene terephthalate were dominant, whereas in sediments, polyethylene and polyethylene terephthalate were more prevalent. Fibers dominated surface water, while fragments dominated sediments. Additives like dibutyl sebacate and ethyl hexyl epoxy soyate were also identified. Polymer hazard index (PHI) and potential ecological risk index (PERI) also predicted the risks imposed by the hazardous polymers. Tourist locations with anthropogenic disturbances have a higher MP abundance in surface water, while both semi-urban and tourist locations contribute to MP pollution in sediments. These findings demonstrate that anthropogenic activities strongly influence MP pollution in the Narmada River and highlight the urgent need for region-specific management strategies.
纳尔马达河是印度灌溉、饮用和水电项目的重要水源。它穿过农村、农业、半城市和旅游密集地区,使其容易受到人为压力。我们提出,微塑料(MP)的丰度和聚合物的多样性在这些人为干扰地区有所不同,旅游和半城市贡献大于农村农业地区。为了验证这一点,我们对中上游流域(地表水和沉积物)进行了评估。形态学表征(形状、大小、颜色)使用立体显微镜和粒度分析仪进行,化学成分通过ATR-FTIR和µFTIR测定。地表水中MPs的平均浓度为4738 ± 5303 particles/m³ ,沉积物中MPs的平均浓度为290071 ± 199929 particles/m³ 。19种不同的聚合物,包括聚氨酯和聚氯乙烯等危险聚合物,被识别出复杂的化学足迹。地表水中以聚丙烯、聚乙烯和聚对苯二甲酸乙二醇酯为主,而沉积物中以聚乙烯和聚对苯二甲酸乙二醇酯为主。表层水以纤维为主,沉积物以碎片为主。添加剂如癸二酸二丁酯和乙基己基环氧大豆酸酯也被确定。利用聚合物危害指数(PHI)和潜在生态风险指数(PERI)预测了危险聚合物的潜在生态风险。受人为干扰的旅游地地表水中MP丰度较高,而半城市和旅游地都对沉积物中的MP污染有贡献。这些研究结果表明,人为活动对纳尔马达河的多聚氰胺污染有强烈的影响,并强调了迫切需要制定针对特定区域的管理策略。
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引用次数: 0
The multi-barrier fate of strobilurin fungicides in Dendrobium officinale: uptake, sequestration in root cell walls, and high cumulative dietary risk 石斛杀菌剂strobilurin在铁皮石斛中的多屏障命运:吸收、根细胞壁的固存和高累积饮食风险。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-03-02 DOI: 10.1016/j.ecoenv.2026.119965
Yuan Lei , Hui Ye , Nan Fang , Jinhua Jiang , Yuqin Luo , Xiangyun Wang , Hongmei He , Jianzhong Yu , Xueping Zhao , Zhiqiang Kong , Changpeng Zhang
The high residual levels and prolonged persistence of strobilurin fungicides prompted this systematic investigation into the environmental fate, accumulation mechanisms, and dietary exposure risks of five key compounds: azoxystrobin, kresoxim-methyl, picoxystrobin, pyraclostrobin, and trifloxystrobin. A hydroponic system was employed to simulate post-application uptake. Root exposure resulted in significant accumulation (bioconcentration factors: 1.6–49) but limited translocation to stems (bioconcentration factors: 0.008–0.31, translocation factor < 0.1), whereas foliar exposure led to effective retention in leaves (translocation factor < 1). To elucidate the underlying mechanisms, correlation analyses revealed that translocation was governed by molecular properties: root-to-stem movement correlated with molecular weight, and leaf-to-stem movement with water solubility (R² > 0.71, p < 0.05). Uptake pathway studies indicated that four fungicides primarily entered roots apoplastically, whereas kresoxim-methyl relied more on the symplastic route. Uptake was predominantly passive, though azoxystrobin and trifloxystrobin appeared to involve membrane transporters, suggesting interspecific differences. Critically, subcellular analysis identified root cell walls as the dominant sink, sequestering 55–88% of absorbed fungicides, which fundamentally limited upward mobility. Based on these fate parameters and integrated with consumption data of 73 crops, probabilistic cumulative exposure assessment predicted an unacceptable chronic risk for children under 14 years, with hazard quotients reaching 3896%. This work elucidates a multi-barrier defense mechanism in plants and underscores the necessity of cumulative risk assessment for medicinal crops under multi-pathway exposure.
