Ecotoxicology and Environmental Safety最新文献

{"title":"Cellular and metabolic impacts of repeated sub-acute exposures to biomass-burning extracts in vitro.","authors":"Michal Pardo, Chunlin Li, Amani Jabali, Yinon Rudich","doi":"10.1016/j.ecoenv.2024.117491","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117491","url":null,"abstract":"<p><p>The increasing exposure to biomass-burning emissions underscores the need to understand their toxicological impacts on human health. In this study, we developed a laboratory model to evaluate the effects of single and repeated sub-acute exposures to water-soluble wood tar (WT) extracts, a product of biomass burning, on human lung, liver, and immune cells. Using representative cell lines for different tissues, we examined the cytotoxic effects under conditions mimicking sub-acute environmental exposure levels relevant to humans. Our findings indicate that repeated sub-acute exposures to water-soluble WT extracts significantly enhance the inflammatory response, evidenced by increased IL6, IL8, and TNFa cytokine levels, compared to a single exposure. Additionally, oxidative stress responses were more pronounced with increased lipid peroxidation and HMOX1, GCLC and CYP1A1 gene expression following repeated exposures. Metabolomics analyses of polar and lipid metabolites revealed changes related to energy production and consumption that emerge even after a single exposure at sub-acute levels and vary across different cell types representing the different tissues. Impaired cellular respiration, measured by oxygen consumption rate, corroborates the observed changes. These results provide important insights into the cellular mechanisms driving the response to biomass-burning exposure and highlight the potential health risks associated with sub-acute exposure to environmental pollutants.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117491"},"PeriodicalIF":6.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142805673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Air pollution exposure and prevalence of non-alcoholic fatty liver disease and related cirrhosis: A systematic review and meta-analysis.","authors":"Xingyi He, Shipeng Zhang, Qinglin Bai, Moshen Pan, Yanjie Jiang, Weiwei Liu, Wei Li, Yuanyuan Gong, Xueping Li","doi":"10.1016/j.ecoenv.2024.117469","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117469","url":null,"abstract":"<p><strong>Background and objective: </strong>A systematic review and meta-analysis were used to investigate the relationship between air pollution exposure and the prevalence of non-alcoholic fatty liver disease (NAFLD) and its related cirrhosis. Through this study, we hope to clarify the potential public health risks of air pollution as an environmental exposure factor.</p><p><strong>Methods: </strong>Through a comprehensive and systematic search of the EMBASE, PubMed, Web of Science, and Cochrane library databases, studies published up to March 30, 2024, that met the eligibility criteria were identified. The meta-analysis aimed to determine the association between air pollution exposure and NAFLD risk. Subgroup analyses were conducted based on regional economic development after adjusting for confounding factors. The combined odds ratio (OR) was calculated, publication bias was assessed using funnel plots, and consideration was given to heterogeneity among study-specific relative risks.</p><p><strong>Results: </strong>This review included 14 observational studies (including 7 cohort studies and 7 cross-sectional studies) involving 43,475,41 participants. The pooled analysis showed that PM_2.5, NO_x, PM₁₀, PM_2.5-10, passive smoking, PM₁, and air pollution from solid fuels were positively associated with the incidence and prevalence of NAFLD and its related cirrhosis. The risk ratios for PM_2.5, NO_x, PM₁₀, PM_2.5-10, passive smoking, and air pollution from solid fuels for NAFLD and its related cirrhosis were 1.33 (95 % CI: 1.25, 1.42), 1.19 (95 % CI: 1.14, 1.23), 1.27 (95 % CI: 1.05, 1.55), 1.05 (95 % CI: 1.00, 1.11), 1.53 (95 % CI: 1.12, 2.09), 1.50 (95 % CI: 0.86, 2.63), and 1.18 (95 % CI: 0.85, 1.63), respectively. In contrast, the risk ratio for O₃ was 0.75 (95 % CI: 0.69, 0.83), suggesting that O₃ may lower the incidence and prevalence of NAFLD and its related cirrhosis. We also conducted subgroup analyses based on the level of national development to examine the impact of PM_2.5 on NAFLD and its related cirrhosis. The results showed that the risk of NAFLD and its related cirrhosis associated with PM_2.5 in developing countries was 1.41 (95 % CI: 1.29, 1.53), which was higher than 1.20 (95 % CI: 1.12, 1.29) in developed countries.