Ecotoxicology and Environmental Safety最新文献

{"title":"Heavy metals promote the formation of multidrug-tolerant Staphylococcus aureus and Escherichia coli persisters","authors":"Seongeun Baek ,&nbsp;Jinbeom Seo ,&nbsp;Taegwan Yun ,&nbsp;Jin Kim ,&nbsp;YuJin Shin ,&nbsp;Jiwoo Choi ,&nbsp;JuOae Chang ,&nbsp;Inseo Kim ,&nbsp;Yung-Hun Yang ,&nbsp;Wooseong Kim ,&nbsp;Wonsik Lee","doi":"10.1016/j.ecoenv.2025.118014","DOIUrl":"10.1016/j.ecoenv.2025.118014","url":null,"abstract":"<div><div>Bacterial persisters are dormant phenotypic variants that are tolerant to antibiotics, contributing to treatment failure and the emergence of antimicrobial resistance. Although the formation of persisters has been extensively studied in regards to bacterial infections and treatment, such as antibiotic exposure or intracellular survival within macrophages, the role of environmental stressors in persister formation remains largely unexplored. In this study, we investigate the role of environmental heavy metals, specifically arsenic (As), cadmium (Cd), and mercury (Hg), in promoting persister cell formation in <em>Staphylococcus aureus</em> and <em>Escherichia coli</em>. Log-phase cultures were exposed to heavy metals (5 mM As, 1.25 mM Cd, 4 µM Hg for <em>S. aureus</em>; 12.5 mM As, 2 mM Cd, and 15 µM Hg for <em>E. coli</em>) for 0.5 h to induce persister cells. We observed that exposure to these metals induced persister cell formation, confirmed by intracellular ATP levels through microscopy and luciferase assays, as well as by reactive oxygen species (ROS) levels using carboxy-H2DCFDA. Short-term heavy metal exposure strongly depleted intracellular ATP while generating ROS. Moreover, we observed enhanced expression of genes involved in the SOS response, including <em>recA</em>, <em>umuC</em>, <em>dinB</em>, <em>rexA</em>, <em>rexB</em>, <em>sulA</em>, <em>rpoS</em>, and <em>soxR</em>, as measured by qPCR. This response was likely induced by elevated ROS levels following heavy metal exposure. Furthermore, we demonstrate that heavy metal-induced bacterial persisters exhibited a substantially increased emergence of antibiotic resistance, as shown by ciprofloxacin resistance developing in the presence of heavy metals. Therefore, our results clearly demonstrate that heavy metals can induce persister cells by depleting cellular ATP and generating ROS, and these bacterial responses to heavy metals substantially contribute to antibiotic resistance. These findings highlight the intricate relationship between environmental heavy metals, bacterial persister formation, and antibiotic resistance, emphasizing the need for a “One Health” strategy to address the growing antibiotic resistance crisis.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"293 ","pages":"Article 118014"},"PeriodicalIF":6.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143600731","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":"Assessing the health hazards of low-dose ethylmercury: Neurochemical and behavioral impacts in neonatal mice through matrix metalloproteinase activation and brain-derived neurotrophic factor release","authors":"Min Heui Yoo ,&nbsp;Tae-Youn Kim ,&nbsp;Ho-Kyong Kim ,&nbsp;Ji-Hyun Yoo ,&nbsp;Byoung-Seok Lee ,&nbsp;Jae-Young Koh","doi":"10.1016/j.ecoenv.2025.118031","DOIUrl":"10.1016/j.ecoenv.2025.118031","url":null,"abstract":"<div><div>Ethylmercury (EtHg) primarily enters the body through contaminated fish and mercury-containing vaccines, raising concerns about its neurotoxic risks, particularly for infants and young children. Although its neurodevelopmental impact has been suggested, research remains inconclusive. Given that neurite outgrowth, matrix metalloproteinase (MMP) activity, and brain-derived neurotrophic factor (BDNF) expression play critical roles in brain development and synaptic plasticity, we hypothesized that EtHg exposure disrupts these processes, leading to behavioral abnormalities. To test this hypothesis, we utilized a neonatal mouse model, exposing mice to a specific dose of EtHg comparable to potential human exposure levels. The exact dosage and exposure conditions were carefully selected to reflect real-world exposure scenarios. Our findings revealed that EtHg exposure led to significant alterations in brain development, including increased brain size and cortical thickness. These structural changes were accompanied by notable impairments in social interactions and behavioral patterns. Further analysis indicated that these effects were likely mediated by increased microglial activation and elevated BDNF expression in the cerebral cortex. Overall, our study suggests that EtHg disrupts neurodevelopment by activating microglia, leading to physiological and morphological changes in the brain. These findings highlight the need for further research on EtHg neurotoxicity and its implications for vulnerable populations, particularly infants and young children.