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Long-term air pollution exposure and cardiovascular disease progression in rheumatoid arthritis: A prospective cohort study using multi-state model analysis
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2025-04-15 DOI: 10.1016/j.ecoenv.2025.118187
Yu-Xuan Zhang , Bin-Bin Feng , Ma Ruo-Wei , Lin Zhu , Yong-Yong Liu , Yu-Ye Zuo , Hai-Feng Pan , Guo-Cui Wu

Background

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.

Methods

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 (PM2.5, PM10, NO2, and NOx) 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.

Results

During a median follow-up of 12.69 years, 3422 participants developed RA, of whom 424 subsequently developed CVD. PM2.5 and NO2 showed the most extensive effects across transition stages. Per IQR increase in PM2.5 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.

Conclusion

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.
{"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<sub>2.5</sub>, PM<sub>10</sub>, NO<sub>2</sub>, and NO<sub>x</sub>) 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<sub>2.5</sub> and NO<sub>2</sub> showed the most extensive effects across transition stages. Per IQR increase in PM<sub>2.5</sub> 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 NO<sub>2</sub> 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}
引用次数: 0
Adolescent cetylpyridinium chloride exposure impairs homologous recombination repair and induces granulosa cell apoptosis and follicular atresia via FOXM1/CREBBP complex suppression
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2025-04-15 DOI: 10.1016/j.ecoenv.2025.118193
LiYao Ma , Xin Yin , Yan Zhang , Yidan Ma , Yanqing Geng , Xinyi Mu , Rufei Gao , Xuemei Chen , Junlin He
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 in vivo and in vitro. Mechanistically, CPC inhibited the FOXM1/CREBBP interaction and inhibited HR repair gene transcription, including MRE11 and NBS1. 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.
{"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}
引用次数: 0
Unraveling the role of abnormal AMPK and CRMP-2 phosphorylation in developmental fluoride neurotoxicity: Implications for synaptic damage and neurological disorders 揭示 AMPK 和 CRMP-2 磷酸化异常在发育期氟化物神经毒性中的作用:对突触损伤和神经系统疾病的影响
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2025-04-15 DOI: 10.1016/j.ecoenv.2025.118192
Jingjing Zhang , Panpan Xu , Yue Zhang , Tingting Li , Xueman Ding , Li Liu , Ping Yao , Qiang Niu
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.
{"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 F<sub>1</sub> 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}
引用次数: 0
Electroacupuncture alleviates diesel exhaust particles-induced inflammatory response in lung through dopamine inhibition of NLRP3 signaling pathway 电针通过多巴胺抑制 NLRP3 信号通路缓解柴油废气颗粒诱发的肺部炎症反应
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2025-04-14 DOI: 10.1016/j.ecoenv.2025.118184
Yuanting Xie , Jing Han , Qianfeng Wang , Xinyi Fang , Bin Pan , Dongyang Han , Jingyu Li , Wenpu Shao , Xiaoqing Hong , Wenyue Tu , Wenye Geng , Weihua Li , Zhanzhuang Tian , Renjie Chen , Yanyi Xu , Haidong Kan
Fine particulate matter (PM2.5) remains a major environmental problem both in China and worldwide. Extensive researches have indicated that PM2.5 exposure can lead to various adverse health effects through pulmonary and systemic inflammation, making it crucial to explore effective individual intervention strategies. Electroacupuncture, an ancient Chinese medical treatment, has been proven safe and effective for treating some diseases, however, its potential in preventing PM2.5-induced toxicity remains unclear. This study aimed to explore the potential of electroacupuncture in mitigating pulmonary inflammation induced by diesel exhaust particles (DEP). Electroacupuncture was administered 15 minutes before intratracheal instillation of DEP, and the results showed that it markedly reduced DEP-induced pulmonary inflammation, as evidenced by significantly decreased pro-inflammatory markers at both gene and protein levels in lung, via regulating the macrophage polarization. Further analysis indicated that electroacupuncture promoted the production and release of dopamine from the adrenal medulla of mice, which then translocated to lung via circulation and inhibited the pulmonary NLRP3/caspase-1 signaling pathway. In addition, the time effectiveness experiment suggested that the anti-inflammatory effect of electroacupuncture against DEP can last for 48 hours. These findings suggest that electroacupuncture holds potential as a therapeutic intervention for health issues caused by PM2.5 exposure.