</p><p><strong>Conclusion: </strong>The study findings show that PM_2.5, NO_x, PM₁₀, PM_2.5-10, passive smoking, PM₁, and air pollution from solid fuels can increase an individual's risk of developing NAFLD and its related cirrhosis; while O₃ can reduce the risk. In developing countries, the risk level of NAFLD and its related cirrhosis due to PM_2.5 is higher than that in developed countries.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117469"},"PeriodicalIF":6.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142805682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Allelopathic effects on vegetative propagation, physiological-biochemical characteristic of Alternanthera philoxeroides (Mart.) Griseb from Cinnamomum camphora (L.) Presl.","authors":"Xiaxia Wang, Haixia Wang, Yanlei Zhang, Yan Li, Qi Jia, Ziyi Wang, Juan Sun","doi":"10.1016/j.ecoenv.2024.117403","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117403","url":null,"abstract":"<p><p>Alternanthera philoxeroides (Mart.) Griseb is a well-known invasive plant species worldwide. Cinnamomum camphora (L.) Presl. is a plant species that is rich in allelopathic substances which can impede the growth of many other plants. In this study, the allelopathic effects of C. camphora on the growth and development, and physiological-biochemical characteristics of A. philoxeroides were investigated. The findings revealed that the leaves of C. camphora exhibited the capability to suppress the asexual reproduction of A. philoxeroides. The addition of C. camphora leaves resulted in inhibition of the fresh weight, stem length, and stem node number of A. philoxeroides new stems, with the strength of inhibition increasing in proportion to the quantity of C. camphora leaves added. Furthermore, the inhibitory effect of C. camphora leaves on A. philoxeroides was significantly amplified under high temperatures (≥ 30°C). Two allelochemicals had strong inhibitory effects on the vegetative reproduction of A. philoxeroides. The inhibition intensities were all up to 100 % on stem vegetative propagation, were 90.40 % and 100 % on root vegetative propagation from camphor and linalool, respectively. Physiological-biochemical analyses of roots indicated that the two allelochemicals promoted the accumulation of hydrogen peroxide and MDA, disrupting the balance of antioxidant enzyme systems. The two allelochemicals had a strong inhibitory effect on CAT activity and a strong promoting effect on POD activity. The effect on SOD activity was greatly affected by the type and concentration of allelochemicals. Moreover, the two allelochemicals significantly inhibited the accumulation of osmotic regulating substance. The contents of soluble sugar, soluble protein, and proline were significantly down-regulated. In summary, the allelochemicals from C. camphora induced damage to biological membranes, disrupting antioxidant enzyme systems and inhibiting osmoregulation. This resulted in the retardation of growth, development, and potential mortality of A. philoxeroides. These findings would contribute to the knowledge base for A. philoxeroides prevention and control, and enrich the understanding of C. camphora allelopathic substances.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117403"},"PeriodicalIF":6.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142805700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of co-exposure to polycyclic aromatic hydrocarbons and vitamin D with early lung dysfunction: Mediating roles of metabolic score-visceral adiposity index.","authors":"Baihao Lin, Wanlu Liu, Hank-Han Wang, Haixia Qian, Xinyu Zhu, Mengya Xu, Yuyu Zheng, Nada Alhazmi, Yansen Bai","doi":"10.1016/j.ecoenv.2024.117496","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117496","url":null,"abstract":"<p><strong>Background: </strong>Preserved ratio impaired spirometry (PRISm) and airflow obstruction are recognized as critical early signs of chronic obstructive pulmonary disease (COPD). While these conditions arise from concurrent exposure to toxicants and essential nutrients, how vitamin D modifies the pulmonary toxicity induced by polycyclic aromatic hydrocarbons (PAHs) and the metabolic mechanisms involved is still unclear.</p><p><strong>Methods: </strong>Based on the National Health and Nutrition Examination Survey (NHANES) 2007-2012, data on urinary PAH metabolites (ΣOH-PAHs), serum vitamin D metabolite levels [Σ25(OH)D], and pulmonary function tests [forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and FEV1/FVC] from 2189 participants, including 369 subjects with early lung dysfunction, defined as PRISm or airflow obstruction. Multiple metabolic disorder indicators were calculated using biochemical markers. The interaction effects between vitamin D and PAHs were evaluated using multiple linear and logistic regression models. Causal mediation analyses and structural equation modeling were employed to investigate the mediating roles of metabolic indicators.