strobilurin杀菌剂的高残留水平和长期持久性促使我们对五种关键化合物的环境命运、积累机制和饮食暴露风险进行了系统的调查:偶氮氧嘧菌酯、甲基甲氧苄菌酯、吡氧嘧菌酯、吡氯嘧菌酯和三氯嘧菌酯。采用水培系统模拟施用后的吸收。根系暴露导致了显著的积累(生物浓度因子:1.6-49),但向茎部的转运有限(生物浓度因子:0.008-0.31,转运因子< 0.1),而叶面暴露导致了叶片的有效滞留(转运因子< 1)。为了阐明潜在的机制,相关分析表明,易位受分子特性的控制:根到茎的运动与分子量相关,叶到茎的运动与水溶性相关(R²> 0.71,p
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引用次数: 0
Membrane-translocated SO₂/₃-PRDX3 disrupts cystine uptake and GPX4 activity: A pivotal mechanism of boron-induced renal ferroptosis in broiler 膜易位SO₂/₃-PRDX3破坏胱氨酸摄取和GPX4活性:硼诱导肉鸡肾铁下沉的关键机制。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-03-02 DOI: 10.1016/j.ecoenv.2026.119969
Yuanxu Li , Yumeng Li , Mingyang Guo , Yating Tian , Mengran Wang , Jiangli Huang , Weiqian Su , Zhonghua Liu , Wenlan Yu
Boron (B), a widely utilized non-metallic element in industrial, agricultural, and medical applications, has garnered significant attention due to its documented reproductive and developmental toxicity. Although the kidney plays a pivotal role in boron metabolism and excretion, the precise mechanisms underlying its nephrotoxicity remain incompletely elucidated. This study systematically investigated the toxic effects of boron exposure on chicken kidneys and its underlying molecular mechanisms, employing both in vivo chicken kidney tissues and an in vitro model of primary chicken renal tubular epithelial cells. Our findings demonstrate that boron exposure significantly impaired growth performance and renal function in broilers, induced histopathological alterations in kidney tissues, disrupted renal iron metabolism homeostasis, and triggered ferroptosis. Mechanistic exploration revealed that during boron-induced ferroptosis, peroxiredoxin 3 (PRDX3) underwent hyperoxidation (forming SO2/3-PRDX3) and aberrantly translocated to the cell membrane. Intriguingly, the membrane localization of SO2/3-PRDX3 impaired cellular cystine uptake, consequently inhibiting the synthesis of the critical antioxidant tripeptide glutathione (GSH), thereby exacerbating the ferroptosis process. Furthermore, dysfunctional SO2/3-PRDX3 could affect the core antioxidant activity of glutathione peroxidase 4 (GPX4), weakening cellular defenses against lipid peroxidation. In conclusion, boron exposure induces renal damage in chickens by activating the ferroptosis pathway. This activation is mediated through PRDX3 hyperoxidation, its subsequent membrane translocation, and the resulting impairment of cysteine uptake and GSH biosynthesis. SO2/3-PRDX3 dysfunction represents a critical molecular event in boron-induced nephrotoxicity in broiler chickens.
硼(B)是一种广泛应用于工业、农业和医疗应用的非金属元素,由于其记录的生殖和发育毒性而引起了极大的关注。尽管肾脏在硼的代谢和排泄中起着关键作用,但其肾毒性的确切机制仍未完全阐明。本研究利用鸡肾脏组织和体外原代鸡肾小管上皮细胞模型,系统研究了硼暴露对鸡肾脏的毒性作用及其潜在的分子机制。我们的研究结果表明,硼暴露显著损害肉仔鸡的生长性能和肾功能,诱导肾脏组织病理改变,破坏肾铁代谢稳态,并引发铁下垂。机制探索表明,在硼诱导的铁凋亡过程中,过氧化物还蛋白3 (PRDX3)发生过氧化(形成SO2/3-PRDX3)并异常易位到细胞膜上。有趣的是,SO2/3-PRDX3的膜定位损害了细胞对胱氨酸的摄取,从而抑制了关键抗氧化剂三肽谷胱甘肽(GSH)的合成,从而加剧了铁死亡过程。此外,SO2/3-PRDX3功能失调会影响谷胱甘肽过氧化物酶4 (GPX4)的核心抗氧化活性,削弱细胞对脂质过氧化的防御能力。综上所述,硼暴露通过激活铁下垂途径诱导鸡肾损伤。这种激活是通过PRDX3过氧化、随后的膜易位以及由此导致的半胱氨酸摄取和谷胱甘肽生物合成的损害介导的。SO2/3-PRDX3功能障碍是肉仔鸡硼致肾毒性的一个关键分子事件。
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引用次数: 0
Physical exercise alleviates PM2.5-induced damage by repairing adipose mitochondria dysfunction in mice 体育锻炼通过修复小鼠脂肪线粒体功能障碍减轻pm2.5引起的损伤。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-20 DOI: 10.1016/j.ecoenv.2026.119896
Bingru Nan , Kun Pan , Chuan Xu , Jinzhuo Zhao , Jie Zhang
Physical exercise (PE) can mitigate fine particulate matter (PM2.5)-associated metabolic disorders, but its impacts on adipose mitochondrial health under PM2.5 exposure remain unclear. Here, we performed a 4-month exposure study in C57BL/6 mice (filtered air, PM2.5, and PM2.5 plus PE) and evaluated systemic metabolic phenotypes (body and adipose weights, serum lipids, intraperitoneal glucose tolerance test, and intraperitoneal insulin tolerance test), adipose mitochondrial ultrastructure, and mitochondrial proteomes in brown adipose tissue (BAT) and epididymal white adipose tissue (eWAT). PM2.5 exposure reduced mitochondrial number and area and caused ultrastructural injury in both adipose depots, accompanied by impaired glucose homeostasis. PE attenuated these phenotypic alterations but did not fully normalize them. Mitochondrial proteomics combined with an integrative stepwise analytical framework identified 6 candidate effector proteins in BAT and 18 in eWAT whose abundance patterns were consistent with PM2.5 injury and partial PE restoration. Functional annotation suggested enrichment in pathways related to gene expression and protein homeostasis, membrane stability, and respiratory chain assembly in BAT, and protein sorting, post-translational modification, antioxidant activity, ion homeostasis, and energy metabolism in eWAT. These findings suggest that PE may alleviate PM2.5-associated adipose mitochondrial dysfunction through coordinated changes across multiple pathways in a tissue-specific manner.