{"title":"Electroacupuncture alleviates diesel exhaust particles-induced inflammatory response in lung through dopamine inhibition of NLRP3 signaling pathway","authors":"Yuanting Xie ,&nbsp;Jing Han ,&nbsp;Qianfeng Wang ,&nbsp;Xinyi Fang ,&nbsp;Bin Pan ,&nbsp;Dongyang Han ,&nbsp;Jingyu Li ,&nbsp;Wenpu Shao ,&nbsp;Xiaoqing Hong ,&nbsp;Wenyue Tu ,&nbsp;Wenye Geng ,&nbsp;Weihua Li ,&nbsp;Zhanzhuang Tian ,&nbsp;Renjie Chen ,&nbsp;Yanyi Xu ,&nbsp;Haidong Kan","doi":"10.1016/j.ecoenv.2025.118184","DOIUrl":"10.1016/j.ecoenv.2025.118184","url":null,"abstract":"<div><div>Fine particulate matter (PM<sub>2.5</sub>) remains a major environmental problem both in China and worldwide. Extensive researches have indicated that PM<sub>2.5</sub> exposure can lead to various adverse health effects through pulmonary and systemic inflammation, making it crucial to explore effective individual intervention strategies. Electroacupuncture, an ancient Chinese medical treatment, has been proven safe and effective for treating some diseases, however, its potential in preventing PM<sub>2.5</sub>-induced toxicity remains unclear. This study aimed to explore the potential of electroacupuncture in mitigating pulmonary inflammation induced by diesel exhaust particles (DEP). Electroacupuncture was administered 15 minutes before intratracheal instillation of DEP, and the results showed that it markedly reduced DEP-induced pulmonary inflammation, as evidenced by significantly decreased pro-inflammatory markers at both gene and protein levels in lung, <em>via</em> regulating the macrophage polarization. Further analysis indicated that electroacupuncture promoted the production and release of dopamine from the adrenal medulla of mice, which then translocated to lung <em>via</em> circulation and inhibited the pulmonary NLRP3/caspase-1 signaling pathway. In addition, the time effectiveness experiment suggested that the anti-inflammatory effect of electroacupuncture against DEP can last for 48 hours. These findings suggest that electroacupuncture holds potential as a therapeutic intervention for health issues caused by PM<sub>2.5</sub> exposure.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143825470","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
Ginsenoside Rg1 alleviates ochratoxin A-induced liver inflammation in ducklings: Involvement of intestinal microbiota modulation and the TLR4/NF-κB pathway inhibition
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2025-04-14 DOI: 10.1016/j.ecoenv.2025.118186
Shuangshuang Zhai , Xin Peng , Cheng Liu , Ran Zhang , Chunlong Jin , Xiayu Jiang , Peishi Feng , Yuting Liang , Xi Yuan , Jinqiu Zhang , Ye Yang
Ochratoxin A (OTA) is a toxic fungal secondary metabolite that triggers liver inflammation in animals. OTA could disrupt intestinal microbiota balance by promoting Gram-negative bacteria growth and activating the Toll-like receptor 4 (TLR4)/Nuclear factor-kappa B (NF-κB) signaling pathway, thereby inducing liver inflammation. Ginsenoside Rg1 (Rg1) is an active component of ginseng, exhibits anti-inflammatory, antibacterial, and antioxidative properties, particularly against gram-negative bacteria. Rg1 has been shown to maintain intestinal microbiota homeostasis and inhibit the TLR4 signaling pathway to alleviate liver inflammation. Given these established mechanisms, the aim of this study was to explore the preventive effect of Rg1 in countering OTA-induced liver inflammation through modulation of intestinal microbiota and the TLR4/NF-κB signaling pathway. The results revealed that Rg1 reduced OTA residues in the cecum and enhanced intestinal barrier function. Moreover, Rg1 ameliorated the intestinal microbiota composition in OTA-treated ducklings by decreasing the relative abundance of lipopolysaccharide (LPS)-related bacteria. Rg1 also increases the abundance of short-chain fatty acid (SCFA)-producing bacteria. Additionally, Rg1 supplementation with OTA decreased the accumulation of LPS in tissues and inhibited the TLR4/NF-κB signaling pathway. Intriguingly, Rg1 maintained its beneficial effects in OTA-treated ducklings even after antibiotic treatment by inhibiting the TLR4/NF-κB pathway. These findings emphasized the importance of intestinal microbiota homeostasis and TLR4/NF-κB pathway suppression in the anti-inflammatory action of Rg1 during OTA-induced liver inflammation.
