Pub Date : 2025-04-23DOI: 10.1016/j.ecoenv.2025.118169
Mengwei Han , Jinlong Lai , Yongbing Zhu , Bin Dong , Qing Wang, Sanping Zhao
High concentrations of energetic compounds in soil pose a serious threat to the ecology and human health. In this study, a combination of plant–microbe remediation was used to remediate soil contaminated with high TNT concentrations. This study aimed to reveal the remediation efficiency, metabolic potential, and microbial community structure in high-concentration TNT-contaminated soils following combined remediation. Five plants and microorganisms were combined to remediate soil contaminated with high concentrations of TNT (1434 mg/kg). The TNT residues in the soil were only 69–125 mg/kg after 60 days. The combined plant-microbe remediation enhanced the soil nitrogen cycle, carbon cycle, and phosphorus metabolism. Untargeted metabolome gas chromatography-mass spectrometry analysis showed that the combined remediation restored fatty acid metabolism, amino acid metabolism, and sugar metabolism pathways in TNT-contaminated soil. Subsequent 16S rRNA diversity analysis showed that the combined microbial agents occupied soil ecological niches. Interaction network analysis showed that phytomicrobial remediation improved the rate of recovery of TNT-contaminated soil by reshaping the microbial structure and metabolic cycles.
{"title":"The mechanism of plants and effective microorganisms combined remediation of heavily TNT-contaminated soil","authors":"Mengwei Han , Jinlong Lai , Yongbing Zhu , Bin Dong , Qing Wang, Sanping Zhao","doi":"10.1016/j.ecoenv.2025.118169","DOIUrl":"10.1016/j.ecoenv.2025.118169","url":null,"abstract":"<div><div>High concentrations of energetic compounds in soil pose a serious threat to the ecology and human health. In this study, a combination of plant–microbe remediation was used to remediate soil contaminated with high TNT concentrations. This study aimed to reveal the remediation efficiency, metabolic potential, and microbial community structure in high-concentration TNT-contaminated soils following combined remediation. Five plants and microorganisms were combined to remediate soil contaminated with high concentrations of TNT (1434 mg/kg). The TNT residues in the soil were only 69–125 mg/kg after 60 days. The combined plant-microbe remediation enhanced the soil nitrogen cycle, carbon cycle, and phosphorus metabolism. Untargeted metabolome gas chromatography-mass spectrometry analysis showed that the combined remediation restored fatty acid metabolism, amino acid metabolism, and sugar metabolism pathways in TNT-contaminated soil. Subsequent 16S rRNA diversity analysis showed that the combined microbial agents occupied soil ecological niches. Interaction network analysis showed that phytomicrobial remediation improved the rate of recovery of TNT-contaminated soil by reshaping the microbial structure and metabolic cycles.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"297 ","pages":"Article 118169"},"PeriodicalIF":6.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859599","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}
Pub Date : 2025-04-23DOI: 10.1016/j.ecoenv.2025.118195
Jackson Nkoh Nkoh , Ting Ye , Chenjing Shang , Chunyuan Li , Jianguang Tu , Sihui Li , Zuping Wu , Pengyu Chen , Quaid Hussain , Seraphine Nkie Esemu
Environmental pollution severely affects ecological functions/health, and nondegradable pollutants such as heavy metals (HMs) cause significant damage to living organisms. Escherichia coli is one of the most studied life forms, and its response to oxidative stress is driven by a complex ensemble of mechanisms driven by transcriptomic-level adjustments. However, the magnitude of the physiological, metabolic, and biochemical alterations and their relationships with transcriptomic changes remain unclear. Studying the growth of E. coli in Cd-, Cu-, and Ni-polluted media at pH 5.0, we observed that (i) downregulation of the alkyl hydroperoxide complex, glutathione reductase, and glutathione S-transferase by Cd inhibited H2O2 degradation, and the accumulated H2O2 was respectively 2.7, 1.7, and 2.4 times greater than that in the control, Cu, and Ni treatments; (ii) Zn-associated resistance protein (ZraP) was the major scavenger of Cd, with a 140.7-fold increase in its expression; (iii) the P-type Cu+ transporter (CopA), multicopper oxidase (CueO), and heteromultimeric transport system (CusCBAF) controlled the excretion and detoxification of Cu; (iv) the Cd2+/Zn2+/Pb2+-exporting P-type ATPase (ZntA) and transcriptional activator ZntR were the major transporters of Ni; (v) Cd upregulated biofilm formation and synthesis of secondary metabolites more than Cu and Ni, which resulted in increased adsorption and improved tolerance; and (vi) the activity of superoxide dismutase in Cu-spiked cells was 153.2 %, 141.7 %, and 172.7 % higher and corresponded to 85.7 %, 524.5 %, and 491.5 % lower O2●⁻ in the control, Cd-, and Ni-spiked cells, respectively. This study reveals E. coli's preferential tolerance mechanisms to Cd rather than Cu and Ni and demonstrates mechanisms for its survival in highly polluted environments.
