Ecotoxicology and Environmental Safety最新文献

{"title":"Assessing the impact of urban form on PM2.5 concentration along roads in a city with mobile monitoring and machine learning models","authors":"Mingyue Xi ,&nbsp;Xuegang Chen ,&nbsp;Jiayu Fan","doi":"10.1016/j.ecoenv.2025.118789","DOIUrl":"10.1016/j.ecoenv.2025.118789","url":null,"abstract":"<div><div>Due to urbanization, air pollution has become one of the most serious environmental problems, threatening human health and causing adverse effects on other environments. In order to improve air quality, it is necessary to analyze the relationship between urban form and air pollution and propose optimization strategies. This study is dedicated to collecting PM_2.5 concentration data on different grades of roads through mobile monitoring technology, which is then corrected using national fixed monitoring stations. At the same time, combining the meteorological data obtained during the experiment by fixed-point monitoring, RF model was used to deeply analyze the influence of urban form on PM_2.5 concentration, providing a scientific and effective reference basis for urban planning. The results showed that the PM_2.5 concentration in autumn was significantly higher than that in summer, and the pollution in the southern region was heavier than that in the northern region. The influence of different urban forms on buffer radius is different. Mean building height, population density, floor area ratio and impervious surface proportion are the key urban form indicators affecting PM_2.5. In future urban planning, it is recommended to reasonably control building heights within a 500-meter buffer zone along roads, optimize urban building layouts, and promote population relocation from old urban areas to expand urban green space and alleviate PM_2.5 pollution in Urumqi. Therefore, quantitative analysis of the relationship between PM_2.5 concentrations and urban form elements can assist decision-makers in urban planning and management.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"303 ","pages":"Article 118789"},"PeriodicalIF":6.1,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144772056","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":"Exposure to persistent organic pollutants and sarcopenia: Revealing associations, mediated modifications, and potential mechanisms","authors":"Jinlong Tao ,&nbsp;Jinchan Zhai ,&nbsp;Jiaqi Yang ,&nbsp;Qiang Niu ,&nbsp;Yunhua Hu ,&nbsp;Yizhong Yan","doi":"10.1016/j.ecoenv.2025.118783","DOIUrl":"10.1016/j.ecoenv.2025.118783","url":null,"abstract":"<div><h3>Background</h3><div>Sarcopenia contributes significantly to the global disease burden, and identifying its risk factors is essential for prevention. However, the effects of persistent organic pollutants (POPs) on sarcopenia remain underexplored.</div></div><div><h3>Objective</h3><div>This study assessed the association between mixed POPs exposure and sarcopenia and explored the mediating roles of inflammation and oxidative stress, along with potential molecular targets.</div></div><div><h3>Methods</h3><div>A total of 2106 participants from the National Health and Nutrition Examination Survey (NHANES) were analyzed. Data included 19 POPs across four categories: polychlorinated biphenyls (PCBs), organochlorine pesticides (OCPs), per- and polyfluoroalkyl substances (PFAS), and polybrominated diphenyl ethers (PBDEs), as well as sarcopenia status and covariates. Logistic regression and restricted cubic splines assessed individual effects, while weighted quantile sum regression (WQS), Bayesian kernel machine regression (BKMR), and quantile-based g-computation examined mixed effects. Mediation analysis evaluated the roles of inflammation and oxidative stress, and network pharmacology identified potential pathways and targets.</div></div><div><h3>Results</h3><div>The WQS index for mixed POPs exposure was inversely associated with sarcopenia, with PCB146 contributing the most. In BKMR models, PFHS (PIP=0.65) was the top contributor to sarcopenia risk In separate WQS regression models, exposure to PCBs and PBDEs was significantly inversely associated with the risk of sarcopenia, with odds ratios (ORs) of 0.66 (95 % CI: 0.46, 0.96) and 0.74 (95 % CI: 0.57, 0.98), respectively. In contrast, OCP exposure showed a significant positive association with sarcopenia (OR: 1.86, 95 % CI: 1.31, 2.63). No significant association was found between PFAS exposure and sarcopenia (<em>P</em> &gt; 0.05). Lower exposure showed a stronger negative effect for PCBs and PBDEs, whereas OCPs had the opposite trend. Inflammation mediated the effects of PCB187 and ppDDE, explaining 3.54 % and 2.87 %, respectively. CDKN1A, NFKBIA, CSF1R, and TFRC were key genes.