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"293 ","pages":"Article 118031"},"PeriodicalIF":6.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143600736","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":"Efficient evaluation of osteotoxicity and mechanisms of endocrine disrupting chemicals using network toxicology and molecular docking approaches: triclosan as a model compound","authors":"Zhongyuan Wang,&nbsp;Jian Wang,&nbsp;Qiang Fu,&nbsp;Hui Zhao,&nbsp;Zaijun Wang,&nbsp;Yuzhong Gao","doi":"10.1016/j.ecoenv.2025.118030","DOIUrl":"10.1016/j.ecoenv.2025.118030","url":null,"abstract":"<div><div>This study aimed to demonstrate the utility of a network toxicology strategy in elucidating osteotoxicity and the molecular mechanisms of endocrine-disrupting chemicals (EDCs) using triclosan exposure in postmenopausal osteoporosis (PMOP) as a case study. The potential targets of triclosan were identified using the Comparative Toxicogenomics Database, SwissTargetPrediction, and TargetNet. PMOP-related targets were obtained from GeneCards, DisGeNET, and DrugBank. A total of 478 overlapping genes between disease targets and triclosan effectors were identified. Subsequent analysis using STRING and Cytoscape, applying the Matthews correlation coefficient algorithm, identified five core genes: STAT3, TP53, EGFR, MYC, and JUN. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses performed using R revealed that triclosan-induced PMOP is primarily associated with disrupted endocrine signaling and activation of the Phosphoinositide 3-kinase (PI3K)-Protein kinase B (Akt) signaling pathway. Molecular docking using CB-Dock2 confirmed strong binding affinities between triclosan and the core targets. Collectively, these results indicate that triclosan adversely affects bone health by disrupting endocrine regulation and energy metabolism through the PI3K-Akt pathway. This study establishes a theoretical framework for understanding how long-term triclosan exposure induces or exacerbates PMOP by investigating the underlying molecular mechanisms. These findings present a novel paradigm for evaluating the health risks posed by environmental pollutants.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"293 ","pages":"Article 118030"},"PeriodicalIF":6.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143600732","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":"Uranium’s hazardous effects on humans and recent developments in treatment","authors":"Yahya Faqir ,&nbsp;Ziang Li ,&nbsp;Talaal Gul ,&nbsp;Zahoor ,&nbsp;Ziwei Jiang ,&nbsp;Libing Yu ,&nbsp;Chengjia Tan ,&nbsp;Xi Chen ,&nbsp;Jiahua Ma ,&nbsp;Jiafu Feng","doi":"10.1016/j.ecoenv.2025.118043","DOIUrl":"10.1016/j.ecoenv.2025.118043","url":null,"abstract":"<div><div>Uranium, a naturally occurring element, is predominantly recognized for its role as fuel in both civilian and military energy sectors. Concerns have been raised regarding the adverse environmental impacts and health risks associated with uranium mining due to the exposure it causes. Such exposure leads to systemic toxicity, affecting pulmonary, hepatic, renal, reproductive, neurological, and bone health. This review identifies significant research gaps regarding detoxification methods for uranium contamination and recommends further advancements, including genetic modification and exploration of plant compounds. A comprehensive review of published research materials from diverse sources of uranium, including various treatments and hazardous impacts on the human body, was conducted. Additionally, a PRISMA analysis was performed in this study. This review emphasizes the importance of collaboration and the formulation of research-informed regulations to effectively safeguard vulnerable communities from the consequences of contamination. Public discourse often emphasizes the significance of radiotoxicity; however, the non-radioactive chemotoxicity of uranium has been identified as a significant risk factor for environmental exposures, contingent upon species, enrichment, and exposure route. Given these serious health consequences, several methods are being investigated to ameliorate uranium toxicity. In response to these concerns, several techniques, such as phytomedicinal treatments, biochemical approaches, and chelation therapy, have been investigated to minimize the adverse effects of uranium exposure in the human body.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"293 ","pages":"Article 118043"},"PeriodicalIF":6.