</p><p><strong>Results: </strong>PAHs and vitamin D had opposite effects on lung function parameters [FEV1: β (95 CIs) = -0.01 (-0.02, -0.01) vs. 0.01 (0.01, 0.04); FVC: β (95 CIs) = -0.01 (-0.02, 0.01) vs. 0.04 (0.01, 0.06)] and risk of early lung dysfunction [OR (95 CIs) = 1.22 (1.06, 1.40) vs. 0.52 (0.37, 0.73)]. Decreased associations of ΣOH-PAHs with FEV1, FVC, and early lung dysfunction, as well as with metabolic score-visceral adiposity index (MSV) were visualized with increased Σ25(OH)D among subjects with body mass index (BMI) < 28 kg/m². Furthermore, 2.18 %, 18.20 %, 5.70 %, and 4.70 % of the associations of co-exposure to ΣOH-PAHs and Σ25(OH)D with FEV1, FVC, FEV1/FVC, and early lung dysfunction disease were mediated by MSV.</p><p><strong>Conclusions: </strong>Our findings indicated that vitamin D antagonizes the hazardous effects of PAHs on early lung dysfunction by metabolic alteration, providing new insight into the identification of the underlying high-risk populations and accessible prevention and intervention measures for attenuating PAH-induced lung dysfunction.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117496"},"PeriodicalIF":6.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142805705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insecticide chlorfenapyr confers induced toxicity in human cells through mitochondria-dependent pathways of apoptosis.","authors":"Longfei Wang, Zheng Qu, Yifan Xu, Guangqing Yu, Xiangyang Liu, Meizi Wang, Shiheng An, Xinming Yin, Risong Na, Youwu Hao","doi":"10.1016/j.ecoenv.2024.117502","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117502","url":null,"abstract":"<p><p>Pesticides are always used in the environment, the unexpected effects of pesticides on the environment and non-target organisms need to be continuously studied. Insecticide chlorfenapyr (Chl) is widely used in agriculture and also recommended for public health use (e.g., providing protection from malaria). Here we study toxic effects of Chl on human alveolar carcinoma cells (A549) and human normal liver cells (L02) in vitro. Chl's ability to induce DNA damage and apoptosis in human cells was confirmed through alkaline comet assay, immunofluorescence assay, and flow cytometric analysis. Further research showed that Chl induced mitochondrial damage (the collapse of mitochondrial membrane potential and the opening of mitochondrial permeability transition pore) with up-regulated expression of Bax/Bcl-2 leads to the release of cytochrome c from mitochondria which in turn activated the apoptotic pathway. Meanwhile, the key protein PARP is cleaved during apoptosis, resulting in the inhibition of DNA damage repair. In short, human A549 and L02 cells exposed to Chl were experiencing DNA damage and apoptosis linked to mitochondria. The results of this study supply theoretical understanding of Chl's toxicity on human cells, and can attract attention on the potential threat of insecticide Chl to human health.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117502"},"PeriodicalIF":6.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142805675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polystyrene nanoplastics promote the blood-brain barrier dysfunction through autophagy pathway and excessive erythrophagocytosis.","authors":"Eun-Hye Kim, Seung Mi Baek, Han Jin Park, Yiying Bian, Han Young Chung, Ok-Nam Bae","doi":"10.1016/j.ecoenv.2024.117471","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117471","url":null,"abstract":"<p><p>There is increasing concern regarding the risks posed by plastics to human health. Nano-sized plastics enter the body through various exposure routes. Although nano-sized particles circulate through the bloodstream and access the blood-brain barrier (BBB), the harmful impacts of nano-sized plastics on BBB function including endothelial cells are not well known. In this study, polystyrene nanoplastics (PS-NP) resulted in hyperpermeability and damaged tight junction proteins in brain endothelial cells. We identified that PS-NP increased intracellular iron levels by inhibiting the autophagy pathway in brain endothelial cells. Our study showed that dysregulated autophagy pathways led to increased BBB permeability induced by PS-NP treatment. In addition, PS-NP caused excessive erythrophagocytosis in brain endothelial cells via damaged red blood cells. PS-NP-treated RBCs (NP-RBC) induced the BBB dysfunction and increased intracellular iron levels and ferroptosis in brain endothelial cells. We provide novel insights into the potential risks of nano-sized plastics in BBB function by interaction between cells as well as direct exposure. Our study will help to understand the cardiovascular toxicity of nano-sized plastics.