环境污染严重影响生态功能/健康，重金属等不可降解污染物对生物造成重大损害。大肠杆菌是研究最多的生命形式之一，其对氧化应激的反应是由转录组水平调节驱动的复杂机制集合驱动的。然而，生理、代谢和生化变化的幅度及其与转录组变化的关系仍不清楚。研究了大肠杆菌在pH 5.0、Cd、Cu和Ni污染的培养基中的生长情况，发现(1)Cd对烷基过氧化氢复合物、谷胱甘肽还原酶和谷胱甘肽s -转移酶的下调抑制了H2O2的降解，H2O2的累积量分别是对照、Cu和Ni处理的2.7倍、1.7倍和2.4倍；（ii） Zn-associated resistance protein （ZraP）是主要的Cd清道夫，其表达量增加了140.7倍；（iii） p型铜转运体（CopA）、多铜氧化酶（CueO）和异多聚转运系统（CusCBAF）控制着铜的排泄和解毒；（iv） Cd2+/Zn2+/Pb2+输出p型atp酶（ZntA）和转录激活剂ZntR是Ni的主要转运体；(v) Cd比Cu和Ni更能上调生物膜的形成和次生代谢物的合成，从而导致吸附增加和耐受性提高；（vi） cu -毒化细胞的超氧化物歧化酶活性比O2 -毒化细胞高153.2 %、141.7 %和172.7 %，与对照、Cd-毒化细胞和ni -毒化细胞的超氧化物歧化酶活性分别低85.7 %、524.5 %和491.5 %。本研究揭示了大肠杆菌对镉的优先耐受机制，而不是对铜和镍的优先耐受机制，并揭示了其在高污染环境中的生存机制。
{"title":"Deciphering the mechanisms for preferential tolerance of Escherichia coli BL21 to Cd(II) over Cu(II) and Ni(II): A combined physiological, biochemical, and multiomics perspective","authors":"Jackson Nkoh Nkoh , Ting Ye , Chenjing Shang , Chunyuan Li , Jianguang Tu , Sihui Li , Zuping Wu , Pengyu Chen , Quaid Hussain , Seraphine Nkie Esemu","doi":"10.1016/j.ecoenv.2025.118195","DOIUrl":"10.1016/j.ecoenv.2025.118195","url":null,"abstract":"<div><div>Environmental pollution severely affects ecological functions/health, and nondegradable pollutants such as heavy metals (HMs) cause significant damage to living organisms. <em>Escherichia coli</em> is one of the most studied life forms, and its response to oxidative stress is driven by a complex ensemble of mechanisms driven by transcriptomic-level adjustments. However, the magnitude of the physiological, metabolic, and biochemical alterations and their relationships with transcriptomic changes remain unclear. Studying the growth of <em>E. coli</em> in Cd-, Cu-, and Ni-polluted media at pH 5.0, we observed that (i) downregulation of the alkyl hydroperoxide complex, glutathione reductase, and glutathione S-transferase by Cd inhibited H<sub>2</sub>O<sub>2</sub> degradation, and the accumulated H<sub>2</sub>O<sub>2</sub> was respectively 2.7, 1.7, and 2.4 times greater than that in the control, Cu, and Ni treatments; (ii) Zn-associated resistance protein (ZraP) was the major scavenger of Cd, with a 140.7-fold increase in its expression; (iii) the P-type Cu<sup>+</sup> transporter (CopA), multicopper oxidase (CueO), and heteromultimeric transport system (CusCBAF) controlled the excretion and detoxification of Cu; (iv) the Cd<sup>2+</sup>/Zn<sup>2+</sup>/Pb<sup>2+</sup>-exporting P-type ATPase (ZntA) and transcriptional activator ZntR were the major transporters of Ni; (v) Cd upregulated biofilm formation and synthesis of secondary metabolites more than Cu and Ni, which resulted in increased adsorption and improved tolerance; and (vi) the activity of superoxide dismutase in Cu-spiked cells was 153.2 %, 141.7 %, and 172.7 % higher and corresponded to 85.7 %, 524.5 %, and 491.5 % lower O<sub>2</sub><sup>●</sup>⁻ in the control, Cd-, and Ni-spiked cells, respectively. This study reveals <em>E. coli</em>'s preferential tolerance mechanisms to Cd rather than Cu and Ni and demonstrates mechanisms for its survival in highly polluted environments.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"297 ","pages":"Article 118195"},"PeriodicalIF":6.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143863323","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}
Pub Date : 2025-04-22DOI: 10.1016/j.ecoenv.2025.118213
Yi Tian , Liping Li , Zhongmou Sun , Jiamin Liu , Chen Qiu , Ji Zhou , Xinghuai Sun , Yuan Lei
This study aims to investigate the influence of ozone exposure on mouse corneas and human corneal epithelial cells (HCEC) to better understand its impact on corneal health and the underlying molecular mechanisms. Elevated cyclic ozone exposure was applied to both mouse corneas and HCECs to assess its effects on corneal structure and cellular response. Ozone exposure induced corneal stromal thinning (27.88 %), increased epithelial thickness (22.44 %), and disrupted epithelial barrier function. Inflammatory responses and nitrative stress, marked by inflammatory cell infiltration and heightened 3-nitrotyrosine levels, coupled with the upregulation of NLRP3, caspase-1 