Ecotoxicology and Environmental Safety最新文献

{"title":"Polystyrene microplastics disrupt adrenal steroid synthesis in male mice via mitochondrial dysfunction.","authors":"Ying Xiong, Zhe Chen, Hanmin Xiang, Yi Liu, Yanlin Wang","doi":"10.1016/j.ecoenv.2024.117528","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117528","url":null,"abstract":"<p><p>Microplastics have gained significant social attention, as they can enter our bodies through food and drinking water. The adrenal gland is essential for the maintenance of metabolic homeostasis and stress responses. Nevertheless, the effects of microplastics on the steroid synthesis in the adrenal cortex was still unclear. In this study, through both in vivo and in vitro models, we found that polystyrene microplastics (PS-MPs) impaired adrenal steroid synthesis, leading to a reduction in corticosterone levels. In vivo, we further observed that chronic exposure to PS-MPs (0.25, 0.5 and 1 mg/d for 4 weeks) could induce abnormal mitochondrial morphology and functional disruptions of adrenal glands in male mice, along with an imbalance in cellular oxidative stress, manifested as increased level of reactive oxygen species, diminished antioxidant activity (glutathione peroxidase and superoxide dismutase). In vitro, these occurrences coincided with an elevated rate of cell apoptosis observed in adrenocortical cells following exposure to PS-MPs. We proposed that mitochondrial dysfunction not only directly influenced the biosynthetic processes of steroid hormones but also induced cell apoptosis through the initiation of cellular oxidative stress. The latter may represent a common mechanism underlying the multi-organ toxicity induced by PS-MPs in the body. Our findings would provide new insights for the development of more effective environmental protection measures and the reduction of plastic pollution.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"290 ","pages":"117528"},"PeriodicalIF":6.2,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823710","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":"Structure-activity relationship and in silico docking analysis of dicarboximide fungicides on 17β-hydroxysteroid dehydrogenase 1 of human, rat, and pig.","authors":"Huiqian Chen, Sailing Chen, Yunbing Tang, Yingfen Ying, Shaowei Wang, Yang Zhu, Yiyan Wang, Ren-Shan Ge, Ping Duan","doi":"10.1016/j.ecoenv.2024.117529","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117529","url":null,"abstract":"<p><p>Dicarboximide fungicides, including captafol, captan, cyclohexylthiophthalimide, folpet, and procymidone, represent a distinct category of fungicides. 17β-Hydroxysteroid dehydrogenase 1 (17β-HSD1) catalyzes the conversion of estrone to estradiol in mammals. Yet, the impact of these fungicides on 17β-HSD1 activity remains unknown. In this study, we investigated their inhibition using human placental cytosols, rat and pig ovarian cytosols. Our observations revealed that dicarboximide fungicides significantly inhibited human 17β-HSD1 activity. Among them, captan showed the strongest potency, with its IC₅₀ of 1.28 μM, whereas procymidone had an IC₅₀ of 100.71 μM. However, both rat and pig 17β-HSD1 enzymes were less sensitive to the inhibition of these fungicides compared to the human enzyme, with captan displaying an IC₅₀ of 5.65 μM for the rat enzyme and 7.36 μM for the pig enzyme. Correlation analysis indicated a positive correlation between IC₅₀ values and LogP. Docking analysis revealed that these fungicides bound to cofactor or between the steroid and cofactor binding sites. The dithiothreitol treatment demonstrated that the formation of irreversible bonds between dicarboximide fungicides and the cysteine residues played a key role in the inhibition of 17β-HSD1 activity. In conclusion, dicarboximide fungicides inhibit 17β-HSD1 depending on lipophilicity, species, and cysteine residue interactions.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"290 ","pages":"117529"},"PeriodicalIF":6.2,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823714","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":"Interaction between walkability and fine particulate matter on ischemic heart disease: A prospective cohort study in China.","authors":"Jiayun Zhang, Peng Shen, Yixing Wang, Zihan Li, Lisha Xu, Jie Qiu, Jingjing Hu, Zongming Yang, Yonghao Wu, Zhanghang Zhu, Hongbo Lin, Zhiqin Jiang, Liming Shui, Mengling Tang, Mingjuan Jin, Feng Tong, Kun Chen, Jianbing Wang","doi":"10.1016/j.ecoenv.2024.117520","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117520","url":null,"abstract":"<p><strong>Background: </strong>Previous studies have suggested that neighborhoods characterized by higher walkability are related to a reduced risk of ischemic heart disease (IHD), whereas exposure to PM_2.5 is positively associated with risk of IHD. Nevertheless, their joint impact on IHD warrants further investigation.