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117471"},"PeriodicalIF":6.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142805776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"L-selenomethionine inhibits small intestinal ferroptosis caused by ammonia exposure through regulating ROS-mediated iron metabolism.","authors":"Xinxin Zhang, Lepeng Gu, Ying Chen, Tianqi Wang, Houjuan Xing","doi":"10.1016/j.ecoenv.2024.117477","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117477","url":null,"abstract":"<p><p>Ammonia is an important component of PM2.5 and PM10, and is also a major harmful gas in intensive and large-scale pig houses, which poses a potential threat to the health of farmers and animals. Intestinal tract is the largest immune organ in the body and is also an important target organ for ammonia exposure. However, the potential toxicity mechanism of ammonia exposure to the intestine remains unclear. L-selenomethionine is an important source of organic selenium with the advantages of high bioavailability, safety and high efficiency. In order to explore the mechanism of ammonia enterotoxicity and the mitigation effect of L-selenomethionine on ammonia enterotoxicity, multi-dimensional ammonia toxicity models and L-selenomethionine intervention models were established in vivo and in vitro. The results showed that ammonia exposure up-regulated the levels of iron, ROS, MDA, and LPO in the small intestinal tissue and the IPEC-J2 cell, down-regulated the activities of antioxidant enzymes and the content of GSH, inhibited the Nrf2 pathway, significantly altered the expression of ferroptosis (TFR-1, FPN-1, FTH1, SLC7A11, GPX4, ACSL4) and intestine tight junctions (Claudin-1, Occludin, ZO-1) genes. Compared with the ammonia exposure group, L-selenomethionine group could significantly improve the changes of these ferroptosis indicators by affecting ROS and iron levels through Nrf2 pathway. Our results indicated that L-selenomethionine inhibited small intestinal epithelial cells ferroptosis caused by ammonia exposure through regulating ROS-mediated iron metabolism.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117477"},"PeriodicalIF":6.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142805677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NLRP3 inflammasome activation and disruption of IRS-1/PI3K/AKT signaling: Potential mechanisms of arsenic-induced pancreatic beta cells dysfunction in rats.","authors":"Yonglian Liu, Wenjuan Wang, Bing Liang, Zhonglan Zou, Aihua Zhang","doi":"10.1016/j.ecoenv.2024.117504","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117504","url":null,"abstract":"<p><p>Environmental exposure to arsenic is associated with significant health risks, including diabetogenic effects linked to pancreatic dysfunction. The NOD-like receptor protein 3 (NLRP3) inflammasome has been implicated in various metabolic abnormalities; however, its specific role in arsenic-induced pancreatic dysfunction remains insufficiently understood. This study aimed to elucidate the involvement and underlying mechanisms of the NLRP3 inflammasome in arsenic-induced pancreatic beta cells dysfunction through in vivo and in vitro models. In rat models, arsenic exposure was found to activate the NLRP3 inflammasome, as evidenced by pathomorphological changes and the expression of inflammasome activation markers. These pathological changes were accompanied by disruptions in the insulin signaling pathway, characterized by increased phosphorylation of insulin receptor substrate 1 (IRS-1) at Ser616, reduced expression of phosphatidylinositol 3-kinase (PI3K) and phosphorylated protein kinase B (AKT) at Ser473, and significant decreases in downstream targets, including the nuclear translocation of PDX-1, membrane translocation of glucose transporter 2 (GLUT2), and glucokinase (GCK) expression. In vitro, NaAsO₂-treated INS-1 cells exhibited a dose-dependent reduction in glucose-stimulated insulin secretion. Furthermore, arsenic exposure in these cells activated the NLRP3 inflammasome, suppressed the IRS-1/PI3K/AKT signaling pathway, and downregulated insulin secretion regulatory molecules (PDX-1, GLUT2, and GCK). Notably, these arsenic-induced effects were reversed by MCC950, an NLRP3 inflammasome inhibitor, and Extendin-4, an agonist of the IRS-1/PI3K/AKT signaling pathway. Collectively, these findings demonstrate that NLRP3 inflammasome activation disrupts the IRS-1/PI3K/AKT signaling pathway, contributing to arsenic-induced pancreatic beta cells dysfunction in rats.