Ecotoxicology and Environmental Safety最新文献

{"title":"The temporal, spatial and population heterogeneity of the associations between ambient temperature and injury by animal in China: A nationwide case-crossover study","authors":"Weiquan Zeng ,&nbsp;Pengpeng Ye ,&nbsp;Mengen Guo ,&nbsp;Yuan Wang ,&nbsp;Jianxiong Hu ,&nbsp;Xiao Deng ,&nbsp;Guanhao He ,&nbsp;Ye Jin ,&nbsp;Tao Liu ,&nbsp;Cuirong Ji ,&nbsp;Sujuan Chen ,&nbsp;Leilei Duan ,&nbsp;Yanfang Guo ,&nbsp;Yuliang Er ,&nbsp;Wenjun Ma","doi":"10.1016/j.ecoenv.2025.118206","DOIUrl":"10.1016/j.ecoenv.2025.118206","url":null,"abstract":"<div><h3>Introduction</h3><div>This study aimed to examine the temporal, spatial and population heterogeneity in the association between temperature and injury by animal in China and to assess the future burden attributed to temperature changes.</div></div><div><h3>Methods</h3><div>Injury by specific animal data during 2006–2017 and 2019–2021 were obtained from National Injury Surveillance System in China, and meteorological data were obtained from the fifth generation of European ReAnalysis-Land. Conditional logistic regression combined with a distributed lag nonlinear model was applied to investigate the association of temperature with injury by animal. Additionally, we projected future trends in animal-related injury burden linked to temperature changes.</div></div><div><h3>Results</h3><div>This study included a total of 859,321 injury cases by animal. The excess risk (ER) on injury by animal increased 1.57 % [95 % confidence interval (CI): 1.48 %-1.67 %] for a 1°C temperature rise with much higher risk for injury by non-mammalian (ER=7.54 %, 95 %CI: 7.12 %-7.96 %) than that for injury by mammalian (ER=1.75 %, 95 %CI: 1.62 %-1.87 %). Among injury by mammalian, dog bites showed the highest risk (ER=2.01 %, 95 %CI: 1.86 %-2.15 %), while snake injury was most affected by temperature (ER=11.82 %, 95 %CI: 10.44 %-13.21 %) among injury by non-mammalian. We observed significant population heterogeneity with higher ER for male, children &lt; 5 years and farmer. We also observed spatial heterogeneity with higher risk for warm region or southern and central China. Temporally, the top three associations between temperature and animal injury risk were observed in 2009, 2020 and 2010, however, the difference was not statistically significant. Projections indicate that under the SSP585 scenario, the temperature-attributable fraction of animal-related injuries in China will increase by 13.89 % (95 % CI: 9.19 %-18.63 %) in the 2090 s compared to the 2010s baseline.</div></div><div><h3>Conclusions</h3><div>High temperature significantly increase injury by animal with significant spatial, temporal, population, and animal heterogeneity. Future temperature rise will increase the burden of injury by animal.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118206"},"PeriodicalIF":6.2,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834147","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":"Association of exposure to organochlorine pesticides with the antioxidant bilirubin: Mediation analysis in the NHANES","authors":"Shan-Shan Huang ,&nbsp;Xiao Shuang Yu ,&nbsp;Xiao-Na Yi ,&nbsp;Tong Lin ,&nbsp;Shuang-Shuang Han ,&nbsp;Ying Tang ,&nbsp;Hai-Yan Mao ,&nbsp;Zhou-Xin Yang","doi":"10.1016/j.ecoenv.2025.118197","DOIUrl":"10.1016/j.ecoenv.2025.118197","url":null,"abstract":"<div><div>Exposure to organochlorine pesticides (OCPs) has been linked to adverse health effects through oxidative stress. Bilirubin, an endogenous antioxidant, may play a key role in regulating oxidative stress. This study utilized NHANES data (2007–2016) to investigate the relationship between exposure to seven OCPs and serum total bilirubin (TB) levels in American adults, as well as potential mediating effects. Among the 6583 adults studied, HCB, β-HCCH, p, p′-DDE, p, p′-DDT, OXYCHLOR, and T-NONA were all significantly and positively correlated with TB levels among the seven OCPs analyzed (p &lt; 0.05). HCB, β-HCCH, and OXYCHLOR showed inverted \"J\"-, a similar \"S\"-, and \"U\"-shaped nonlinear relationships with TB, respectively (p for nonlinear &lt; 0.05). OXYCHLOR had the strongest cumulative effect, and platelets partially mediated the association between p, p′-DDE, p, p′-DDT, T-NONA, OXYCHLOR, and TB. Exposure to OPCs was significantly positively associated with antioxidant TB levels, and platelets played a partially negative mediating role in this association. This finding suggests that OCPs exposure may adversely affect human health by impacting the redox system.