</div></div><div><h3>Conclusion</h3><div>Excessive OCPs was positively associated with sarcopenia, whereas PCBs, PFAS, and PBDEs showed inverse associations. CDKN1A, NFKBIA, CSF1R, and TFRC may be key targets through which POPs influence sarcopenia development.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"303 ","pages":"Article 118783"},"PeriodicalIF":6.1,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144772054","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":"The impact of environmental toxicants on gestational diabetes mellitus: Investigating the mediating role of high-density lipoprotein cholesterol","authors":"Hui Chen ,&nbsp;Jinghua Du ,&nbsp;Xian Wang ,&nbsp;Lifan Cui ,&nbsp;Qingyou Wu ,&nbsp;Yan Zhu ,&nbsp;Yuan Guo","doi":"10.1016/j.ecoenv.2025.118810","DOIUrl":"10.1016/j.ecoenv.2025.118810","url":null,"abstract":"<div><div>Gestational diabetes mellitus (GDM) is a significant metabolic disorder characterized by the elevated glucose level first detected during pregnancy, influencing approximately 14 % of pregnancies globally. Given the rising prevalence of environmental toxicants and their potential impact on maternal health, it is imperative to explore the relationship between environmental exposures and GDM. This study aimed to investigate the mediating role of high-density lipoprotein cholesterol (HDLC) in this context, demonstrating that exposure to environmental toxicants may influence GDM risk through some pathways. Data from the 2007–2020 waves of the National Health and Nutrition Examination Survey (NHANES) were analyzed to assess the association between exposure to 89 environmental toxicants and GDM incidence. A comprehensive evaluation was conducted to identify toxicant-GDM associations, with a particular concentration on volatile organic compounds (VOCs) and certain metals. Additionally, network pharmacology approaches were employed to predict candidate molecular targets of VOCs and elucidate protein-protein interactions (PPIs) linked to GDM pathophysiology. The Similarity Ensemble Approach (SEA) and STRING databases were utilized to construct a PPI network. The findings revealed that 29 environmental toxicants exhibited a positive association with GDM, notably among VOCs and selected metals. HDL-C emerged as a potential surrogate marker for systemic inflammation, mediating the correlation between toxicant exposure and GDM risk. Network pharmacology analysis further revealed key pathways and protein targets implicated in the relationship between environmental exposures and GDM pathogenesis. These findings highlight the critical role of environmental toxicants in shaping maternal health outcomes and GDM susceptibility. By identifying HDL-C as a mediator, this study offers novel insights into the inflammatory mechanisms driving GDM development. Public health strategies must prioritize addressing environmental toxicant exposure to reduce GDM risk and improve maternal-fetal health outcomes.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"303 ","pages":"Article 118810"},"PeriodicalIF":6.1,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144772055","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":"Evaluating the association between exposure to multiple metals and adverse pregnancy outcomes based on a multi−step statistical analysis strategy","authors":"Tao Yu ,&nbsp;Dongyang Zhang ,&nbsp;Zelian Li ,&nbsp;Muxin Zhai ,&nbsp;Weilong Lin ,&nbsp;Shiwei Ren ,&nbsp;Dongmei Ji ,&nbsp;Yunxia Cao ,&nbsp;Chunmei Liang ,&nbsp;Yuanyuan Yang","doi":"10.1016/j.ecoenv.2025.118768","DOIUrl":"10.1016/j.ecoenv.2025.118768","url":null,"abstract":"<div><h3>Background</h3><div>Adverse pregnancy outcomes (APOs) pose a serious threat to the safety of both the mother and the fetus. The association between metal exposure during pregnancy and the risk of APOs remains inconsistent. Therefore, this study aimed to evaluate the association between exposure to multiple metals and the risk of APOs based on a multi−step statistical analysis strategy.