Pub Date : 2025-04-23DOI: 10.1016/j.ecoenv.2025.118225
Wenhao Ouyang , Chenjie Zhu , Yudi Li , Hong Huang , Fangming Li , Li Ling
Synthetic chemicals like triethyl citrate (TEC) are widely used in food packaging, pharmaceuticals, and cosmetics. Despite being considered safe, there are concerns about TEC's potential neurotoxic effects. In this study, we used network toxicology and molecular docking to examine TEC's impact on the nervous system. We identified 229 targets related to neurotoxicity and found that TEC may affect key processes such as cell death, inflammation, and neuronal health. Molecular docking showed strong interactions between TEC and proteins like MAPK3, SRC, CASP3, TNF, and BCL2, suggesting a risk of neural damage and the need for further research to assess TEC's safety.
{"title":"Assessing the neurotoxic risks of triethyl citrate in daily environmental exposure using network toxicology and molecular docking","authors":"Wenhao Ouyang , Chenjie Zhu , Yudi Li , Hong Huang , Fangming Li , Li Ling","doi":"10.1016/j.ecoenv.2025.118225","DOIUrl":"10.1016/j.ecoenv.2025.118225","url":null,"abstract":"<div><div>Synthetic chemicals like triethyl citrate (TEC) are widely used in food packaging, pharmaceuticals, and cosmetics. Despite being considered safe, there are concerns about TEC's potential neurotoxic effects. In this study, we used network toxicology and molecular docking to examine TEC's impact on the nervous system. We identified 229 targets related to neurotoxicity and found that TEC may affect key processes such as cell death, inflammation, and neuronal health. Molecular docking showed strong interactions between TEC and proteins like MAPK3, SRC, CASP3, TNF, and BCL2, suggesting a risk of neural damage and the need for further research to assess TEC's safety.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"297 ","pages":"Article 118225"},"PeriodicalIF":6.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143863328","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}
Arsenic (As) is classified as a Group 1 carcinogen by the International Agency for Research on Cancer (IARC). Exposure to As has been associated with an increased risk of various cancers, particularly lung cancer. However, the precise molecular mechanisms contributing to this carcinogenesis are not well understood. In our study, we analyzed transcriptomic data from the GEO database (GSE36684), identifying 764 differentially expressed genes (DEGs) in BEAS-2B cells treated with environmentally relevant doses of As for 8 weeks. A KEGG pathway enrichment analysis suggested that the FoxO pathway activation might be a novel key signaling event in As-induced carcinogenesis. We further analyzed the expression of 11 DEGs involved in the FoxO pathway using the TCGA-LUSC dataset. The findings revealed that four genes displayed expression patterns in tumor tissues consistent with those observed after As treatment in GEO dataset. Among them, USP7 was upregulated, while ATM, S1PR1, and PLK2 were downregulated in cancer tissues. High USP7 expression was specifically linked to a poor prognosis in lung squamous cell carcinoma (LUSC). To explore the role of USP7 in As-induced malignant transformation, BEAS-2B cells were exposed to NaAsO2 concentrations of 0.2 μM and 2 μM for up to 20 weeks. Experimental results confirmed that NaAsO2 treatment suppressed the FoxO transcriptional activity by upregulating USP7 expression, subsequently downregulating ATM and PLK2 expression, which led to abnormalities in cell cycle regulation and apoptosis. Notably, knocking down USP7 in As-transformed cells resulted in significant reductions in cell proliferation, colony formation, and tumor formation ability in nude mice, indicating the USP7-regulated FOXO3A pathway could be central to As-induced lung carcinogenesis. Moreover, our research demonstrated that USP7 inhibited FOXO3A’s ability to translocate from the cytoplasm to the nucleus by affecting its monoubiquitination status. Additionally, we speculated that As-induced the elevation of USP7 expression due to the excessive inflammatory cytokines secretion and the activation of mTORC1/WTAP pathway. These findings offer novel insights into the molecular mechanisms underlying As-mediated lung cancer.