were observed in mice cornea. Additionally, ozone exposure induced diminished cell viability, nitrative stress, and activation of the NLRP3/caspase-1/GSDMD pathway in HCECs, which were mitigated by anti-nitration agent MnTMPyP treatment. In summary, the study elucidated the mechanisms underlying ozone-induced corneal toxicity, highlighting nitrative stress and NLRP3 inflammasome-mediated pyroptosis. These findings suggest the importance of minimizing ozone exposure and also provide potential therapeutic strategies targeting nitrative stress and inflammasome activation to prevent ozone-related tissue damage.
{"title":"Decoding ozone's impact on the cornea: disruption of barrier integrity and its molecular drivers","authors":"Yi Tian , Liping Li , Zhongmou Sun , Jiamin Liu , Chen Qiu , Ji Zhou , Xinghuai Sun , Yuan Lei","doi":"10.1016/j.ecoenv.2025.118213","DOIUrl":"10.1016/j.ecoenv.2025.118213","url":null,"abstract":"<div><div>This study aims to investigate the influence of ozone exposure on mouse corneas and human corneal epithelial cells (HCEC) to better understand its impact on corneal health and the underlying molecular mechanisms. Elevated cyclic ozone exposure was applied to both mouse corneas and HCECs to assess its effects on corneal structure and cellular response. Ozone exposure induced corneal stromal thinning (27.88 %), increased epithelial thickness (22.44 %), and disrupted epithelial barrier function. Inflammatory responses and nitrative stress, marked by inflammatory cell infiltration and heightened 3-nitrotyrosine levels, coupled with the upregulation of NLRP3, caspase-1 were observed in mice cornea. Additionally, ozone exposure induced diminished cell viability, nitrative stress, and activation of the NLRP3/caspase-1/GSDMD pathway in HCECs, which were mitigated by anti-nitration agent MnTMPyP treatment. In summary, the study elucidated the mechanisms underlying ozone-induced corneal toxicity, highlighting nitrative stress and NLRP3 inflammasome-mediated pyroptosis. These findings suggest the importance of minimizing ozone exposure and also provide potential therapeutic strategies targeting nitrative stress and inflammasome activation to prevent ozone-related tissue damage.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118213"},"PeriodicalIF":6.2,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855255","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}
Pub Date : 2025-04-22DOI: 10.1016/j.ecoenv.2025.118188
Ziang Guo , Yuxuan Tan , Chuhang Lin , Haiying Li , Qianqian Xie , Zhengtian Lai , Xiao Liang , Lei Tan , Chunxia Jing
Background
The evidence linking endocrine-disrupting chemicals (EDCs) to anxiety in adults is currently sparse, while the effects of various categories of EDCs on the risk of anxiety, along with the underlying mechanisms, remain poorly understood.
Methods
Four EDCs—polycyclic aromatic hydrocarbons (PAHs), phenols, pesticides, and phthalates—were quantified in 3927 adults from the National Health and Nutrition Examination Survey (NHANES) (2007–2012). We employed five statistical models to assess the individual and joint impacts of EDCs on anxiety risk. Causal mediation analysis frameworks were constructed to explore the mediating role of oxidative stress (OS). We identified potential biological mechanisms linking analytes to outcomes using the Comparative Toxicogenomics Database (CTD), MalaCards, and Open Targets, followed by enrichment analyses with Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG).
Results
In individual chemical analyses, nine PAHs were significantly associated with increased anxiety risk (P < 0.05). Mixed-effects analyses showed that co-exposure to EDCs positively correlated with anxiety, primarily due to 2-hydroxyfluorene (2-FLU) and 3-hydroxyfluorene (3-FLU). Bilirubin mediated 5.42 % of the anxiety linked to the PAH mixture. The inflammatory genes TNF and IL-6 were identified as key biological stressors, with enrichment analysis indicating significant involvement in reactive oxygen species metabolic processes and the AGE-RAGE signaling pathway.