</div></div><div><h3>Methods</h3><div>A birth cohort study including 707 pregnant women was performed in the present study, and 182 women were ultimately diagnosed with APOs. Blood levels of arsenic (As), cadmium (Cd), mercury (Hg), lead (Pb), barium (Ba), cobalt (Co), chromium (Cr), manganese (Mn), molybdenum (Mo), nickel (Ni), thallium (Tl), and vanadium (V) were measured in pregnant women. Multi-step statistical analyses were conducted to evaluate the associations between metals exposure and APO risk. First, cluster and scatter clustering analyses were used to assess the overlap for high exposure levels of metals among participants. Second, binary logistic regression was performed to assess the association between each single metal level and APO risk, respectively. Third, weighted quantile sum (WQS) regression and quantile-based g-computation (QGC) were conducted to identify the key metals contributing most to APO risk. Finally, Bayesian kernel machine regression (BKMR) evaluated the joint effects of these key metals on APO risk.</div></div><div><h3>Results</h3><div>The results from cluster analyses revealed that there were substantial overlaps for high exposure levels of metals among pregnant women. Higher blood levels of Ba and Tl were associated with an increased APO risk (Ba: adjusted odds ratio [aOR] = 2.03, 95 % confidence interval [CI]: 1.33–3.10; Tl: aOR = 1.73, 95 % CI: 1.13–2.63). Consistently, results from the WQS regression model suggested that Ba (0.27), Tl (0.16), Pb (0.01) and V (0.01) were major contributors to APO risk (p &lt; 0.05), which was further supported by the results from QGC regression model. The BKMR model indicated that the mixtures of Ba, Tl, Pb and V, identified through the WQS and QGC models, were positively associated with the risk of APOs.</div></div><div><h3>Conclusions</h3><div>In this study, we observed substantial overlaps in high exposure levels of metals among pregnant women. Ba, Tl, Pb, and V were identified as the major contributors to the risk of APOs. Co-exposure to these metals was linked to an increased risk of APOs. This highlights the importance of avoiding metal exposure during pregnancy to protect maternal and fetal health.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"303 ","pages":"Article 118768"},"PeriodicalIF":6.1,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144766626","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":"HMGA2/PHGDH axis-mediated glycolysis under hypoxia is required for cadmium-induced A549 cell migration","authors":"Chunpeng Gao ,&nbsp;Qiuxuan Xie ,&nbsp;Li Li ,&nbsp;Shengxiang Luo ,&nbsp;Jianhui Fan ,&nbsp;Jun Cao","doi":"10.1016/j.ecoenv.2025.118787","DOIUrl":"10.1016/j.ecoenv.2025.118787","url":null,"abstract":"<div><div>Cadmium (Cd) is a widespread environmental contaminant, which has been classified as a human carcinogen. Phosphoglycerate dehydrogenase (PHGDH), the first rate-limiting enzyme involved in the serine biosynthesis pathway, was reported to be able to indicate poor prognosis for cancers. In this study, we investigated the possible mechanism of PHGDH in Cd-induced cell migration. Firstly, 2 μM Cd increased the expression of PHGDH protein in A549 cells and HELF cells. Similarly, Cd exposure (0.5 and 1 mg/kg) led to increased PHGDH expression in lung tissue of male BALB/c mice. Silencing PHGDH suppressed Cd-triggered aerobic glycolysis while enhancing oxidative phosphorylation (OXPHOS), suggesting that PHGDH plays a critical role in the metabolic adjustments caused by Cd exposure. Secondly, the heightened expression of HMGA2 triggered PHGDH, and the Chromatin immunoprecipitation (ChIP) assay revealed HMGA2 protein binds directly to the promoter region of the <em>PHGDH</em> gene. Furthermore, HMGA2/PHGDH axis was determined to be involved in Cd-induced aerobic glycolysis. Using CoCl₂ (100 μM) to induce hypoxia and YC-1 (10 μM), the inhibitor of HIF-1α, we demonstrated that HIF-1α might initiate Cd-elevated HMGA2 and PHGDH. Collectively, HIF-1α-elevated HMGA2 regulated <em>PHGDH</em> transcriptionally by binding to the <em>PHGDH</em> promoter, resulting metabolic reprogramming from OXPHOS to glycolysis, which mediated Cd-induced cell migration. This study potentially offers a new approach for prevention of lung cancer.