{"title":"Role of the USP7/FOXO3A axis in environmentally relevant doses of arsenic-induced lung carcinogenesis: Insights from bioinformatics analysis and model of human epithelial cell malignant transformation","authors":"Xiaoyu Chen, Yuqing Wang, Ziqi Liu, Yujie He, Huan Gao, Xinchao Guan, Liping Chen, Shen Chen, Xiumei Xing, Wen Chen, Daochuan Li, Qing Wang","doi":"10.1016/j.ecoenv.2025.118224","DOIUrl":"10.1016/j.ecoenv.2025.118224","url":null,"abstract":"<div><div>Arsenic (As) is classified as a Group 1 carcinogen by the International Agency for Research on Cancer (IARC). Exposure to As has been associated with an increased risk of various cancers, particularly lung cancer. However, the precise molecular mechanisms contributing to this carcinogenesis are not well understood. In our study, we analyzed transcriptomic data from the GEO database (GSE36684), identifying 764 differentially expressed genes (DEGs) in BEAS-2B cells treated with environmentally relevant doses of As for 8 weeks. A KEGG pathway enrichment analysis suggested that the FoxO pathway activation might be a novel key signaling event in As-induced carcinogenesis. We further analyzed the expression of 11 DEGs involved in the FoxO pathway using the TCGA-LUSC dataset. The findings revealed that four genes displayed expression patterns in tumor tissues consistent with those observed after As treatment in GEO dataset. Among them, USP7 was upregulated, while ATM, S1PR1, and PLK2 were downregulated in cancer tissues. High USP7 expression was specifically linked to a poor prognosis in lung squamous cell carcinoma (LUSC). To explore the role of USP7 in As-induced malignant transformation, BEAS-2B cells were exposed to NaAsO<sub>2</sub> concentrations of 0.2 μM and 2 μM for up to 20 weeks. Experimental results confirmed that NaAsO<sub>2</sub> treatment suppressed the FoxO transcriptional activity by upregulating USP7 expression, subsequently downregulating ATM and PLK2 expression, which led to abnormalities in cell cycle regulation and apoptosis. Notably, knocking down USP7 in As-transformed cells resulted in significant reductions in cell proliferation, colony formation, and tumor formation ability in nude mice, indicating the USP7-regulated FOXO3A pathway could be central to As-induced lung carcinogenesis. Moreover, our research demonstrated that USP7 inhibited FOXO3A’s ability to translocate from the cytoplasm to the nucleus by affecting its monoubiquitination status. Additionally, we speculated that As-induced the elevation of USP7 expression due to the excessive inflammatory cytokines secretion and the activation of mTORC1/WTAP pathway. These findings offer novel insights into the molecular mechanisms underlying As-mediated lung cancer.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"297 ","pages":"Article 118224"},"PeriodicalIF":6.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859600","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.2025.118210
Shen-Tong Wang , Qi Yang , Ming-Kun Liu , Li Li , Wei Wang , Shou-Du Zhang , Guo-Fan Zhang
Ocean and coastal acidification (OCA) poses a significant and rapidly emerging threat to mollusks. The physiological resilience of mollusks to OCA varies considerably; however, the underlying molecular mechanisms remain poorly understood. Seawater in estuaries, being more susceptible to acidification than that in open coastal zones, may enhance the tolerance of resident mollusks to low pH levels. Here, we conducted a comparative analysis between estuarine oysters (Crassostrea ariakensis) and Pacific oysters (Crassostrea gigas) using physiological phenotype and transcriptomic analyses to reveal differential acid-tolerance mechanisms in response to constant pH of 7.8. Our findings indicated that survival and respiration rates of C. ariakensis, which inhabits estuaries with fluctuating pH levels, were higher than those of C. gigas, which inhabits open coastal zones with relative stable pH conditions. Acid-responsive genes identified in C. gigas, including molecular chaperones and immune-related genes, exhibited higher constitutive expression in C. ariakensis under control conditions. Co-expression analyses revealed that C. ariakensis mitigated the effects of low pH by expressing genes involved in ion transporter activity and translation control. C. gigas activated genes associated with glycolipid metabolism while inhibiting cell division during acid stress. These findings suggested that C. ariakensis has evolved into a more energy-efficient regulatory network than C. gigas, incorporating both front-loading and responsive mechanisms to maintain acidbase homeostasis. This study is the first to investigate acid-tolerance differences between mollusks inhabiting estuarine and open coastal environments and provides critical insights into the resilience of mollusks in increasingly acidified oceans.