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143600654","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":"Exogenous proline mediates OsNPR1 to regulate the innate pool of IAA in response to Cr exposure in rice plants","authors":"Abid Ullah,&nbsp;Peng Tian,&nbsp;Yi Kang,&nbsp;Xiao-Zhang Yu","doi":"10.1016/j.ecoenv.2025.117955","DOIUrl":"10.1016/j.ecoenv.2025.117955","url":null,"abstract":"<div><div>Indole acetic acid (IAA) orchestrates a myriad of physiological and biochemical responses in plants under stressful conditions, highlighting its indispensable role in plant resilience. The widespread contamination of chromium (Cr) poses a significant threat to rice cultivation, as its accumulation in plants disrupts various metabolic processes, consequently hindering growth. Of course, the utilization of exogenous growth regulators, including proline (Pro), has notably surged as a strategy to mitigate stress in plants. Pro can trigger the activation of other growth-regulating molecules, including IAA, to coordinate stress responses. To explore the complex interaction between exogenous Pro and the endogenous pool of IAA under Cr(VI) toxicity, a hydroponic system was established. The rice plants treated with exogenous Pro in coupled with Cr(VI) [Cr(VI)+Pro] showed significantly greater content of IAA than the plants not treated with exogenous Pro [Cr(VI)-Pro]. The expression analysis of genes involved in the speciation of IAA reactions reveals that the downregulation of <em>OsNPR1</em> under “Cr(VI)+Pro” treatments might be the crucial player in increasing the IAA content in rice plants. The increase in IAA by Pro treatment under Cr toxicity might lead to an improvement in root activity and root architecture elements. Importantly, no significant difference was observed in the accumulation of Cr in [Cr(VI)-Pro]- and [Cr(VI)+Pro]-treated rice plants. These results reveal that exogenous Pro can improve plant growth by inducing IAA accumulation in plant tissues exposed to Cr(VI) toxicity, without increasing Cr toxicity in plants.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"294 ","pages":"Article 117955"},"PeriodicalIF":6.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143601010","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 the drug carbamazepine on the structure and functioning of a freshwater aquatic ecosystem","authors":"Elien Versteegen ,&nbsp;Miia Häkkinen ,&nbsp;Dailing Wu ,&nbsp;Ineke Heikamp-de Jong ,&nbsp;Ivo Roessink ,&nbsp;Edwin T.H.M. Peeters ,&nbsp;Paul J. van den Brink","doi":"10.1016/j.ecoenv.2025.118009","DOIUrl":"10.1016/j.ecoenv.2025.118009","url":null,"abstract":"<div><div>Carbamazepine, a widely used psychotropic drug, has been frequently detected in surface waters due to its poor removal in conventional wastewater treatment and slow dissipation in aquatic systems. While carbamazepine’s ecotoxicological effects have frequently been researched, most research focuses on high concentrations and single species, with only a few studies including more ecological complexity and environmentally relevant concentrations. With a mesocosm experiment, we investigated the long-term ecological effects of environmentally relevant concentrations of carbamazepine (0.001–100 µg/L, performed in triplicate) on 1200 L freshwater ecosystems to provide more ecologically relevant insights. The study intended to identify sensitive species and assess the overall impact on the structure and functioning of the aquatic ecosystem. The composition of macroinvertebrate, zooplankton and microbial communities, primary producers and several physicochemical variables were analysed over a 14-week exposure period to determine the effects of a range of carbamazepine concentrations. While sublethal effects on invertebrates may have gone undetected, any potential sublethal impacts did not translate into lasting population-level consequences. We found that exposure to environmentally realistic concentrations of carbamazepine in aquatic mesocosms did not impact water quality, primary producers, or invertebrate and bacterial communities. The findings suggest that carbamazepine, at current environmental levels, is unlikely to harm freshwater ecosystems that exclude larger predators like fish.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"294 ","pages":"Article 118009"},"PeriodicalIF":6.