{"title":"Ginsenoside Rg1 alleviates ochratoxin A-induced liver inflammation in ducklings: Involvement of intestinal microbiota modulation and the TLR4/NF-κB pathway inhibition","authors":"Shuangshuang Zhai ,&nbsp;Xin Peng ,&nbsp;Cheng Liu ,&nbsp;Ran Zhang ,&nbsp;Chunlong Jin ,&nbsp;Xiayu Jiang ,&nbsp;Peishi Feng ,&nbsp;Yuting Liang ,&nbsp;Xi Yuan ,&nbsp;Jinqiu Zhang ,&nbsp;Ye Yang","doi":"10.1016/j.ecoenv.2025.118186","DOIUrl":"10.1016/j.ecoenv.2025.118186","url":null,"abstract":"<div><div>Ochratoxin A (OTA) is a toxic fungal secondary metabolite that triggers liver inflammation in animals. OTA could disrupt intestinal microbiota balance by promoting Gram-negative bacteria growth and activating the Toll-like receptor 4 (TLR4)/Nuclear factor-kappa B (NF-κB) signaling pathway, thereby inducing liver inflammation. Ginsenoside Rg1 (Rg1) is an active component of ginseng, exhibits anti-inflammatory, antibacterial, and antioxidative properties, particularly against gram-negative bacteria. Rg1 has been shown to maintain intestinal microbiota homeostasis and inhibit the TLR4 signaling pathway to alleviate liver inflammation. Given these established mechanisms, the aim of this study was to explore the preventive effect of Rg1 in countering OTA-induced liver inflammation through modulation of intestinal microbiota and the TLR4/NF-κB signaling pathway. The results revealed that Rg1 reduced OTA residues in the cecum and enhanced intestinal barrier function. Moreover, Rg1 ameliorated the intestinal microbiota composition in OTA-treated ducklings by decreasing the relative abundance of lipopolysaccharide (LPS)-related bacteria. Rg1 also increases the abundance of short-chain fatty acid (SCFA)-producing bacteria<em>.</em> Additionally, Rg1 supplementation with OTA decreased the accumulation of LPS in tissues and inhibited the TLR4/NF-κB signaling pathway. Intriguingly, Rg1 maintained its beneficial effects in OTA-treated ducklings even after antibiotic treatment by inhibiting the TLR4/NF-κB pathway. These findings emphasized the importance of intestinal microbiota homeostasis and TLR4/NF-κB pathway suppression in the anti-inflammatory action of Rg1 during OTA-induced liver inflammation.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143825388","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
Integration of histopathology, transcriptomics and non-targeted metabolomics reveals toxic effects of thiamethoxam under acute stress in mirror carp (Cyprinus carpio var. Longke-11 mirror) 组织病理学、转录组学和非靶向代谢组学的整合揭示了噻虫嗪在镜鲤(Cyprinus carpio var.)
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2025-04-14 DOI: 10.1016/j.ecoenv.2025.118162
Dongchang Guo , Wenyang Song , Manhong Liu , Haixia Jiang , Xiaolong Wang , Zhiying Jia , Bin Xu
In recent years, the increasing application of thiamethoxam (THM), coupled with its high leaching and solubility in water, has led to growing concerns regarding THM residues in aquatic environments, which may pose toxic effects on aquatic organisms, particularly fish. However, the toxicological mechanisms of THM in freshwater fish remain unclear. In this study, using histopathology, transcriptomics, and non-targeted metabolomics, the toxic effects of different concentrations of THM under acute stress (96 h) were investigated in mirror carp (Cyprinus carpio var. Longke-11 mirror). The results showed that under acute THM stress, liver tissues of the mirror carp exhibited vacuolation, cellular degeneration, and enhanced cytoplasmic eosinophilia, while gill tissues displayed epithelial structure loss, epithelial cell detachment, degeneration, and vacuolation, with the severity of lesions increasing with exposure concentration. Transcriptomic analysis revealed that the number of differentially expressed genes (DEGs) increased with the concentration of THM. Genes related to immune response and antioxidant stress were mostly downregulated, while genes related to inflammation and apoptosis were predominantly upregulated. The downregulation of common DEGs (SLC7A11, ITLN, CDH17) further confirmed these results. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed significant enrichment in pathways related to inflammation and oxidative stress, with the NF-kappa B signaling pathway identified as the key pathway affected. Metabolomic analysis showed that differentially expressed metabolites (SCMs) associated with amino acid and lipid metabolism were significantly downregulated. The downregulation of SCM acetylcysteine further affected the antioxidant capacity of mirror carp. Moreover, different concentrations of THM affected phenylalanine metabolism, cysteine and methionine metabolism, and biosynthesis of unsaturated fatty acids in the liver of mirror carp. Integrated analysis of apoptosis-related factors (TP53INP1, PRF1, Sphingosine) upregulation and anti-apoptotic factors (Bcl2l1) downregulation suggested that THM induces apoptosis in mirror carp cells. These results indicate that THM stress affects the immune system, amino acid, and lipid metabolism in mirror carp, leading to inflammation, oxidative stress, and apoptosis. This study provides preliminary insights into the toxic mechanisms of THM in fish and can serve as a scientific basis for THM risk assessment and environmental protection.