海洋和沿岸酸化（OCA）对软体动物构成了巨大且迅速出现的威胁。软体动物对海洋酸化的生理适应能力差别很大，但对其潜在的分子机制仍然知之甚少。河口地区的海水比沿海开放地区的海水更容易受到酸化的影响，这可能会增强常驻软体动物对低pH值的耐受性。在这里，我们利用生理表型和转录组分析对河口牡蛎（Crassostrea ariakensis）和太平洋牡蛎（Crassostrea gigas）进行了比较分析，以揭示它们在恒定 pH 值为 7.8 时的不同耐酸机制。我们的研究结果表明，栖息在 pH 值波动的河口的 C. ariakensis 的存活率和呼吸率高于栖息在 pH 值相对稳定的开阔沿海地区的 C. gigas。在控制条件下，在千吉鱼中发现的酸反应基因，包括分子伴侣蛋白和免疫相关基因，在阿里雅克斯鱼中有较高的组成型表达。共表达分析表明，C. ariakensis 通过表达参与离子转运活性和翻译控制的基因来减轻低 pH 值的影响。千头椿激活了与糖脂代谢有关的基因，同时在酸胁迫期间抑制了细胞分裂。这些研究结果表明，与千足虫相比，阿里亚克氏千足虫已经进化成了一种更节能的调控网络，它结合了前负荷和响应机制来维持酸碱平衡。这项研究首次调查了栖息在河口和开放沿海环境中的软体动物的耐酸性差异，为软体动物在日益酸化的海洋中的恢复能力提供了重要的见解。
{"title":"Comparative transcriptomic analysis reveals a differential acid response mechanism between estuarine oyster (Crassostrea ariakensis) and Pacific oyster (Crassostrea gigas)","authors":"Shen-Tong Wang , Qi Yang , Ming-Kun Liu , Li Li , Wei Wang , Shou-Du Zhang , Guo-Fan Zhang","doi":"10.1016/j.ecoenv.2025.118210","DOIUrl":"10.1016/j.ecoenv.2025.118210","url":null,"abstract":"<div><div>Ocean and coastal acidification (OCA) poses a significant and rapidly emerging threat to mollusks. The physiological resilience of mollusks to OCA varies considerably; however, the underlying molecular mechanisms remain poorly understood. Seawater in estuaries, being more susceptible to acidification than that in open coastal zones, may enhance the tolerance of resident mollusks to low pH levels. Here, we conducted a comparative analysis between estuarine oysters (<em>Crassostrea ariakensis</em>) and Pacific oysters (<em>Crassostrea gigas</em>) using physiological phenotype and transcriptomic analyses to reveal differential acid-tolerance mechanisms in response to constant pH of 7.8. Our findings indicated that survival and respiration rates of <em>C. ariakensis</em>, which inhabits estuaries with fluctuating pH levels, were higher than those of <em>C. gigas</em>, which inhabits open coastal zones with relative stable pH conditions. Acid-responsive genes identified in <em>C. gigas</em>, including molecular chaperones and immune-related genes, exhibited higher constitutive expression in <em>C. ariakensis</em> under control conditions. Co-expression analyses revealed that <em>C. ariakensis</em> mitigated the effects of low pH by expressing genes involved in ion transporter activity and translation control. <em>C. gigas</em> activated genes associated with glycolipid metabolism while inhibiting cell division during acid stress. These findings suggested that <em>C. ariakensis</em> has evolved into a more energy-efficient regulatory network than <em>C. gigas</em>, incorporating both front-loading and responsive mechanisms to maintain acid<img>base homeostasis. This study is the first to investigate acid-tolerance differences between mollusks inhabiting estuarine and open coastal environments and provides critical insights into the resilience of mollusks in increasingly acidified oceans.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"297 ","pages":"Article 118210"},"PeriodicalIF":6.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859598","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.2025.118230
Yong-sheng Yang , Xu-wei Tang , Ji-fu Wu , Zhi-ying Zhan, Zhi-jian Hu, Fei He
Background
Lung cancer remains a leading cause of cancer-related deaths globally, influenced by environmental and lifestyle factors. However, evidence on the impact of multiple air pollutants is limited. Moreover, their combined effect of air pollutants and dietary patterns on lung cancer remains unclear.