</p><p><strong>Methods: </strong>This prospective cohort study was performed in Yinzhou, Ningbo, China, comprising 47,516 participants. Individual-level walkability and PM_2.5 were evaluated using a commercial walkability database and a land use regression (LUR) model, respectively. Hazard ratios (HRs) and 95 % confidence intervals (95 % CIs) were calculated using two Cox proportional hazards models: one based on two-year average PM_2.5 levels prior to baseline, and the other incorporating time-varying PM_2.5 assessed on a monthly scale. Dose-response relationships were explored using restricted cubic spline (RCS) functions. Interactions on both additive and multiplicative scales were assessed via relative excess risk due to interaction (RERI) and likelihood-ratio tests. Joint effects were explored and visualized using a 3D wireframe plot.</p><p><strong>Results: </strong>Over a median follow-up of 5.14 years, 1735 incident cases of IHD were identified. Adjusted HRs (95 % CIs) were 1.56 (1.34-1.81) per 10 μg/m³ increase in PM_2.5 and 0.96 (0.94-0.98) per 10-unit increase in walkability, with both exposures exhibiting non-linear dose-response relationships. Walkability and PM_2.5 were positively correlated (r_s = 0.12, P < 0.001), and a multiplicative interaction was detected (P_interaction = 0.019).</p><p><strong>Conclusion: </strong>Walkability was inversely associated with risk of IHD, whereas exposure to PM_2.5 was positively associated with IHD. Notably, the pernicious effects of PM_2.5 could be attenuated in areas with higher levels of walkability. Our findings underscore the significance of walkable urban design, air quality improvement, as preventive strategies for IHD.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"290 ","pages":"117520"},"PeriodicalIF":6.2,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823707","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":"Abnormal methylation of Mill1 gene regulates osteogenic differentiation involved in various phenotypes of skeletal fluorosis in rats and methionine intervention.","authors":"Niannian Chen, Jing Zhang, Congyu Yin, Yudan Liao, Lei Song, Ting Hu, Xueli Pan","doi":"10.1016/j.ecoenv.2024.117519","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117519","url":null,"abstract":"<p><p>Excessive fluoride intake can lead to skeletal fluorosis. Nutritional differences in the same fluoride-exposed environment result in osteosclerosis, osteoporosis, and osteomalacia. DNA methylation has been found to be involved in skeletal fluorosis and is influenced by environment and nutrition. In a previous study, we screened eight genes with differential methylation associated with various phenotypes of skeletal fluorosis. By combining gene functions, Mill1 gene was selected for subsequent experiments. First, we found that the Mill1 gene was hypomethylated and upregulated in osteosclerosis skeletal fluorosis, whereas it was hypermethylated and downregulated in osteoporosis/osteomalacia skeletal fluorosis. Similar results were obtained in the cell experiments. Subsequently, we validated the regulation of Mill1 gene methylation using DNMT1 and TET2 enzyme inhibitors. Furthermore, we knockdown and overexpression experiments confirmed its downregulation inhibited osteogenic differentiation, whereas osteogenic differentiation was promoted by its overexpression. These findings imply that abnormal methylation of the Mill1 gene triggered by fluoride under diverse nutritional conditions, regulates its expression and participates in osteogenic differentiation, potentially resulting in various phenotypes of skeletal fluorosis. Eventually, we use methionine for interventions both in vivo and in vitro. The results indicated that under normal nutrition and fluoride exposure followed by methionine intervention, the methylation levels of the Mill1 gene increased, whereas its high expression and enhanced osteogenic differentiation were restrained. This study offers a theoretical foundation for understanding the mechanism behind the various phenotypes of skeletal fluorosis through the perspective of DNA methylation and for employing nutrients to intervene in skeletal fluorosis.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"290 ","pages":"117519"},"PeriodicalIF":6.2,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823652","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":"Mechanisms underlying the effects of cyanogenesis on development and reproduction of Tetranychus urticae: Insights from enzyme activity and gene expression aspects.","authors":"Mufeng Wu, Xiao Liang, Ying Liu, Chunling Wu, Xingkui An, Zihua Zhao, Guifeng Hao, Ijiti Oluwole Gregory, Zhihong Li, Qing Chen","doi":"10.1016/j.ecoenv.2024.117523","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117523","url":null,"abstract":"<p><p>Cyanogenic plants can release toxic hydrogen cyanide (HCN) to defend against herbivory by hydrolyzing the cyanogenic glycosides (CNGs) with its β-glucosidases (β-GLUs). Numerous studies have speculated this CNG-mediated toxicity by a plant-pest interaction manner. However, the specific toxic effect of HCN was not well-demonstrated because of the interference of other ingested metabolites. Additionally, the physiological- and biochemical-based mode of action of