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143601011","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":"Residential greenness, air pollution, genetic predisposition and the risk of lung cancer","authors":"Yiqun Zhu ,&nbsp;Yao Wu ,&nbsp;Zhuanxing Zhu ,&nbsp;Huaying Liang ,&nbsp;Qinyu Chang ,&nbsp;Fengyu Lin ,&nbsp;Dianwu Li ,&nbsp;Jun Cheng ,&nbsp;Pinhua Pan ,&nbsp;Yuming Guo ,&nbsp;Yan Zhang","doi":"10.1016/j.ecoenv.2025.118027","DOIUrl":"10.1016/j.ecoenv.2025.118027","url":null,"abstract":"<div><h3>Background</h3><div>Growing evidence suggests that greenness is associated with multiple health outcomes, but its association with lung cancer risk remains limited and far from consistent. In particular, it is unclear whether this association varies across different types of lung cancer and whether it is influenced by factors such as genetics, air pollution, and physical activity.</div></div><div><h3>Method</h3><div>This prospective cohort study included 425108 participants aged 37–73 years from the UK Biobank. Residential greenness was estimated with the normalized difference vegetation index (NDVI) and the enhanced vegetation index (EVI) within the 500 m buffer. Cox proportional hazards regression was performed to evaluate the hazard ratios (HR) and 95 % confidence intervals (CI) of the relationship between greenness and risk of lung cancer. A genetic risk was calculated using 18 independent susceptibility loci for lung cancer. Mediation analysis was conducted to assess the indirect effects through air pollutants (including PM_2.5, PM₁₀, NO₂, NO_x) and physical activity.</div></div><div><h3>Results</h3><div>During a median follow-up of 14.0 years, 3814 lung cancer cases identified. An inversely linear correlation between residential greenness and incident lung cancer was found. Specifically, each interquartile range increase in NDVI and EVI within the 500 m buffer was linked to 8 % (HR 0.92, 95 % CI: 0.88, 0.96) and 9 % (HR 0.91, 95 % CI: 0.87, 0.94) decreased in lung cancer risk, respectively. Moreover, the association was particularly pronounced for adenocarcinoma (HR 0.88, 95 % CI: 0.83, 0.94 for NDVI; HR 0.87, 95 % CI: 0.82, 0.92 for EVI). Mediation analysis suggested that reductions in PM_2.5 exposure and increased physical activity accounted for approximately 45 % and 1.5 % of the observed association.</div></div><div><h3>Conclusion</h3><div>Increased residential greenness was linearly associated with reduced risk of lung cancer, particularly adenocarcinoma, and such an association may be substantially mediated by mitigating air pollutants, especially PM_2.5 and increased physical activity. The study provides promising evidence and strategy of improving greenness during urbanization to reduce the risk of lung adenocarcinoma in the context of the grimmer trend of rapidly increasing risk of adenocarcinoma.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"294 ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143592632","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":"Exploring the neurotoxic effects of cylindrospermopsin in early development of zebrafish: An integrated impact of oxidative stress, inflammatory response, and apoptosis","authors":"Xu Zhang ,&nbsp;Jie Hu ,&nbsp;Jiaxue Jian ,&nbsp;Haixia Liu ,&nbsp;Xuefei Zhou ,&nbsp;Yalei Zhang ,&nbsp;Guoyan Zou ,&nbsp;Li Zhou ,&nbsp;Jian Wang","doi":"10.1016/j.ecoenv.2025.118021","DOIUrl":"10.1016/j.ecoenv.2025.118021","url":null,"abstract":"<div><div>The increasing global spread of cyanobacteria and their toxin Cylindrospermopsin (CYN) is a growing concern.This study aimed to examine the toxic effects of CYN on the early neurodevelopment of zebrafish, and to identify the underlying mechanisms. The findings indicated that zebrafish exposed to varying concentrations of CYN exhibited general developmental toxicity, including typical malformations, diminished embryonic movement, and shortened body length. The length of zebrafish larvae was shortened by 4.8 and 6.1 % in the 0.2 and 2 μm exposure groups, Furthermore, CYN was observed to impede neuronal development and motor behaviour in zebrafish. Concomitantly, CYN markedly elevated reactive oxygen species (ROS) levels and modified catalase (CAT) and superoxide dismutase (SOD) activities. Compared with the control group, zebrafish larvae in the 0.2 and 2 μm exposure groups showed a significant decrease of 17.7 and 43.2 % in CAT activity and a significant increase of 51.4 and 84.4 % in SOD activity, indicating that CYN induces oxidative stress. Furthermore, the fluorescence quantification and acridine orange staining assay conducted on additional <em>Tg(lyz:dsRed)</em> transgenic lines provided further evidence that CYN induced an inflammatory response and apoptosis, a finding that was also verified at the gene level. This study not only provides new insights into the mechanisms of CYN toxicity, but also provides important scientific evidence for risk assessment of environmental pollutants and the conservation of aquatic organisms.