Conclusion
This study highlights the association between EDCs and anxiety in a representative U.S. population, indicating that exposure to PAHs may elevate anxiety risk through OS, inflammation, and the AGE-RAGE signaling pathway. Further longitudinal study were merited to support our results.
{"title":"Unraveling the connection between endocrine-disrupting chemicals and anxiety: An integrative epidemiological and bioinformatic perspective","authors":"Ziang Guo , Yuxuan Tan , Chuhang Lin , Haiying Li , Qianqian Xie , Zhengtian Lai , Xiao Liang , Lei Tan , Chunxia Jing","doi":"10.1016/j.ecoenv.2025.118188","DOIUrl":"10.1016/j.ecoenv.2025.118188","url":null,"abstract":"<div><h3>Background</h3><div>The evidence linking endocrine-disrupting chemicals (EDCs) to anxiety in adults is currently sparse, while the effects of various categories of EDCs on the risk of anxiety, along with the underlying mechanisms, remain poorly understood.</div></div><div><h3>Methods</h3><div>Four EDCs—polycyclic aromatic hydrocarbons (PAHs), phenols, pesticides, and phthalates—were quantified in 3927 adults from the National Health and Nutrition Examination Survey (NHANES) (2007–2012). We employed five statistical models to assess the individual and joint impacts of EDCs on anxiety risk. Causal mediation analysis frameworks were constructed to explore the mediating role of oxidative stress (OS). We identified potential biological mechanisms linking analytes to outcomes using the Comparative Toxicogenomics Database (CTD), MalaCards, and Open Targets, followed by enrichment analyses with Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG).</div></div><div><h3>Results</h3><div>In individual chemical analyses, nine PAHs were significantly associated with increased anxiety risk (<em>P</em> < 0.05). Mixed-effects analyses showed that co-exposure to EDCs positively correlated with anxiety, primarily due to 2-hydroxyfluorene (2-FLU) and 3-hydroxyfluorene (3-FLU). Bilirubin mediated 5.42 % of the anxiety linked to the PAH mixture. The inflammatory genes TNF and IL-6 were identified as key biological stressors, with enrichment analysis indicating significant involvement in reactive oxygen species metabolic processes and the AGE-RAGE signaling pathway.</div></div><div><h3>Conclusion</h3><div>This study highlights the association between EDCs and anxiety in a representative U.S. population, indicating that exposure to PAHs may elevate anxiety risk through OS, inflammation, and the AGE-RAGE signaling pathway. Further longitudinal study were merited to support our results.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118188"},"PeriodicalIF":6.2,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855257","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}
Pub Date : 2025-04-22DOI: 10.1016/j.ecoenv.2025.118199
Mingkai Huang , Junjie Wen , Chenyang Lu , Xuliang Cai , Changxing Ou , Zhenan Deng , Xinyi Huang , Enli Zhang , Kian Fan Chung , Jie Yan , Nanshan Zhong , Qingling Zhang
Background
The relationship between residential greenness and asthma remains a topic of interest, especially in understanding the pathways involved and how genetic factors might influence this association. This study aimed to explore the association between residential greenness and asthma incidence, while also examining potential mediating pathways and the role of genetic susceptibility.
Methods
Data were analyzed from two independent cohorts: the UK Biobank and the Chinese Biomarkers for the Prediction of Respiratory Disease Outcomes (C-BIOPRED) study. Greenness was measured by normalized difference vegetation index (NDVI). Polygenic risk scores were constructed from 145 asthma-associated single nucleotide polymorphisms. Cox proportional hazard models and logistics regression models were used to assess the association between residential greenness and asthma incidence, and mediation analysis was conducted to explore potential mediators.
Results
Over a median follow-up of 11.85 years in UK Biobank, higher NDVI exposure was associated with reduced asthma incidence (hazard ratio per IQR increase in NDVI300 m: 0.965, 95 % CI: 0.949–0.982). The association was more pronounced among non-smokers and individuals with highest genetic risk. PM2.5 mediated 40.4 % (95 % CI: 5.1 %–76.4 %) of the protective effect. In the C-BIOPRED study, greenness was inversely associated with severe asthma (odd ratio: 0.645, 95 % CI: 0.441–0.943) and improved clinical outcomes.
Conclusion
Residential greenness is associated with a lower risk of asthma, particularly in genetically susceptible and socioeconomically disadvantaged populations, partially through improving air quality. Our findings advocate for integrating green space optimization into urban planning as a precision public health strategy.