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117504"},"PeriodicalIF":6.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142805775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brassica rapa selenium transporter NPF2.20 (BrNPF2.20) accounts for Se-enrichment in Chinese cabbage.","authors":"Xiaoting Hu, Yucheng Chen, Weihong Xu","doi":"10.1016/j.ecoenv.2024.117466","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117466","url":null,"abstract":"<p><p>Selenium (Se) is an essential nutrient for the human body and breeding highly Se-enriched Chinese cabbage varieties is an important means of addressing Se deficiency in individuals in certain regions. The genus Brassica has a strong ability to enrich Se; however, the primary molecular mechanism of Se enrichment remains unclear. We screened for high- and low-Se-enriched Chinese cabbage varieties from 39 different genotypes and identified a key candidate gene for Se enrichment, namely, BrNPF2.20 (BraA07g035670.3.1 C), located on the cell membrane. The expression level of BrNPF2.20 in the high-Se-enriched Chinese cabbage variety P2 was significantly higher than that in the low-Se-enriched variety P6. Heterologous expression of BrNPF2.20 increased the sensitivity of yeast to Se. The overexpression of BrNPF2.20 significantly increased the Se content in Arabidopsis plants, whereas silencing BrNPF2.20 in Chinese cabbage leaves reduced the Se content. Cell selenium mainly in the cell wall may be the physiological and biochemical mechanism of the high-Se-enriched vareity in response to selenium stress. BrNPF2.20 promoted the transport and accumulation of Se from root to shoot in Chinese cabbage maybe by increasing GSH-Px activity or regulating sulfate transporter family genes related to Se absorption and transport. This study not only deepens our understanding of Se transport from Chinese cabbage root to the ground part, but also provides a new idea for breeding Se-rich Chinese cabbage varieties by promoting SeMet transport.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117466"},"PeriodicalIF":6.2,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-world outdoor air exposure effects in a model of the human airway epithelium - A comparison of healthy and asthmatic individuals using a mobile laboratory setting.","authors":"Pavel Rossner, Helena Libalova, Tereza Cervena, Michal Sima, Zuzana Simova, Kristyna Vrbova, Antonin Ambroz, Zuzana Novakova, Fatima Elzeinova, Anezka Vimrova, Lubos Dittrich, Michal Vojtisek, Martin Pechout, Michal Vojtisek-Lom","doi":"10.1016/j.ecoenv.2024.117495","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117495","url":null,"abstract":"<p><p>We developed a mobile laboratory allowing field exposure of lung tissue models to ambient air at localities with various pollution sources (Background, Industrial, Traffic, Urban) in different seasons (summer/fall/winter). In samples originating from healthy and asthmatic individuals, we assessed the parameters of toxicity, lipid peroxidation and immune response; we further performed comprehensive monitoring of air pollutants at sampling sites. We measured lactate dehydrogenase (LDH) and adenylate kinase (AK) production and transepithelial electrical resistance (TEER), analyzed 15-F_2t-isopostane (IsoP) and a panel of 20 cytokines/chemokines/growth factors. In the ambient air, we detected particulate matter (PM), and other relevant chemicals (benzene, benzo[a]pyrene (BaP), NOx). In the Traffic locality, we found very high concentrations of ultrafine particles and NOx and observed low TEER values in the exposed samples, indicating significant traffic-related toxicity of the ambient air. In the Urban locality, sampled in winter, we observed high PM and BaP levels. We found lower AK levels in samples from healthy individuals exposed in this locality than in the asthmatic samples. In the samples from the Industrial locality, sampled in summer, we detected higher concentrations of TNFα, MIP-1α, Eotaxin, GROα, GM-CSF, IL-6 and IL-7 than in the Urban locality samples. We hypothesize that pollen or other plant-related components of the ambient air were responsible for this response. In conclusion, our data proved the feasibility of our mobile laboratory for field measurements of the biological response of lung tissue models exposed to ambient air, reflecting not only the levels of toxic compounds, but also season-specific parameters.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117495"},"PeriodicalIF":6.2,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142793945","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}