{"title":"Integration of histopathology, transcriptomics and non-targeted metabolomics reveals toxic effects of thiamethoxam under acute stress in mirror carp (Cyprinus carpio var. Longke-11 mirror)","authors":"Dongchang Guo ,&nbsp;Wenyang Song ,&nbsp;Manhong Liu ,&nbsp;Haixia Jiang ,&nbsp;Xiaolong Wang ,&nbsp;Zhiying Jia ,&nbsp;Bin Xu","doi":"10.1016/j.ecoenv.2025.118162","DOIUrl":"10.1016/j.ecoenv.2025.118162","url":null,"abstract":"<div><div>In recent years, the increasing application of thiamethoxam (THM), coupled with its high leaching and solubility in water, has led to growing concerns regarding THM residues in aquatic environments, which may pose toxic effects on aquatic organisms, particularly fish. However, the toxicological mechanisms of THM in freshwater fish remain unclear. In this study, using histopathology, transcriptomics, and non-targeted metabolomics, the toxic effects of different concentrations of THM under acute stress (96 h) were investigated in mirror carp (<em>Cyprinus carpio</em> var. <em>Longke-11 mirror</em>). The results showed that under acute THM stress, liver tissues of the mirror carp exhibited vacuolation, cellular degeneration, and enhanced cytoplasmic eosinophilia, while gill tissues displayed epithelial structure loss, epithelial cell detachment, degeneration, and vacuolation, with the severity of lesions increasing with exposure concentration. Transcriptomic analysis revealed that the number of differentially expressed genes (DEGs) increased with the concentration of THM. Genes related to immune response and antioxidant stress were mostly downregulated, while genes related to inflammation and apoptosis were predominantly upregulated. The downregulation of common DEGs (<em>SLC7A11, ITLN, CDH17</em>) further confirmed these results. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed significant enrichment in pathways related to inflammation and oxidative stress, with the NF-kappa B signaling pathway identified as the key pathway affected. Metabolomic analysis showed that differentially expressed metabolites (SCMs) associated with amino acid and lipid metabolism were significantly downregulated. The downregulation of SCM acetylcysteine further affected the antioxidant capacity of mirror carp. Moreover, different concentrations of THM affected phenylalanine metabolism, cysteine and methionine metabolism, and biosynthesis of unsaturated fatty acids in the liver of mirror carp. Integrated analysis of apoptosis-related factors (<em>TP53INP1, PRF1, Sphingosine</em>) upregulation and anti-apoptotic factors (Bcl2l1) downregulation suggested that THM induces apoptosis in mirror carp cells. These results indicate that THM stress affects the immune system, amino acid, and lipid metabolism in mirror carp, leading to inflammation, oxidative stress, and apoptosis. This study provides preliminary insights into the toxic mechanisms of THM in fish and can serve as a scientific basis for THM risk assessment and environmental protection.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118162"},"PeriodicalIF":6.2,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143828948","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
Transcriptomics uncover inhibition of repair and wound healing pathways in Atlantic halibut (Hippoglossus hippoglossus) after crude oil exposure 转录组学发现原油暴露后大西洋比目鱼(Hippoglossus hippoglossus)的修复和伤口愈合途径受到抑制
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2025-04-14 DOI: 10.1016/j.ecoenv.2025.118151
Elin Sørhus , Kai K. Lie , Sonnich Meier , Tomasz Furmanek , Birgitta Norberg , Prescilla Perrichon
Accidental oil spills significantly threaten marine ecosystems and fisheries, impacting biodiversity and ecological health. This study examines the downstream transcriptomic responses of Atlantic halibut larvae exposed to crude oil during organogenesis. Findings show concentration-dependent transcriptional abnormalities. Pathway analysis at 10 days post-hatch (dph), 11 days after cessation of oil exposure, indicates downregulation of inflammatory and reparative pathways. By 18 dph, tissue-specific analyses reveal activation of these pathways, especially in head tissues, alongside upregulation of neuronal signaling pathways. This highlights the complex relationship between oil exposure and transcriptional responses, emphasizing recovery mechanisms represented by regulation of inflammatory, repair and wound healing pathways following oil exposure. The activation of repair pathways in surviving larvae suggests compensatory processes to address oil-induced damage. These novel insights enhance understanding of the molecular mechanisms of oil toxicity and the lasting effects on marine organisms.