{"title":"Residential greenness, genetic susceptibility, and asthma risk: Mediating roles of air pollution in UK and Chinese populations","authors":"Mingkai Huang , Junjie Wen , Chenyang Lu , Xuliang Cai , Changxing Ou , Zhenan Deng , Xinyi Huang , Enli Zhang , Kian Fan Chung , Jie Yan , Nanshan Zhong , Qingling Zhang","doi":"10.1016/j.ecoenv.2025.118199","DOIUrl":"10.1016/j.ecoenv.2025.118199","url":null,"abstract":"<div><h3>Background</h3><div>The relationship between residential greenness and asthma remains a topic of interest, especially in understanding the pathways involved and how genetic factors might influence this association. This study aimed to explore the association between residential greenness and asthma incidence, while also examining potential mediating pathways and the role of genetic susceptibility.</div></div><div><h3>Methods</h3><div>Data were analyzed from two independent cohorts: the UK Biobank and the Chinese Biomarkers for the Prediction of Respiratory Disease Outcomes (C-BIOPRED) study. Greenness was measured by normalized difference vegetation index (NDVI). Polygenic risk scores were constructed from 145 asthma-associated single nucleotide polymorphisms. Cox proportional hazard models and logistics regression models were used to assess the association between residential greenness and asthma incidence, and mediation analysis was conducted to explore potential mediators.</div></div><div><h3>Results</h3><div>Over a median follow-up of 11.85 years in UK Biobank, higher NDVI exposure was associated with reduced asthma incidence (hazard ratio per IQR increase in NDVI<sub>300 m</sub>: 0.965, 95 % CI: 0.949–0.982). The association was more pronounced among non-smokers and individuals with highest genetic risk. PM<sub>2.5</sub> mediated 40.4 % (95 % CI: 5.1 %–76.4 %) of the protective effect. In the C-BIOPRED study, greenness was inversely associated with severe asthma (odd ratio: 0.645, 95 % CI: 0.441–0.943) and improved clinical outcomes.</div></div><div><h3>Conclusion</h3><div>Residential greenness is associated with a lower risk of asthma, particularly in genetically susceptible and socioeconomically disadvantaged populations, partially through improving air quality. Our findings advocate for integrating green space optimization into urban planning as a precision public health strategy.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118199"},"PeriodicalIF":6.2,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859473","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}
Pub Date : 2025-04-21DOI: 10.1016/j.ecoenv.2025.118218
Xiangbin You , Zhuo Zhang , Guijuan Tian , Yapei Zhang , Yanru Pei , Yanxue Wu , Gan Li , Qiankun Wang , Youbing Yang
The widespread presence of polystyrene microplastics in the environment, and their significant accumulation, has led to their recognition as a major global ecological problem. There has been a lot of research on how microplastics affect the physiology of aquatic species, but less research on the mechanism of the impact on livestock and poultry microplastics. This paper primarily investigates the negative consequences of microplastic exposure on the health of quail and explores the underlying mechanisms. The study revealed that exposure to polystyrene microplastics notably decreased the body weight, growth rate, and muscle quality of quail. Histopathological analysis indicated significant damage in the liver, lungs, and testicles of quail exposed to microplastics. Furthermore, microplastics reduced the antioxidant capacity of quail and upregulated the expression of inflammatory factors, suggesting the induction of oxidative stress and inflammatory responses. Alterations in the composition and abundance of gut microbes were also observed in quail exposed to polystyrene microplastics; and found an increased abundance of potentially pro-inflammatory bacteria. In conclusion, the findings demonstrate that microplastics have adverse effects on quail health by impacting growth performance, oxidative stress, inflammatory responses, and gut microflora balance.