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"303 ","pages":"Article 118787"},"PeriodicalIF":6.1,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144766713","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":"Chondroitin sulfate A-selenium nanoparticles protect chondrocytes from T-2 toxin-induced oxidative stress and mitochondrial dysfunction through activating autophagy by the SIRT1-AMPK-FOXO3 pathway","authors":"Huan Deng ,&nbsp;Jinyan Lin ,&nbsp;Yude Jiang ,&nbsp;Abebe Feyissa Amhare ,&nbsp;Lichun Qiao ,&nbsp;Jun Wang ,&nbsp;Jing Han","doi":"10.1016/j.ecoenv.2025.118797","DOIUrl":"10.1016/j.ecoenv.2025.118797","url":null,"abstract":"<div><div>T-2 toxin is known to cause tissue and cellular damage, with chondrocytes being particularly vulnerable. In contrast, chondroitin sulfate A-selenium nanoparticles (CSA-SeNP) have shown cartilage-protective properties, although the precise molecular mechanism remains incompletely elucidated. This study used T-2 toxin and CSA-SeNP to treat human C28/I2 chondrocytes, and studied their effects on SIRT1-AMPK-FOXO3 pathway and oxidative damage, mitochondrial dysfunction, impaired autophagy, and apoptosis. Autophagy was evaluated by acridine orange (AO) and dansylcadaverine (MDC) staining, transmission electron microscopy observation, and mRFP-GFP-LC3 adenovirus. Oxidative stress (ROS, MDA, SOD, CAT, T-AOC) and mitochondrial function (ATP, SDH, ATPases, membrane potential) were assessed. Western blotting analyzed the expression level of the SIRT1-AMPK-FOXO3 pathway, autophagy markers, and apoptosis. We found that 4-hour exposure to 5 and 20 ng/mL, as well as 12-hour exposure to 5 ng/mL of T-2 toxin, activated the SIRT1-AMPK-FOXO3 pathway compensatively, inducing autophagy but inhibiting degradation of autolysosome, leading to oxidative damage, mitochondrial dysfunction, and increased apoptosis. 12-hour exposure to 20 ng/mL T-2 toxin inhibited this pathway and autophagy, causing serious damage to chondrocytes. CSA-SeNP alleviated the inhibition of the SIRT1-AMPK-FOXO3 pathway induced by T-2 toxin, reducing oxidative damage, mitochondrial dysfunction and apoptosis, thereby restoring autophagy to protect chondrocytes. In summary, T-2 toxin's effects on chondrocyte autophagy were dose- and time-dependent. CSA-SeNP protected against T-2 toxin by activating the SIRT1-AMPK-FOXO3 pathway, suggesting its potential for chondrocyte protection. This study may provide new insights into the development of T-2 toxin detoxification strategies and the method for prevention and treatment of chondrocyte damage.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"303 ","pages":"Article 118797"},"PeriodicalIF":6.1,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144772167","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":"Acute effects of mercury on brine shrimp: First evidence highlighting the molecular mechanism through integrated transcriptome and metabolomic analysis","authors":"Hangyu Lin ,&nbsp;Yanlin Wei ,&nbsp;Junjie Huang ,&nbsp;Qun Lu ,&nbsp;Song Zhu ,&nbsp;Jianguang Qin ,&nbsp;Shengqi Su ,&nbsp;Tao He","doi":"10.1016/j.ecoenv.2025.118795","DOIUrl":"10.1016/j.ecoenv.2025.118795","url":null,"abstract":"<div><div>Mercury poses significant hazards to aquatic organisms, causing neurotoxicity, and metabolic disorders. Research on the dynamic distribution of mercury within zooplankton is limited, and the metabolic mechanisms of mercury in zooplankton remain unclear. In this study, we employed a mercury-specific fluorescent probe (aggregation-induced emission luminogen, AIEgen) to visualize the in vivo distribution of Hg²⁺ and MeHg in brine shrimp. Both Hg²⁺ and MeHg accumulated predominantly in the head, ocellus, midgut, and midgut–hindgut transition, with Hg²⁺ further affecting the hindgut and anal opening. Transcriptomics and metabolomics analyses revealed that Hg²⁺ exposure in the midgut likely induced the efflux activity of ABC transporters. The linoleic acid metabolism, α-linolenic acid metabolism, tryptophan metabolism, and retinol metabolism pathways were potentially associated with MeHg accumulation in the head and ocellus. Additionally, the cytochrome P450 pathway participated in detoxification. Enzyme assays and multi-omics data further demonstrated that both Hg²⁺ and MeHg elicited oxidative stress and impaired growth, development, and energy metabolism in brine shrimp. Integrated omics analysis revealed that glutathione metabolism is highly associated with Hg²⁺, while glycerophospholipid metabolism is highly associated with MeHg. Our study revealed the toxicity effects of mercury in zooplankton brine shrimp and promoted the understanding of the underlying mechanism and coping strategies for mercury toxicity in the zooplankton of the aquatic food chain.