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118197"},"PeriodicalIF":6.2,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834961","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":"Lithium carbonate exposure disrupts neurodevelopment by perturbing primary cilia and ER homeostasis","authors":"Zhen Guan,&nbsp;Yingchao Liang,&nbsp;Zhiqiang Zhu,&nbsp;Aiyun Yang,&nbsp;Shen Li,&nbsp;Xiuwei Wang ,&nbsp;Jianhua Wang","doi":"10.1016/j.ecoenv.2025.118200","DOIUrl":"10.1016/j.ecoenv.2025.118200","url":null,"abstract":"<div><div>Lithium, which is widely used in medicine and batteries, has become increasingly prevalent in the environment, raising concerns about its impact on human health. Lithium carbonate (Li₂CO₃) is a common treatment and relapse prevention method for bipolar disorder. It can freely cross the placental barrier; however, lithium treatment is accompanied by side effects, particularly in women of reproductive age. Among these, neural tube defects (NTDs) have the most severe impact on nervous system development; however, their underlying mechanisms remain unclear. This study explored the potential mechanisms by which Li₂CO₃ exposure contributes to NTDs. Pregnant mice were intraperitoneally injected with Li₂CO₃ (360 mg/kg), which mimicked high-exposure scenarios such as an unintended pregnancy during lithium therapy or exposure to industrial contamination. Embryos were assessed for morphological changes, primary cilia length, and endoplasmic reticulum (ER) homeostasis using histological analysis, scanning electron microscopy, PCR array analysis, immunofluorescence, and quantitative real-time PCR. Network and bioinformatics analyses were used to identify primary molecular targets and pathways. We also evaluated the effects of inositol supplementation on cilia during Li₂CO₃ exposure. The results revealed that treatment with Li₂CO₃ at 360 mg/kg induced exencephaly in some embryos, reduced primary cilia length, and dysregulated cilia-associated gene expression in the neural tube. PCR Array, network metabolism, and immunofluorescence analyses revealed that HSP90AB1, a critical regulator of ER homeostasis, was upregulated in Li₂CO₃-treated embryos with NTDs. Li₂CO₃ exposure disturbed ER homeostasis in the developing brain. Interestingly, inositol supplementation partially rescued ciliogenesis impairment in lithium-treated NIH3T3 cells. Li₂CO₃ exposure disrupted primary ciliary development and ER homeostasis in the embryonic neural tube. Maintaining adequate maternal inositol levels during Li₂CO₃ exposure before and during pregnancy prevents NTDs. These findings help in better understanding and reassessing the risks associated with lithium, especially in terms of maternal and fetal health.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118200"},"PeriodicalIF":6.2,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834145","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":"Ambient low-level benzene, genetic factors, and heart failure incidence among urban adults","authors":"Yongxuan Li ,&nbsp;Yujia Bao ,&nbsp;Jiawei Gu ,&nbsp;Zheshen Han ,&nbsp;Xiaobei Deng ,&nbsp;Wei Mu ,&nbsp;Hui Wang ,&nbsp;Hongchao Qi ,&nbsp;Lefei Han ,&nbsp;Jinjun Ran","doi":"10.1016/j.ecoenv.2025.118207","DOIUrl":"10.1016/j.ecoenv.2025.118207","url":null,"abstract":"<div><div>Ambient benzene, a representative volatile organic compound (VOC) primarily resulting from rapid industrialization and urbanization, is also of great concern as an urban air toxic. The global benzene market is experiencing steady growth, driven by its use in industrial manufacturing. Currently, population epidemiological evidence about the effects of ambient benzene on heart failure (HF) incidence is still inadequate, especially at low levels of long-term exposure. Leveraging data from 277,585 urban residents in the UK Biobank, the study utilized Cox regression models adjusted for potential confounders to evaluate the association between low-concentration benzene exposure and HF risk. The investigation also assessed potential interactions between genetic predisposition and ambient benzene by applying relative excess risk due to interaction (RERI) metrics and interaction significance testing. Furthermore, the effect of ambient benzene on cardiac functional parameters was estimated using multiple linear regression models. This study demonstrated that per interquartile range increment of ambient benzene was related to the elevated HF risk (hazard ratios = 1.22, 95 % confidence interval (CI): 1.07–1.39] from the time-dependent Cox model. An additive interaction between ambient benzene and genetic risk was observed (RERI = 0.18, 95 % CI: 0.01–0.36). Ambient benzene exposure demonstrated significant correlations with modifications in cardiac functional parameters, such as ventricular end-diastolic and end-systolic volumes. Prolonged exposure to low-concentration ambient benzene may elevate the likelihood of developing HF, which provides the necessary evidence for the systematic risk assessment of ambient benzene and promotes the formulation and updating of air quality guidelines worldwide.