Methods
This study used UK Biobank data to assess the impact of mixed air pollutants (PM10, PM2.5, NO2, NOx, and SO2) on lung cancer risk, with pollution scores based on weighted regression coefficients. Diet quality was measured using the Mediterranean Diet-based Healthy Diet Score. Cox proportional hazard models were used to calculate the hazard ratios (HRs) and 95 % confidence intervals (CIs).
Results
Our analysis included 327,147 participants with 3705 incident lung cancer cases. Higher exposure to air pollutants significantly increased lung cancer risk (HR: 1.41, 95 % CI: 1.34–1.48 per interquartile range (IQR) increase in air pollution score). Per IQR increase, HRs (95 % Cis) for individual pollutants were as follows: PM10,1.25(1.19–1.32), PM2.5, 1.50(1.41–1.59), NO2, 1.35(1.29–1.42), NOx, 1.29(1.24–1.34), and SO2, 1.20(1.15–1.26). Conversely, a higher healthy diet score was associated with lower lung cancer risk, with each IQR increase corresponding to an HR of 0.88 (95 % CI: 0.85–0.90). The combination of high air pollution and an unhealthy diet showed synergistic effects (synergy index: 1.40, 95 % CI: 1.11–1.76), further elevating lung cancer risk.
Conclusions
Poor dietary habits exacerbate the adverse effects of long-term air pollution exposure on lung cancer risk. Public health interventions promoting dietary improvements and reducing air pollution are critical for lung cancer prevention.
{"title":"Mitigating air pollution’s impact on lung cancer in a large-scale longitudinal study: The unexplored potential of dietary interventions","authors":"Yong-sheng Yang , Xu-wei Tang , Ji-fu Wu , Zhi-ying Zhan, Zhi-jian Hu, Fei He","doi":"10.1016/j.ecoenv.2025.118230","DOIUrl":"10.1016/j.ecoenv.2025.118230","url":null,"abstract":"<div><h3>Background</h3><div>Lung cancer remains a leading cause of cancer-related deaths globally, influenced by environmental and lifestyle factors. However, evidence on the impact of multiple air pollutants is limited. Moreover, their combined effect of air pollutants and dietary patterns on lung cancer remains unclear.</div></div><div><h3>Methods</h3><div>This study used UK Biobank data to assess the impact of mixed air pollutants (PM<sub>10</sub>, PM<sub>2.5</sub>, NO<sub>2</sub>, NO<sub>x</sub>, and SO<sub>2</sub>) on lung cancer risk, with pollution scores based on weighted regression coefficients. Diet quality was measured using the Mediterranean Diet-based Healthy Diet Score. Cox proportional hazard models were used to calculate the hazard ratios (HRs) and 95 % confidence intervals (CIs).</div></div><div><h3>Results</h3><div>Our analysis included 327,147 participants with 3705 incident lung cancer cases. Higher exposure to air pollutants significantly increased lung cancer risk (HR: 1.41, 95 % CI: 1.34–1.48 per interquartile range (IQR) increase in air pollution score). Per IQR increase, HRs (95 % Cis) for individual pollutants were as follows: PM<sub>10</sub>,1.25(1.19–1.32), PM<sub>2.5</sub>, 1.50(1.41–1.59), NO<sub>2</sub>, 1.35(1.29–1.42), NO<sub>x</sub>, 1.29(1.24–1.34), and SO<sub>2</sub>, 1.20(1.15–1.26). Conversely, a higher healthy diet score was associated with lower lung cancer risk, with each IQR increase corresponding to an HR of 0.88 (95 % CI: 0.85–0.90). The combination of high air pollution and an unhealthy diet showed synergistic effects (synergy index: 1.40, 95 % CI: 1.11–1.76), further elevating lung cancer risk.</div></div><div><h3>Conclusions</h3><div>Poor dietary habits exacerbate the adverse effects of long-term air pollution exposure on lung cancer risk. Public health interventions promoting dietary improvements and reducing air pollution are critical for lung cancer prevention.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"297 ","pages":"Article 118230"},"PeriodicalIF":6.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143863324","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.2025.118169
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.
{"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}
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