体育锻炼(PE)可以减轻细颗粒物(PM2.5)相关的代谢紊乱,但其对PM2.5暴露下脂肪线粒体健康的影响尚不清楚。在这里,我们对C57BL/6小鼠(过滤空气、PM2.5和PM2.5加PE)进行了为期4个月的暴露研究,并评估了全身代谢表型(体和脂肪重量、血脂、腹腔内葡萄糖耐量试验和腹腔内胰岛素耐量试验)、脂肪线粒体超微结构和棕色脂肪组织(BAT)和附睾白色脂肪组织(eWAT)的线粒体蛋白质组学。PM2.5暴露减少了两个脂肪库的线粒体数量和面积,并导致超微结构损伤,同时伴有葡萄糖稳态受损。PE减轻了这些表型改变,但并未使其完全正常化。线粒体蛋白质组学结合综合逐步分析框架确定了BAT中的6个候选效应蛋白和eWAT中的18个候选效应蛋白,其丰度模式与PM2.5损伤和部分PE恢复一致。功能注释表明,BAT中与基因表达和蛋白质稳态、膜稳定性和呼吸链组装相关的途径,以及eWAT中与蛋白质分选、翻译后修饰、抗氧化活性、离子稳态和能量代谢相关的途径都有富集。这些发现表明,PE可能通过多种途径以组织特异性方式协调改变,减轻pm2.5相关的脂肪线粒体功能障碍。
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引用次数: 0
Acrylamide exposure induces neurotoxicity via the PI3K/Akt/NF-κB pathway: Evidence from network toxicology and experimental validation 丙烯酰胺暴露通过PI3K/Akt/NF-κB通路诱导神经毒性:网络毒理学证据和实验验证。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-23 DOI: 10.1016/j.ecoenv.2026.119922
Zhaoda Duan , Chunjiao Yu , Qiuxian Yu , Wenjie Yang , Rui Zhang , Qiaoling Ruan , Yongfang Zhao , Shan Yan
Acrylamide (ACR) is a chemical compound widely used in industrial production and food processing, the underlying mechanisms of its neurotoxicity have yet to be fully elucidated. Through the integration of network toxicology, molecular docking, and experimental validation, this study systematically explored the underlying molecular mechanisms of ACR-induced neurotoxicity. Through database analysis, 183 ACR-related targets and 2725 neurotoxicity-associated targets were identified, among which 100 overlapping genes were predominantly enriched in the PI3K/Akt signaling pathway and apoptosis-related biological processes. Molecular docking and molecular dynamics simulations suggested potential interactions between ACR and key target proteins. While causing minimal alterations in peripheral organs, ACR exposure in vivo resulted in hippocampal neuronal disorganization and Nissl body loss, indicating potential neurotoxicity. In vitro studies demonstrated that ACR not only decreased cell viability in PC12 and HT22 cells but also significantly enhanced apoptosis and inflammation, while markedly activating the PI3K/Akt and NF-κB signaling pathway. The significant attenuation of these effects was observed following treatment with the PI3K inhibitor LY294002. These findings suggest that ACR-induced neurotoxicity involves the coexistence and imbalance of survival and inflammatory–apoptotic signaling, providing mechanistic insight into its neurotoxic effects and a theoretical basis for potential preventive strategies.
丙烯酰胺(Acrylamide, ACR)是一种广泛应用于工业生产和食品加工的化合物,其神经毒性的潜在机制尚未完全阐明。本研究通过网络毒理学、分子对接和实验验证相结合,系统探索acr诱导神经毒性的潜在分子机制。通过数据库分析,共鉴定出183个acr相关靶点和2725个神经毒性相关靶点,其中100个重叠基因主要富集于PI3K/Akt信号通路和凋亡相关生物学过程。分子对接和分子动力学模拟表明ACR与关键靶蛋白之间存在潜在的相互作用。虽然对周围器官的影响很小,但体内接触ACR会导致海马神经元组织紊乱和尼氏体丧失,表明潜在的神经毒性。体外研究表明,ACR不仅降低PC12和HT22细胞活力,而且显著增强细胞凋亡和炎症反应,同时显著激活PI3K/Akt和NF-κB信号通路。在使用PI3K抑制剂LY294002治疗后,观察到这些效应的显著衰减。这些发现表明,acr诱导的神经毒性涉及生存和炎症-凋亡信号的共存和不平衡,为其神经毒性作用提供了机制见解,并为潜在的预防策略提供了理论基础。
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Ecotoxicology and Environmental Safety
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