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118207"},"PeriodicalIF":6.2,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143838729","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":"Biodegradation of polypropylene by Bacillus cereus PP-5 isolated from waste landfill","authors":"Huizhen Xue ,&nbsp;Xue Chen ,&nbsp;Zhitong Jiang ,&nbsp;Jinghui Lei ,&nbsp;Jie Zhou ,&nbsp;Weiliang Dong ,&nbsp;Zhoukun Li ,&nbsp;Gang Hu ,&nbsp;Zhongli Cui","doi":"10.1016/j.ecoenv.2025.118205","DOIUrl":"10.1016/j.ecoenv.2025.118205","url":null,"abstract":"<div><div>Waste polypropylene (PP) plastic has caused serious environmental pollution, and biological methods provide a feasible strategy to deal with the environmental pollution and resource waste caused by waste plastics. In this study, we investigated the physicochemical and structural changes of PP plastic degraded by <em>Bacillus cereus</em> PP-5, which was isolated from a waste landfill. After 30-day incubation with PP-5, structural properties of PP powder were analyzed using high-temperature gel permeation chromatography, scanning electron microscopy (SEM), Fourier transform infrared spectroscopy, and differential scanning calorimetry. We found that PP-5 colonized the plastic surface through biofilm, and the bio-deterioration with visible cracks was also observed from the PP surfaces, the carbonyl index of PP-5-treated PP powder was identified as 0.536. Meantime, the weight-average molecular weight and thermal stability of PP decreased, while melting enthalpy and average crystallinity increased after PP-5treatment. Moreover, oxidative cleavage of carbon-carbon bonds of PP was observed from the appearance of quaternary carbon and elevated C<img>O groups of PP-5-treated PP plastics, suggesting microbial oxidation. Our findings elucidate a potential bio-oxidizing mechanism for microbial-driven PP degradation, and also highlight the application prospects in bio-recycling systems, particularly for managing plastic waste in landfills or marine environments.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118205"},"PeriodicalIF":6.2,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834144","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":"Transcriptome analysis reveals the mechanism of tolerance to copper toxicity in the white rot fungus Trametes hirsuta AH28-2","authors":"Chenkai Wang ,&nbsp;Kun Wu ,&nbsp;Na Pang ,&nbsp;Huifang Zhao ,&nbsp;Shenglong Liu ,&nbsp;Xinlei Zhang ,&nbsp;Yazhong Xiao ,&nbsp;Zemin Fang ,&nbsp;Juanjuan Liu","doi":"10.1016/j.ecoenv.2025.118194","DOIUrl":"10.1016/j.ecoenv.2025.118194","url":null,"abstract":"<div><div>Heavy metals, such as copper (Cu), are prevalent in the environment and pose a substantial threat to human health. White rot fungi, especially <em>Trametes</em> spp., display prominent Cu tolerance and removal capacity. However, how <em>Trametes</em> responds to environmental Cu stress remains poorly understood. Here, we found that <em>Trametes hirsuta</em> AH28–2 exhibits Cu removal efficiencies varying from 80.8 % at 1.25 mg/L to 57.6 % at 37 mg/L. Comparative transcriptome analysis identified 812, 1898, and 2110 differentially expressed genes (DEGs) at the Cu concentrations of 1.25, 12.5, and 25 mg/L, respectively. Some DEGs were associated with antioxidant defense systems, secondary metabolite biosynthesis (terpenoids and polyketides), transmembrane transport, and glutathione metabolism, potentially enhancing Cu tolerance. The activities of antioxidant enzymes such as superoxide dismutase, catalase, and laccase were increased under Cu stress. qRT-PCR confirmed the alterations in gene expression and demonstrated that glutathione S-transferases, catalases, cytochrome P450s, and laccases were involved in counteracting Cu-induced stress. Gene silencing experiments further confirmed the crucial roles of laccases in this process. Many transcription factors were enriched under Cu stress, including the Zn2Cys6 family transcription factor GME8421_g (TH8421), which was significantly upregulated at the Cu concentration of 12.5 mg/L. ChIP-seq identified five antioxidant enzyme-encoding genes as direct targets of TH8421, forming a regulatory network that protects against Cu stress. These findings offer insights into the molecular mechanisms driving Cu toxicity tolerance in <em>Trametes</em> fungi.