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"303 ","pages":"Article 118795"},"PeriodicalIF":6.1,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144772053","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":"Diesel exhaust induces gut microbiome dysbiosis and reduced fecal acetate: Role of acetate supplementation","authors":"Rajat Gupta ,&nbsp;Candace Chang ,&nbsp;Laurent Vergnes ,&nbsp;Dawoud Sulaiman ,&nbsp;Fen Yin ,&nbsp;James A. Stewart ,&nbsp;Margarete Mehrabian ,&nbsp;Joel D. Kaufman ,&nbsp;Jonathan P. Jacobs ,&nbsp;Aldons J. Lusis ,&nbsp;Karen Reue ,&nbsp;Michael E. Rosenfeld ,&nbsp;Jesus A. Araujo","doi":"10.1016/j.ecoenv.2025.118654","DOIUrl":"10.1016/j.ecoenv.2025.118654","url":null,"abstract":"<div><div>Air pollution exposure enhances the risk of cardiovascular morbidity and mortality. Epidemiological studies provide strong evidence of a link between exposure to ambient particulate matter with aerodynamic diameter&lt; 2.5 µm (PM_2.5) and development of cardiovascular and metabolic disorders. We have shown that inhaled ultrafine particles (UFP) or whole diesel exhaust (DE), enriched in UFP, induce cardiometabolic effects, including dyslipidemia and hepatic steatosis. However, the pathogenic mechanisms remain unknown. We recently demonstrated that exposure to ambient particulate in the ultrafine-size range altered the gut microbiota composition in various animal models, with a potential to induce systemic effects. Thus, we hypothesized that sub-chronic inhalation exposure to DE leads to gut dysbiosis and altered gut-derived metabolites, likely responsible for some of the metabolic effects. Male apolipoprotein E^-/- (ApoE^-/-) mice, exposed to inhaled DE <em>vs.</em> filtered air (FA) (6 h/day, 5 days/week for 16 weeks) displayed alterations in cecal microbiota composition, which associated with elevated plasma cholesterol and triglycerides, as well as hepatic triglycerides and oxidized lipids. DE exposure upregulated hepatic mRNA and protein levels of 12-lipoxygenase (Alox12), together with significantly reduced fecal acetate levels, correlating with changes in lipids and cecal microbiota composition. Metabolic effects were recapitulated in HepG2 cells treated with DE particles, including elevated <em>Alox12</em> mRNA levels and decreased respiration in isolated mitochondria. Supplementation with gut-derived short chain fatty acid acetate reversed these effects in cells. In conclusion, inhaled DE induced gut microbiome dysbiosis, lipid peroxidation and triglyceride accumulation, likely <em>via</em> mitochondrial dysfunction, which was rescued in cells by acetate supplementation.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"303 ","pages":"Article 118654"},"PeriodicalIF":6.1,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144766627","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":"MXene-nanoparticles foliar application improves wheat morpho-physiological and biochemical traits under cadmium (Cd2+) stress: A novel sustainable approach","authors":"Ghulam Murtaza ,&nbsp;Najmaldin Ezaldin Hassan ,&nbsp;Muhammad Usman ,&nbsp;Gang Deng ,&nbsp;Zeeshan Ahmed ,&nbsp;Basharat Ali ,&nbsp;Asma Majeed ,&nbsp;Hassan Mehmood ,&nbsp;Javed Iqbal ,&nbsp;Mohamed S. Elshikh ,&nbsp;Humaira Rizwana ,&nbsp;Shabir Ahmad ,&nbsp;Rashid Iqbal ,&nbsp;Maximilian Lackner","doi":"10.1016/j.ecoenv.2025.118781","DOIUrl":"10.1016/j.ecoenv.2025.118781","url":null,"abstract":"<div><div>Cadmium (Cd²⁺) pollution is a persistent problem in the agricultural sector. Plants can be treated with nanoparticles (NP) to reduce heavy metal stress. MXene nanoparticles (MX-NPs) were tested for wheat Cd stress relief. Comparative confocal microscopy was used to examine the morphology, physiology, yield, biochemistry, antioxidant enzyme activity, and cell viability of the wheat plants. Cd-stressed plants exhibited a decline in morphological parameters and yield attributes, including leaf area (-49 %), root length (-35 %), shoot length (-18 %), seed