{"title":"The impact of polyethylene microplastics exposure on the, growth performance, reproductive performance, antioxidant capacity, and intestinal microbiota of quails","authors":"Xiangbin You , Zhuo Zhang , Guijuan Tian , Yapei Zhang , Yanru Pei , Yanxue Wu , Gan Li , Qiankun Wang , Youbing Yang","doi":"10.1016/j.ecoenv.2025.118218","DOIUrl":"10.1016/j.ecoenv.2025.118218","url":null,"abstract":"<div><div>The widespread presence of polystyrene microplastics in the environment, and their significant accumulation, has led to their recognition as a major global ecological problem. There has been a lot of research on how microplastics affect the physiology of aquatic species, but less research on the mechanism of the impact on livestock and poultry microplastics. This paper primarily investigates the negative consequences of microplastic exposure on the health of quail and explores the underlying mechanisms. The study revealed that exposure to polystyrene microplastics notably decreased the body weight, growth rate, and muscle quality of quail. Histopathological analysis indicated significant damage in the liver, lungs, and testicles of quail exposed to microplastics. Furthermore, microplastics reduced the antioxidant capacity of quail and upregulated the expression of inflammatory factors, suggesting the induction of oxidative stress and inflammatory responses. Alterations in the composition and abundance of gut microbes were also observed in quail exposed to polystyrene microplastics; and found an increased abundance of potentially pro-inflammatory bacteria. In conclusion, the findings demonstrate that microplastics have adverse effects on quail health by impacting growth performance, oxidative stress, inflammatory responses, and gut microflora balance.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118218"},"PeriodicalIF":6.2,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855091","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}
Pub Date : 2025-04-21DOI: 10.1016/j.ecoenv.2025.118203
Yuan Lin , Qiuping Zhang , Lu Chen , Yingying Liu , Xiaoxi Lin , Xiaoyan Peng , Hua Cao , Yuqing Lei , Xinrui Wang
Neomycin, a widely used aminoglycoside antibiotic, poses potential risks to organism and the environment that remain incompletely evaluated. This study systematically evaluates its toxic effects on zebrafish embryos across physiological, cellular, molecular, and behavioral dimensions. At the physiological level, neomycin exposure induces severe developmental abnormalities, including yolk sac edema, reduced body length, and craniofacial malformations. Developmental disorders of the cardiovascular and hematopoietic systems are confirmed in exposed larvae. In addition, zebrafish larvae exposed to neomycin exhibit significant locomotor deficits, including reduced swimming speed, distance traveled, and impaired responsiveness to light-dark stimulation, indicating reduced activity. Mechanically, neomycin triggers oxidative stress through a dose-dependent elevation of reactive oxygen species (ROS) levels and induces cellular apoptosis through the PI3K/Akt signaling pathway. Collectively, our findings demonstrate that neomycin exerts toxic effects on zebrafish embryonic development, highlighting concerns regarding neomycin exposure risks during early pregnancy and providing critical insights into its potential environmental hazards.
{"title":"Neomycin affects cardiovascular and hematopoietic system via the PI3K/Akt pathway in zebrafish larvae","authors":"Yuan Lin , Qiuping Zhang , Lu Chen , Yingying Liu , Xiaoxi Lin , Xiaoyan Peng , Hua Cao , Yuqing Lei , Xinrui Wang","doi":"10.1016/j.ecoenv.2025.118203","DOIUrl":"10.1016/j.ecoenv.2025.118203","url":null,"abstract":"<div><div>Neomycin, a widely used aminoglycoside antibiotic, poses potential risks to organism and the environment that remain incompletely evaluated. This study systematically evaluates its toxic effects on zebrafish embryos across physiological, cellular, molecular, and behavioral dimensions. At the physiological level, neomycin exposure induces severe developmental abnormalities, including yolk sac edema, reduced body length, and craniofacial malformations. Developmental disorders of the cardiovascular and hematopoietic systems are confirmed in exposed larvae. In addition, zebrafish larvae exposed to neomycin exhibit significant locomotor deficits, including reduced swimming speed, distance traveled, and impaired responsiveness to light-dark stimulation, indicating reduced activity. Mechanically, neomycin triggers oxidative stress through a dose-dependent elevation of reactive oxygen species (ROS) levels and induces cellular apoptosis through the PI3K/Akt signaling pathway. Collectively, our findings demonstrate that neomycin exerts toxic effects on zebrafish embryonic development, highlighting concerns regarding neomycin exposure risks during early pregnancy and providing critical insights into its potential environmental hazards.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118203"},"PeriodicalIF":6.2,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855253","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}
Pub Date : 2025-04-21DOI: 10.1016/j.ecoenv.2025.118196
Seul-Gi Lee , Yoonseo Kim , Sang Woong Park , Min Woo Kim , Jeong-Seop Oh , Shinhye Park , Suemin Lee , Yun Hyeong Lee , Youngin Jeong , Jeong Hwan Park , Myeonghee Lee , Hyewon Shin , Seeun Kim , Young Min Bae , C-Yoon Kim , Hyung Min Chung
Phthalates, known as plasticizers, are endocrine disruptor, and their risks are being highlighted as their use increases worldwide. Di-2-ethylhexyl phthalate (DEHP), the most prevalent of the phthalates, is known to be toxic to humans, and it has recently been reported to be linked to cardiotoxicity. Although many other phthalates are also widely used, data on their cardiotoxic effects are yet to be well established. In this study, we assessed the cardiotoxic potential of various phthalates using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and a microelectrode array-based dual-cardiotoxicity evaluation method previously reported. Cytotoxicity results showed that acute exposure to DEHP, dibutyl phthalate (DBP), benzyl butyl phthalate (BBP), and di-n-octyl phthalate (DnOP) did not affect the viability of hiPSC-CMs. Before examining the functional changes in hiPSC-CMs caused by exposure to these four phthalates, we present changes in field potential (FP) and contractility based on the blocking of major ions for reference. Contrary to concerns, FP results showed a dramatic decrease in spike amplitude, beat period, and FP duration (FPD) at high doses of DBP and BBP rather than DEHP. Interestingly, DnOP resulted in a prolonged FPD, unlike the others. Furthermore, contractility results indicated that, unlike DEHP and DnOP, high doses of DBP and BBP caused beating arrest along with decreased beat amplitude. Overall, this study demonstrated that phthalates other than DEHP can also induce cardiotoxicity, even with acute exposure. It is expected that the application of the established evaluation method will facilitate the development of safe alternatives.