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118194"},"PeriodicalIF":6.2,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143828952","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":"Association between long-term benzene exposure and inflammatory bowel disease in a national cohort: The modifying effect of genetic susceptibility","authors":"Zhi-Hao Xiao ,&nbsp;Shaoni Huang ,&nbsp;Kai Zhao ,&nbsp;Xiaoqin Zhang ,&nbsp;Zhi Li ,&nbsp;Runze Li ,&nbsp;Min Yao ,&nbsp;Shaojun Li ,&nbsp;Cheng Xu","doi":"10.1016/j.ecoenv.2025.118198","DOIUrl":"10.1016/j.ecoenv.2025.118198","url":null,"abstract":"<div><h3>Background</h3><div>This study aimed to investigate the effects of environmental benzene exposure and its interaction with genetic susceptibility on inflammatory bowel disease (IBD), with a specific focus on ulcerative colitis (UC) and Crohn's disease (CD).</div></div><div><h3>Methods</h3><div>A total of 432,727 participants from the UK Biobank who were free of IBD at baseline were included in the analysis. The annual average benzene concentrations during the follow-up period were evaluated by air dispersion models. The study assessed the incidence of IBD in relation to ambient benzene exposure using Cox proportional hazard models and estimated the exposure<img>response relationships using restricted cubic spline models. Additive interactions included relative excess risk due to interaction (RERI) and the attributable proportion (AP) to evaluate the interaction between ambient benzene exposure and genetic predisposition.</div></div><div><h3>Results</h3><div>A significant association was identified between ambient benzene exposure and the incidence of IBD, with hazard ratios (95 % confidence intervals) of 1.06 (1.03, 1.09) for IBD, 1.08 (1.04, 1.12) for UC, and 1.03 (0.98, 1.09) for CD per 0.1 μg/m³ increase. Furthermore, genetic predispositions were found to significantly modify the relationship between ambient benzene exposure and IBD risk. Individuals with the highest genetic risk and benzene exposure had the highest risk of UC.</div></div><div><h3>Conclusion</h3><div>This study provides compelling evidence of the interaction between environmental factors and genetic susceptibility in the pathogenesis of UC. These findings underscore the importance of considering both genetic and environmental influences in future prevention and intervention strategies for IBD.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118198"},"PeriodicalIF":6.2,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143828951","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":"Long-term air pollution exposure and cardiovascular disease progression in rheumatoid arthritis: A prospective cohort study using multi-state model analysis","authors":"Yu-Xuan Zhang ,&nbsp;Bin-Bin Feng ,&nbsp;Ma Ruo-Wei ,&nbsp;Lin Zhu ,&nbsp;Yong-Yong Liu ,&nbsp;Yu-Ye Zuo ,&nbsp;Hai-Feng Pan ,&nbsp;Guo-Cui Wu","doi":"10.1016/j.ecoenv.2025.118187","DOIUrl":"10.1016/j.ecoenv.2025.118187","url":null,"abstract":"<div><h3>Background</h3><div>Patients with rheumatoid arthritis (RA) have a significantly elevated risk of developing cardiovascular disease (CVD), the leading cause of their death. However, the impact of environmental factors on RA progression remains unclear. This study aimed to explore the link between long-term air pollution exposure and the multi-stage progression from a healthy status to RA onset, then CVD development, and finally death.</div></div><div><h3>Methods</h3><div>Utilizing data from 326,059 participants in the UK Biobank, we used a unidirectional multi-state Markov proportional hazards model to analyze the associations between long-term exposure to air pollutants (PM_2.5, PM₁₀, NO₂, and NO_x) and disease progression. The models included transitions from baseline healthy state to RA onset, to subsequent CVD, and to death. Air pollution exposure was assessed using land use regression models, and hazard ratios (HRs) were calculated per interquartile range (IQR) increase in pollutant concentrations.</div></div><div><h3>Results</h3><div>During a median follow-up of 12.69 years, 3422 participants developed RA, of whom 424 subsequently developed CVD. PM_2.5 and NO₂ showed the most extensive effects across transition stages. Per IQR increase in PM_2.5 was associated with increased risks of RA onset (HR: 1.08; 95 %CI: 1.03, 1.12) and RA to death (HR: 1.20; 95 %CI: 1.06, 1.37), while NO₂ was associated with increased risks of RA onset (HR: 1.10; 95 %CI: 1.06, 1.15) and subsequent CVD development (HR: 1.13; 95 %CI: 1.01, 1.28). Notably, valve disorders showed associations with multiple pollutants, and these effects were more pronounced in women and elderly participants.