{"title":"Transcriptomics uncover inhibition of repair and wound healing pathways in Atlantic halibut (Hippoglossus hippoglossus) after crude oil exposure","authors":"Elin Sørhus ,&nbsp;Kai K. Lie ,&nbsp;Sonnich Meier ,&nbsp;Tomasz Furmanek ,&nbsp;Birgitta Norberg ,&nbsp;Prescilla Perrichon","doi":"10.1016/j.ecoenv.2025.118151","DOIUrl":"10.1016/j.ecoenv.2025.118151","url":null,"abstract":"<div><div>Accidental oil spills significantly threaten marine ecosystems and fisheries, impacting biodiversity and ecological health. This study examines the downstream transcriptomic responses of Atlantic halibut larvae exposed to crude oil during organogenesis. Findings show concentration-dependent transcriptional abnormalities. Pathway analysis at 10 days post-hatch (dph), 11 days after cessation of oil exposure, indicates downregulation of inflammatory and reparative pathways. By 18 dph, tissue-specific analyses reveal activation of these pathways, especially in head tissues, alongside upregulation of neuronal signaling pathways. This highlights the complex relationship between oil exposure and transcriptional responses, emphasizing recovery mechanisms represented by regulation of inflammatory, repair and wound healing pathways following oil exposure. The activation of repair pathways in surviving larvae suggests compensatory processes to address oil-induced damage. These novel insights enhance understanding of the molecular mechanisms of oil toxicity and the lasting effects on marine organisms.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143825471","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
Chlorantraniliprole-induced oxidative stress, DNA damage, and apoptosis in Caenorhabditis elegans: Mechanistic insights and ecological risk implications
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2025-04-13 DOI: 10.1016/j.ecoenv.2025.118164
Fengyuan Hu , Mengzhen Yang , Shaohua Han , Guokun Hu , Xiaoxue Ji , Kang Qiao
Chlorantraniliprole (CAP) is one of the most widely used insecticides in the world. CAP is strictly restricted in foodstuff with maximum residual limits (MRLs) from 0.01 to 40 mg/kg set by Chinese national food safety standard. However, a detailed evaluation on its possible acute toxicity and the underlying mechanisms remains inconclusive. In this study, effects of CAP at environmentally relevant concentrations on growth, locomotion, lifespan, reproduction, and antioxidative defense systems were evaluated using the model organism Caenorhabditis elegans. Exposure to CAP notably reduced nematode development, head thrash, and pharyngeal pumping frequency compared with the control. Moreover, CAP at 0.1, 1, and 10 μg/L decreased lifespan of nematodes by 23.73 %, 28.71 %, and 36.23 %, respectively. CAP at 1 and 10 μg/L enhanced the ROS level, reduced the activity of antioxidative enzyme, including CAT and SOD. CAP also regulated mRNA expression levels of daf-16, skn-1, sod-3, gst-4, ced-3, ced-4, ced-9, egl-1, clk-2, and hus-1 in the nematodes, while no significant effect in the mutants was observed. Pearson correlation analysis revealed that significant correlation existed between tested parameters, indicating that CAP caused a series of negative effects in the nematodes. Meanwhile, molecular docking results revealed the potential of CAP to bind with oxidative stress, DNA damage and apoptosis proteins, providing molecular mechanisms for the observed detrimental effects. Therefore, our results suggested that acute exposure to CAP at environmental concentrations caused oxidative stress, DNA damage and apoptosis in the nematodes. Our results shed new light on risk assessment and management of CAP.