{"title":"Evaluation of phthalates induced cardiotoxicity using human iPSCs-derived cardiomyocyte and dual-cardiotoxicity evaluation methods","authors":"Seul-Gi Lee , Yoonseo Kim , Sang Woong Park , Min Woo Kim , Jeong-Seop Oh , Shinhye Park , Suemin Lee , Yun Hyeong Lee , Youngin Jeong , Jeong Hwan Park , Myeonghee Lee , Hyewon Shin , Seeun Kim , Young Min Bae , C-Yoon Kim , Hyung Min Chung","doi":"10.1016/j.ecoenv.2025.118196","DOIUrl":"10.1016/j.ecoenv.2025.118196","url":null,"abstract":"<div><div>Phthalates, known as plasticizers, are endocrine disruptor, and their risks are being highlighted as their use increases worldwide. Di-2-ethylhexyl phthalate (DEHP), the most prevalent of the phthalates, is known to be toxic to humans, and it has recently been reported to be linked to cardiotoxicity. Although many other phthalates are also widely used, data on their cardiotoxic effects are yet to be well established. In this study, we assessed the cardiotoxic potential of various phthalates using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and a microelectrode array-based dual-cardiotoxicity evaluation method previously reported. Cytotoxicity results showed that acute exposure to DEHP, dibutyl phthalate (DBP), benzyl butyl phthalate (BBP), and di-n-octyl phthalate (DnOP) did not affect the viability of hiPSC-CMs. Before examining the functional changes in hiPSC-CMs caused by exposure to these four phthalates, we present changes in field potential (FP) and contractility based on the blocking of major ions for reference. Contrary to concerns, FP results showed a dramatic decrease in spike amplitude, beat period, and FP duration (FPD) at high doses of DBP and BBP rather than DEHP. Interestingly, DnOP resulted in a prolonged FPD, unlike the others. Furthermore, contractility results indicated that, unlike DEHP and DnOP, high doses of DBP and BBP caused beating arrest along with decreased beat amplitude. Overall, this study demonstrated that phthalates other than DEHP can also induce cardiotoxicity, even with acute exposure. It is expected that the application of the established evaluation method will facilitate the development of safe alternatives.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118196"},"PeriodicalIF":6.2,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143852278","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}
Pub Date : 2025-04-21DOI: 10.1016/j.ecoenv.2025.118214
Sae Woong Oh , Eunbi Yu , See-Hyoung Park , Kitae Kwon , Jung Hyun Lee , Heejun Ha , Gyeonghyeon Kim , Hee Seon Shin , Seokhyeon Min , Minkyung Song , Jae Youl Cho , Jongsung Lee
Ammonium chloride is an indoor environmental pollutant released due to industrial emissions, concrete, indoor bacteria, or other sources. In this study, we characterized molecular mechanisms of ammonium chloride-induced cell damage in melanocyte cells, which are a critical effector for pigmentation. Specifically, we investigated the effects of ammonium chloride on pigmentation and its underlying mechanisms, including its involvement in melanogenesis and autophagy. Based on the experiments, we elucidated that ammonium chloride induced and increased melanogenesis by upregulating MITF via AKT-mediated melanogenic signaling pathways. Moreover, ammonium chloride did not exhibit lysosomotropic activity and inhibited autophagy by activating the AKT-mTOR signaling pathway, suggesting that the pigment-regulating mechanism of ammonium chloride was associated with autophagy in pigmented cells. The findings of this study offer new perspectives on the mechanisms involved in ammonium chloride-induced pigmentation and propose a potential approach to mitigate ammonium chloride-induced side effects like hyperpigmentation and hyperammonemia by employing a combined autophagy inducer.