weight (-37 %), seeds per plant (-69 %), root and shoot fresh weight (-55 % and −64 %), carotenoid levels (-40 %), total chlorophyll (-13 %), total soluble sugar (-29 %), total soluble protein (-39 %), antioxidant enzymatic activities (APX, CAT, and SOD by −16 %, −5 %, and −14 %, respectively), and nitrate reductase activity (-65 %) compared to the control group. Stress markers, including MDA (+270 %) and proline (+201 %), increased in plants exposed to Cd. Levels of total flavonoids (+481 %) and phenols (+92 %) were greater in the Cd-treated groups. Foliar application of MX-NPs (1000 ppm) significantly alleviated Cd-induced stress, as demonstrated by increases in shoot length and root length (+41 % and +39 %, respectively), seed weight (+69 %), seeds per plant (+99 %), carotenoid concentration (+30 %), chlorophyll content (+39 %), nitrate reductase activity (+60 %), and total soluble protein (+19 %) compared with the control group. The supplementation of 1000 ppm-MX-NPs with Cd (250 μM) in exposed plants led to an enhancement in antioxidant enzymes, with APX, CAT, and SOD increasing by 76 %, 81 %, and 84 %, respectively. Confocal microscopy revealed that MX-NPs increased cell viability following Cd exposure. In conclusion, MX-NPs foliar spray effectively reduced Cd-induced stress in wheat, promoting sustainable agriculture under 500 μM Cd stress.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"303 ","pages":"Article 118781"},"PeriodicalIF":6.1,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144766625","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":"Toxicological effects of ADB-FUBINACA on early zebrafish development: An analysis utilizing metabolomics","authors":"Yang Luo,&nbsp;LinRong Ying,&nbsp;YiZhou Liu,&nbsp;YiLei Fan,&nbsp;Kai Wang,&nbsp;YanFei Lan,&nbsp;Song Chian","doi":"10.1016/j.ecoenv.2025.118782","DOIUrl":"10.1016/j.ecoenv.2025.118782","url":null,"abstract":"<div><div>ADB-FUBINACA, which is a type-1 indazole cannabinoid receptor (CB1) agonist, is a prevalent synthetic cannabinoid due to its widespread abuse and confiscation. Numerous clinical reports have indicated the potential for ADB-FUBINACA to induce multisystemic bodily harm when smoked, but a comprehensive understanding of its potential toxicity to aquatic life remains largely unexplored. Our study used zebrafish as a model organism to assess the toxic effects of exposure to different doses of ADB-FUBINACA on embryonic development. By integrating a nontargeted metabolomics strategy, we aimed to explore the metabolic pathways that are implicated in the toxic effects of ADB-FUBINACA on the early development of zebrafish. Our findings revealed that exposure to ADB-FUBINACA reduced the heart rate, survival rate, hatching rate, and body length of zebrafish embryos/larvae in a dose-dependent manner. Additionally, we observed lipid disorders and reduced motor behaviour. Moreover, ADB-FUBINACA affected the mechanism of oxidative stress in zebrafish larvae. Compared with the control, high-dose treatment resulted in a 2.19-fold increase in reactive oxygen species (ROS) levels and a 42.56 % decrease in reduced glutathione (GSH) levels. The embryos were subsequently analysed using ultrahigh-performance liquid chromatography-quadrupole-orbitrap-high-resolution mass spectrometry (UHPLC-Q-Orbitrap-HRMS); the results identified 45 differentially abundant metabolites and showed that the arachidonic acid metabolic pathway was significantly activated, the latter of which was suggested by bioinformatics analysis. RT<img>qPCR revealed that <em>lpcat3</em> gene expression was upregulated by 2.51-fold in zebrafish in the ADB-FUBINACA treatment group, whereas <em>gclc</em> gene expression was reduced by 70.94 %. Additionally, the expression of genes related to inflammatory factors and heart development showed varying degrees of change. In summary, our study revealed that ADB-FUBINACA can exert toxic effects on the early development of zebrafish, and its mechanism may involve activating the arachidonic acid metabolic pathway, triggering lipid metabolism disorders, and inducing inflammatory responses and oxidative damage.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"303 ","pages":"Article 118782"},"PeriodicalIF":6.1,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144766624","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}