氯虫苯甲酰胺(CAP)是世界上使用最广泛的杀虫剂之一。中国国家食品安全标准规定,CAP 在食品中的最高残留限量(MRL)为 0.01 至 40 毫克/千克,受到严格限制。然而,对其可能的急性毒性及其潜在机制的详细评估仍无定论。本研究以模式生物秀丽隐杆线虫(Caenorhabditis elegans)为对象,评估了环境相关浓度的 CAP 对其生长、运动、寿命、繁殖和抗氧化防御系统的影响。与对照组相比,暴露于 CAP 会明显降低线虫的发育、头部甩动和咽部抽动频率。此外,0.1、1 和 10 μg/L 的 CAP 会使线虫的寿命分别缩短 23.73%、28.71% 和 36.23%。1 和 10 μg/L 的 CAP 可提高 ROS 水平,降低 CAT 和 SOD 等抗氧化酶的活性。CAP 还能调节线虫体内 daf-16、skn-1、sod-3、gst-4、ced-3、ced-4、ced-9、egl-1、clk-2 和 hus-1 的 mRNA 表达水平,而对突变体则无显著影响。皮尔逊相关分析表明,测试参数之间存在显著相关性,表明 CAP 对线虫产生了一系列负面影响。同时,分子对接结果显示 CAP 有可能与氧化应激蛋白、DNA 损伤蛋白和细胞凋亡蛋白结合,为所观察到的有害效应提供了分子机制。因此,我们的研究结果表明,线虫急性接触环境浓度的 CAP 会导致氧化应激、DNA 损伤和细胞凋亡。我们的研究结果为 CAP 的风险评估和管理提供了新的思路。
{"title":"Chlorantraniliprole-induced oxidative stress, DNA damage, and apoptosis in Caenorhabditis elegans: Mechanistic insights and ecological risk implications","authors":"Fengyuan Hu ,&nbsp;Mengzhen Yang ,&nbsp;Shaohua Han ,&nbsp;Guokun Hu ,&nbsp;Xiaoxue Ji ,&nbsp;Kang Qiao","doi":"10.1016/j.ecoenv.2025.118164","DOIUrl":"10.1016/j.ecoenv.2025.118164","url":null,"abstract":"<div><div>Chlorantraniliprole (CAP) is one of the most widely used insecticides in the world. CAP is strictly restricted in foodstuff with maximum residual limits (MRLs) from 0.01 to 40 mg/kg set by Chinese national food safety standard. However, a detailed evaluation on its possible acute toxicity and the underlying mechanisms remains inconclusive. In this study, effects of CAP at environmentally relevant concentrations on growth, locomotion, lifespan, reproduction, and antioxidative defense systems were evaluated using the model organism <em>Caenorhabditis elegans</em>. Exposure to CAP notably reduced nematode development, head thrash, and pharyngeal pumping frequency compared with the control. Moreover, CAP at 0.1, 1, and 10 μg/L decreased lifespan of nematodes by 23.73 %, 28.71 %, and 36.23 %, respectively. CAP at 1 and 10 μg/L enhanced the ROS level, reduced the activity of antioxidative enzyme, including CAT and SOD. CAP also regulated mRNA expression levels of <em>daf-16</em>, <em>skn-1</em>, <em>sod-3</em>, <em>gst-4</em>, <em>ced-3</em>, <em>ced-4</em>, <em>ced-9</em>, <em>egl-1</em>, <em>clk-2</em>, and <em>hus-1</em> in the nematodes, while no significant effect in the mutants was observed. Pearson correlation analysis revealed that significant correlation existed between tested parameters, indicating that CAP caused a series of negative effects in the nematodes. Meanwhile, molecular docking results revealed the potential of CAP to bind with oxidative stress, DNA damage and apoptosis proteins, providing molecular mechanisms for the observed detrimental effects. Therefore, our results suggested that acute exposure to CAP at environmental concentrations caused oxidative stress, DNA damage and apoptosis in the nematodes<em>.</em> Our results shed new light on risk assessment and management of CAP.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118164"},"PeriodicalIF":6.2,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143823558","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
Efficient removal of cadmium (II) and arsenic (III) from water by nano-zero-valent iron modified biochar-zeolite composite
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2025-04-13 DOI: 10.1016/j.ecoenv.2025.118178
Mengyuan Wu , Lijuan Wu , Wen Zhang , Xianbao Zhong , Runfeng Guo , Ziying Cui , Yajun Yang , Jialong Lv
For the removal of Cd(II) and As(III) from water, this study synthesized a nano-zero-valent iron-loaded biochar-zeolite composite material (nZVI-BCZo) using a liquid-phase reduction method, with biochar, zeolite, and FeSO₄·7H₂O as precursors. The successful incorporation of nZVI onto the BCZo was verified through Scanning Electron Microscopy (SEM), X-ray Diffraction (XRD), X-ray Photoelectron Spectroscopy (XPS), and Fourier Transform Infrared Spectroscopy (FTIR) analyses, which revealed significant modifications in the surface oxygen-containing functional groups. Batch adsorption experiments were conducted to evaluate the adsorption characteristics