{"title":"Ammonium chloride, an environmental pollutant, disrupts melanocyte biology through the regulation of melanosome and autophagy","authors":"Sae Woong Oh , Eunbi Yu , See-Hyoung Park , Kitae Kwon , Jung Hyun Lee , Heejun Ha , Gyeonghyeon Kim , Hee Seon Shin , Seokhyeon Min , Minkyung Song , Jae Youl Cho , Jongsung Lee","doi":"10.1016/j.ecoenv.2025.118214","DOIUrl":"10.1016/j.ecoenv.2025.118214","url":null,"abstract":"<div><div>Ammonium chloride is an indoor environmental pollutant released due to industrial emissions, concrete, indoor bacteria, or other sources. In this study, we characterized molecular mechanisms of ammonium chloride-induced cell damage in melanocyte cells, which are a critical effector for pigmentation. Specifically, we investigated the effects of ammonium chloride on pigmentation and its underlying mechanisms, including its involvement in melanogenesis and autophagy. Based on the experiments, we elucidated that ammonium chloride induced and increased melanogenesis by upregulating MITF via AKT-mediated melanogenic signaling pathways. Moreover, ammonium chloride did not exhibit lysosomotropic activity and inhibited autophagy by activating the AKT-mTOR signaling pathway, suggesting that the pigment-regulating mechanism of ammonium chloride was associated with autophagy in pigmented cells. The findings of this study offer new perspectives on the mechanisms involved in ammonium chloride-induced pigmentation and propose a potential approach to mitigate ammonium chloride-induced side effects like hyperpigmentation and hyperammonemia by employing a combined autophagy inducer.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118214"},"PeriodicalIF":6.2,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143852279","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}
Pub Date : 2025-04-21DOI: 10.1016/j.ecoenv.2025.118208
Agnes Schöndorfer , Sara Kolbenschlag , Peer Bauspiess , Jens Schirmel , Eric Bollinger , Alessandro Manfrin , Mirco Bundschuh
Aquatic biomass and essential nutrients can subsidize terrestrial food webs. However, stressors in the aquatic ecosystem, such as the non-chemical mosquito control agent Bti (Bacillus thuringiensis israelensis), may affect such subsidies by changing the dynamics and diversity of emergent aquatic insects. Such changes in emergence phenology may influence riparian predators with consequences for the terrestrial food web. Here we asked whether repeated Bti application over four consecutive vegetative periods cause similar impacts over these years (i.e., 2020–2023). We used floodplain pond mesocosms and measured insect emergence from control and Bti-treated ponds between April and August in each year. We found significant effects on insect emergence dynamics and community composition only during the first year. This effect disappeared over the three following years. Our observations suggest a shift in community composition, for example, by replacing more Bti-sensitive (i.e., Chironomidae) with more tolerant insect species – a hypothesis that is partially supported by changes in the wider community of emergent aquatic insects during the study. Alternatively, a reduced Bti activity could explain this pattern: The activity could be affected by changes in environmental factors such as the accumulation of organic carbon and fine sediment. All in all, our data point to a higher annual variability in insect emergence dynamics and the community of emergent aquatic insects relative to the impacts caused by Bti.
{"title":"Long-term consequences of Bti applications on aquatic insect emergence: Insights from a 4-year mesocosm study","authors":"Agnes Schöndorfer , Sara Kolbenschlag , Peer Bauspiess , Jens Schirmel , Eric Bollinger , Alessandro Manfrin , Mirco Bundschuh","doi":"10.1016/j.ecoenv.2025.118208","DOIUrl":"10.1016/j.ecoenv.2025.118208","url":null,"abstract":"<div><div>Aquatic biomass and essential nutrients can subsidize terrestrial food webs. However, stressors in the aquatic ecosystem, such as the non-chemical mosquito control agent Bti (<em>Bacillus thuringiensis israelensis</em>), may affect such subsidies by changing the dynamics and diversity of emergent aquatic insects. Such changes in emergence phenology may influence riparian predators with consequences for the terrestrial food web. Here we asked whether repeated Bti application over four consecutive vegetative periods cause similar impacts over these years (i.e., 2020–2023). We used floodplain pond mesocosms and measured insect emergence from control and Bti-treated ponds between April and August in each year. We found significant effects on insect emergence dynamics and community composition only during the first year. This effect disappeared over the three following years. Our observations suggest a shift in community composition, for example, by replacing more Bti-sensitive (i.e., Chironomidae) with more tolerant insect species – a hypothesis that is partially supported by changes in the wider community of emergent aquatic insects during the study. Alternatively, a reduced Bti activity could explain this pattern: The activity could be affected by changes in environmental factors such as the accumulation of organic carbon and fine sediment. All in all, our data point to a higher annual variability in insect emergence dynamics and the community of emergent aquatic insects relative to the impacts caused by Bti.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"296 ","pages":"Article 118208"},"PeriodicalIF":6.2,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855254","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}
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