</div></div><div><h3>Conclusion</h3><div>Long-term exposure to air pollutants was significantly associated with increased risks at multiple transition stages, from RA onset to subsequent CVD development and death, although effect sizes were modest for some transitions. Considering the widespread global exposure to air pollution, these findings emphasize the importance of air pollution control in preventing RA and its cardiovascular complications, especially among susceptible populations.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118187"},"PeriodicalIF":6.2,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834153","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":"Adolescent cetylpyridinium chloride exposure impairs homologous recombination repair and induces granulosa cell apoptosis and follicular atresia via FOXM1/CREBBP complex suppression","authors":"LiYao Ma ,&nbsp;Xin Yin ,&nbsp;Yan Zhang ,&nbsp;Yidan Ma ,&nbsp;Yanqing Geng ,&nbsp;Xinyi Mu ,&nbsp;Rufei Gao ,&nbsp;Xuemei Chen ,&nbsp;Junlin He","doi":"10.1016/j.ecoenv.2025.118193","DOIUrl":"10.1016/j.ecoenv.2025.118193","url":null,"abstract":"<div><div>Cetylpyridinium chloride (CPC), a widely used surfactant, functions as an antimicrobial agent in pharmaceuticals and personal care products (PPCPs). However, its effect on the female reproductive system remains largely unknown. Herein, female mice were gavaged with 0.01, 0.1, or 1 mg CPC/kg body weight (bw)/d during adolescence. Results showed reduced body and ovarian weights, decreased primordial follicle numbers, and increased atretic follicles. Additionally, CPC disrupted serum hormone levels, reduced cell viability and proliferation, and increased apoptosis in granulosa cells. Transcriptomic analysis of primary granulosa cells revealed altered genes in homologous recombination (HR) repair pathway, including the downregulation of FOXM1 and the MRN complex. Further validation demonstrated decreased expression of HR repair components and increased DNA damage in both <em>in vivo</em> and <em>in vitro</em>. Mechanistically, CPC inhibited the FOXM1/CREBBP interaction and inhibited HR repair gene transcription, including <em>MRE11</em> and <em>NBS1</em>. Finally, FOXM1 overexpression partially reversed the detrimental effects of CPC on HR repair and cell proliferation. These results indicate that CPC-induced ovarian dysfunction during adolescence is mediated through FOXM1/CREBBP complex inhibition and homologous recombination repair impairment, potentially increasing the risk for the development of diminished ovarian reserve (DOR) and providing new experimental evidence to assess the reproductive toxicity effects of CPC.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118193"},"PeriodicalIF":6.2,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834154","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":"Unraveling the role of abnormal AMPK and CRMP-2 phosphorylation in developmental fluoride neurotoxicity: Implications for synaptic damage and neurological disorders","authors":"Jingjing Zhang ,&nbsp;Panpan Xu ,&nbsp;Yue Zhang ,&nbsp;Tingting Li ,&nbsp;Xueman Ding ,&nbsp;Li Liu ,&nbsp;Ping Yao ,&nbsp;Qiang Niu","doi":"10.1016/j.ecoenv.2025.118192","DOIUrl":"10.1016/j.ecoenv.2025.118192","url":null,"abstract":"<div><div>Excessive fluoride exposure can be neurotoxic, although the exact mechanism remains unknown. This study aimed to investigate the neurotoxicity of continuous sodium fluoride exposure in offspring rats, focusing on the potential effects of fluoride exposure on hippocampal synaptic function and the role of AMPK and CRMP-2 in synaptic damage. We established an SD rat model of fluoride exposure (25, 50, and 100 mg/L NaF) and found that fluoride exposure damaged the learning and memory ability of F₁ generation rats and caused ultrastructural changes in the hippocampus. Additionally, after the proteomic and phosphoproteomic analysis of rat hippocampal tissues, the Gene Ontology analysis revealed that sodium fluoride was involved in the enrichment of neuronal differentiation, synaptic signaling, and cytoskeleton-related biological processes. The Kyoto Encyclopedia of Genes and Genomes analysis showed that differential genes were enriched in synapse-related signaling pathways. Thus, we screened three differentially expressed proteins related to synaptic function for validation. The Western blotting analysis showed that AMPK and CRMP-2 were hyperphosphorylated in the hippocampus of fluoride-exposed rats. Our study found that abnormal AMPK and CRMP-2 phosphorylation leads to synaptic damage. This may be an important cause of memory impairment in fluorosis, offering new insights into the mechanism of fluoride-induced neurotoxicity.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118192"},"PeriodicalIF":6.2,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143828949","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}