and performance of nZVI-BCZo for Cd(II) and As(III). Under optimal conditions (pH 6.0, temperature of 310 K, and an adsorption time of 360 min), the maximum adsorption capacities for Cd(II) and As(III) were found to be 28.09 mg/g and 186.99 mg/g, respectively. The influence of pH on removal efficiency was more pronounced than that of temperature, with nZVI-BCZo exhibiting a higher affinity for As(III) compared to Cd(II). Kinetic analysis showed that the adsorption process is primarily controlled by chemical adsorption and follows a monolayer adsorption mechanism. Regeneration tests demonstrated that nZVI-BCZo retained good adsorption capacity after three cycles, with adsorption efficiencies of 67.78 % for Cd(II) and 53.04 % for As(III), indicating its potential for repeated use in water treatment applications. The economic evaluation revealed that nZVI-BCZo has a lower processing cost. Therefore, this study established nZVI-BCZo as an efficient, reusable, and cost-effective adsorbent for the treatment of heavy metal-laden water.
{"title":"Efficient removal of cadmium (II) and arsenic (III) from water by nano-zero-valent iron modified biochar-zeolite composite","authors":"Mengyuan Wu ,&nbsp;Lijuan Wu ,&nbsp;Wen Zhang ,&nbsp;Xianbao Zhong ,&nbsp;Runfeng Guo ,&nbsp;Ziying Cui ,&nbsp;Yajun Yang ,&nbsp;Jialong Lv","doi":"10.1016/j.ecoenv.2025.118178","DOIUrl":"10.1016/j.ecoenv.2025.118178","url":null,"abstract":"<div><div>For the removal of Cd(II) and As(III) from water, this study synthesized a nano-zero-valent iron-loaded biochar-zeolite composite material (nZVI-BCZo) using a liquid-phase reduction method, with biochar, zeolite, and FeSO₄·7H₂O as precursors. The successful incorporation of nZVI onto the BCZo was verified through Scanning Electron Microscopy (SEM), X-ray Diffraction (XRD), X-ray Photoelectron Spectroscopy (XPS), and Fourier Transform Infrared Spectroscopy (FTIR) analyses, which revealed significant modifications in the surface oxygen-containing functional groups. Batch adsorption experiments were conducted to evaluate the adsorption characteristics and performance of nZVI-BCZo for Cd(II) and As(III). Under optimal conditions (pH 6.0, temperature of 310 K, and an adsorption time of 360 min), the maximum adsorption capacities for Cd(II) and As(III) were found to be 28.09 mg/g and 186.99 mg/g, respectively. The influence of pH on removal efficiency was more pronounced than that of temperature, with nZVI-BCZo exhibiting a higher affinity for As(III) compared to Cd(II). Kinetic analysis showed that the adsorption process is primarily controlled by chemical adsorption and follows a monolayer adsorption mechanism. Regeneration tests demonstrated that nZVI-BCZo retained good adsorption capacity after three cycles, with adsorption efficiencies of 67.78 % for Cd(II) and 53.04 % for As(III), indicating its potential for repeated use in water treatment applications. The economic evaluation revealed that nZVI-BCZo has a lower processing cost. Therefore, this study established nZVI-BCZo as an efficient, reusable, and cost-effective adsorbent for the treatment of heavy metal-laden water.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118178"},"PeriodicalIF":6.2,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143823557","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
Spatiotemporal dynamics of microcystin contamination in fish across the Lake Chaohu basin under the Yangtze River ten-year fishing ban: Ecological and human health implications 长江十年禁渔期巢湖流域鱼类微囊藻毒素污染的时空动态变化:对生态和人类健康的影响
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2025-04-12 DOI: 10.1016/j.ecoenv.2025.118185
Shengpan Han , Wulai Xia , Jun He , Qianhui Wu , Wenli Xu , Jia Yu , Jun Chen , Ping Xie