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"293 ","pages":"Article 118021"},"PeriodicalIF":6.2,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143592273","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":"Modeling praseodymium toxicity in solution to wheat root elongation using the biotic ligand model theory","authors":"Xiaohong Guo ,&nbsp;Mengjia Li ,&nbsp;Bin Wang ,&nbsp;Haiying Zong ,&nbsp;Fangli Wang ,&nbsp;Xiaoli Huang ,&nbsp;Liu Shuaiqi ,&nbsp;Ningning Song ,&nbsp;Meng Li","doi":"10.1016/j.ecoenv.2025.118023","DOIUrl":"10.1016/j.ecoenv.2025.118023","url":null,"abstract":"<div><div>Praseodymium (Pr[Ⅲ]) is a rare earth element (REE) with chronic toxicity. With the increasing use of REE in various fields, considerable amounts of praseodymium have been released into the environment. Consequently, understanding the toxic effects and ecological risks of Pr(III) on organisms is crucial. This study utilized a soil-simulated solution culture method to investigate the influence of Ca^2 +, K⁺, Na⁺, Mg²⁺, and pH on acute toxicity to wheat through a single-factor control experiment and established a Pr(III) toxicity prediction model based on the biotic ligand model (BLM). These findings demonstrated that increasing the activities of Mg²⁺, Ca²⁺ and H⁺ reduced the toxicity of Pr(III) on wheat root elongation. In contrast, increasing the activities of K⁺ and Na⁺ exhibited no significant effects. Additionally, pH influenced both the solubility and speciation of Pr(III). At pH &lt; 6.5, Pr(III) predominately exists as Pr³⁺ and PrCl²⁺, whereas at pH 7.0, the proportion of PrOH²⁺ significantly increased. Based on DPS9.0 software fitting results, the stability constants were determined as follows: logK_PrBL = 2.54, logK_PrClBL = 3.26, logK_PrOHBL = 3.18, logK_CaBL = 2.50, logK_MgBL = 2.61, logK_HBL = 3.88, and <span><math><msubsup><mrow><mi>f</mi></mrow><mrow><mi>PrBL</mi></mrow><mrow><mn>50</mn><mo>%</mo></mrow></msubsup></math></span> = 0.36. These results suggest that the BLM effectively predicts Pr(III) toxicity by accounting for toxic species such as Pr³⁺, PrCl²⁺, and PrOH²⁺, along with the competition for binding sites by Mg²⁺, Ca²⁺, and H⁺. The improved Pr(III)-BLM performance is believed to be applicable to a wide range of land plants.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"293 ","pages":"Article 118023"},"PeriodicalIF":6.2,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143592020","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":"Maternal exposure to polystyrene nanoplastics induces sex-specific kidney injury in offspring","authors":"Xiuli Chen,&nbsp;Li Wang,&nbsp;Kan Liu,&nbsp;Qiuming Wang,&nbsp;Ranhong Li,&nbsp;Leilei Niu,&nbsp;Haiying Wu","doi":"10.1016/j.ecoenv.2025.118006","DOIUrl":"10.1016/j.ecoenv.2025.118006","url":null,"abstract":"<div><div>Maternal exposure to polystyrene nanoplastics (PS-NPs) during pregnancy and lactation has been linked to adverse effects on offspring kidney development, with sex-specific outcomes. This study investigated the impact of maternal PS-NPs exposure on kidney weight, histology, transcriptomics, and functional pathways in offspring mice. Offspring exposed to PS-NPs exhibited significantly lower body weight (<em>P</em> &lt; 0.05) and an increased kidney-to-body weight ratio (<em>P</em> &lt; 0.05), particularly in males. Histological analysis revealed a reduction in glomerular number in PS-NP-treated groups. Transcriptome profiling identified 758 differentially expressed genes (DEGs) in male and 101 DEGs in female offspring, with males showing a more pronounced alteration in gene expression. KEGG pathway enrichment highlighted disruptions in immune response, cell cycle regulation, and metabolism, with males exhibiting more extensive pathway changes than females. Additionally, PS-NPs exposure increased renal fibrosis (<em>P</em> &lt; 0.05), with molecular analyses confirming sex-specific gene expression patterns linked to fibrosis and apoptosis. Immunohistochemical analysis revealed enhanced macrophage infiltration and cleaved caspase-3 expression, indicating heightened immune and apoptotic responses in males. Further investigation identified small molecules BI-D1870 and Resatorvid as potential therapeutic agents, reducing fibrosis, inflammation, and apoptosis in male and female offspring, respectively. These findings demonstrate that maternal PS-NPs exposure induces sex-specific kidney injury in offspring, disrupting key biological processes and pathways. The study underscores the need for targeted therapeutic interventions to mitigate these effects and highlights potential compounds for future treatment.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"293 ","pages":"Article 118006"},"PeriodicalIF":6.2,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143592280","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}