Microcystins (MCs), produced by harmful cyanobacterial blooms, pose a threat to aquatic ecosystems and public health in the Yangtze River basin, including Lake Chaohu, which implemented a ten-year fishing ban in 2021 for ecological restoration. This study provides the first basin-wide assessment of MC contamination in fish muscle tissues from Lake Chaohu and its major tributaries during the ban's initial phase (2022–2023), with comparisons to pre-ban data. Using UHPLC-MS/MS, we quantified MC-LR and MC-RR in fish from four trophic levels (planktivorous, omnivorous, herbivorous, and carnivorous). Results revealed that MC-RR was the predominant variant, and planktivorous fish exhibited the highest MC levels, followed by omnivorous, herbivorous, and carnivorous species, reflecting dynamics of trophic transfer. Overall, fish MC concentrations were significantly lower during the ban compared to pre-ban levels, demonstrating positive initial effects. Seasonal analysis revealed higher MC levels in warmer seasons, but detectable MCs persisted during cold seasons, reflecting ongoing contamination. Spatially, while fish in the lake exhibited higher MC concentrations, contamination was also detected in riverine fish, highlighting the basin-wide spread. Despite a lower overall health risk from fish consumption relative to the pre-ban period, high consumption of planktivorous species, especially during warm seasons and in lake regions, may still pose potential health risks. Additionally, MCs likely pose ecological risks to fish populations. These findings provide a crucial baseline for evaluating the long-term effectiveness of the fishing ban and underscore the need for integrated watershed management to safeguard both ecological and public health.
{"title":"Spatiotemporal dynamics of microcystin contamination in fish across the Lake Chaohu basin under the Yangtze River ten-year fishing ban: Ecological and human health implications","authors":"Shengpan Han ,&nbsp;Wulai Xia ,&nbsp;Jun He ,&nbsp;Qianhui Wu ,&nbsp;Wenli Xu ,&nbsp;Jia Yu ,&nbsp;Jun Chen ,&nbsp;Ping Xie","doi":"10.1016/j.ecoenv.2025.118185","DOIUrl":"10.1016/j.ecoenv.2025.118185","url":null,"abstract":"<div><div>Microcystins (MCs), produced by harmful cyanobacterial blooms, pose a threat to aquatic ecosystems and public health in the Yangtze River basin, including Lake Chaohu, which implemented a ten-year fishing ban in 2021 for ecological restoration. This study provides the first basin-wide assessment of MC contamination in fish muscle tissues from Lake Chaohu and its major tributaries during the ban's initial phase (2022–2023), with comparisons to pre-ban data. Using UHPLC-MS/MS, we quantified MC-LR and MC-RR in fish from four trophic levels (planktivorous, omnivorous, herbivorous, and carnivorous). Results revealed that MC-RR was the predominant variant, and planktivorous fish exhibited the highest MC levels, followed by omnivorous, herbivorous, and carnivorous species, reflecting dynamics of trophic transfer. Overall, fish MC concentrations were significantly lower during the ban compared to pre-ban levels, demonstrating positive initial effects. Seasonal analysis revealed higher MC levels in warmer seasons, but detectable MCs persisted during cold seasons, reflecting ongoing contamination. Spatially, while fish in the lake exhibited higher MC concentrations, contamination was also detected in riverine fish, highlighting the basin-wide spread. Despite a lower overall health risk from fish consumption relative to the pre-ban period, high consumption of planktivorous species, especially during warm seasons and in lake regions, may still pose potential health risks. Additionally, MCs likely pose ecological risks to fish populations. These findings provide a crucial baseline for evaluating the long-term effectiveness of the fishing ban and underscore the need for integrated watershed management to safeguard both ecological and public health.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118185"},"PeriodicalIF":6.2,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143821277","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
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Ecotoxicology and Environmental Safety
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