HCN were seldom determined. To fill those knowledge gaps, the two-spotted spider mite (TSSM), Tetranychus urticae, was used as a model organism to elucidate the toxic mechanism of HCN. In addition, three CNG-enzyme combinations were screened for effective cyanogenesis and TSSM lethality. Linamarin-β-GLU (lima bean-derived) presented prompt HCN release, and molecular docking indicated higher binding energy and more robust binding sites compared with other two groups, i.e., lotaustralin-β-GLU (lima bean-derived) and amygdalin-β-GLU (almond-derived). Meanwhile, this combination led to higher TSSM mortality. Moreover, we found that the median lethal concentration of this combination will significantly prolong the developmental duration, and decrease the longevity and fecundity of TSSM. Besides, the population growth was also significantly suppressed. Furthermore, the sustainable activation of enzyme activity and the encoding gene expression related to physiological process such as detoxification (cytochrome P450, glutathione S-transferase, UDP-glucuronosyltransferase and β-cyanoalanine synthase), antioxidation (superoxide dismutase, catalase and peroxidase), neural transduction (acetylcholinesterase) and respiration (cytochrome c oxidase) were attributed to the detrimental impact on development and reproduction of TSSM. The present findings can provide insight regarding reasonable utilization of toxic chemicals in pest management and creation of novel pest-resistant germplasm.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"290 ","pages":"117523"},"PeriodicalIF":6.2,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821566","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":"Potential risks of bacterial plant pathogens from thawing permafrost in the Alaskan tundra.","authors":"Dockyu Kim, Mincheol Kim, Sungho Woo, Sungjin Nam, Nu Ri Myeong, Eungbin Kim, Yung Mi Lee","doi":"10.1016/j.ecoenv.2024.117531","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117531","url":null,"abstract":"<p><p>Global warming-induced permafrost thawing raises concerns about the release of dormant microbes, including potentially harmful plant pathogens. However, the potential pathogenic risks associated with the thawing of permafrost remain poorly understood. Here, we conducted a 90-day soil incubation experiment at 4 °C to mimic extended permafrost thawing in Alaskan tundra soils stratified into active (A), transitional (T), and permanently frozen (P) layers. Following incubation, we examined the changes in bacterial abundance and community composition and tested the reactivation and pathogenicity of dormant plant pathogenic bacteria. Bacterial abundance, measured by colony-forming units and 16S rRNA gene copies, distinctly increased in the T and P layers after thawing. These layers also exhibited substantial shifts in bacterial community structure, with Fe-cycling taxa becoming more abundant and permafrost-dominant taxa decreasing in abundance. Notably, we isolated 52 strains with proteolytic activity, and our pathogenicity tests confirmed that Pseudomonas spp. isolates caused potato soft rot symptoms. Some Pseudomonas pathogens were undetectable in the amplicon sequencing data before thawing and emerged only in the thawed T and P layers. Our findings illustrate that permafrost acts as a reservoir of potential plant pathogens, and their resurgence upon thawing poses a potential risk to Arctic ecosystems.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117531"},"PeriodicalIF":6.2,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821561","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":"Cyclopiazonic acid suppresses the function of Leydig cells in prepubertal male rats by disrupting mitofusin 1-mediated mitochondrial function.","authors":"Hang Lin, Ming Su, He Zhu, Yang Yu, Jianmin Sang, Yiyan Wang, Qiqi Zhu, Yang Zhu, Xiaoheng Li, Xingwang Li, Ren-Shan Ge, Huitao Li","doi":"10.1016/j.ecoenv.2024.117503","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117503","url":null,"abstract":"<p><p>This research investigated the impact of cyclopiazonic acid (CPA), a mycotoxin, on the function of progenitor Leydig cells (PLCs) in prepubertal male rats, focusing on its potential disruption of mitochondrial integrity through mitofusin 1 (MFN1) modulation. In vivo, Sprague Dawley rats received CPA (0.2, 1, 5 mg/kg/day) via gavage from postnatal days 21-28 to evaluate PLC function and mitochondrial morphology using serum hormone levels, histology, qPCR, and Western blot analyses. In vitro, rat R2C cells were treated with CPA (0.1, 1, 10 μM) alone or in combination with 100 μM leflunomide to assess PLC development through testosterone measurements, Western blotting, flow cytometry, and Mito-Tracker Green Staining. The findings from in vivo experiments showed that CPA reduced serum testosterone and progesterone levels at 1 mg/kg/day. The qPCR and Western blotting analyses revealed significant alterations in the expression of genes and proteins pertinent to PLC function, such as Scarb1, Star, Cyp11a1, and Cyp17a1. Immunofluorescence staining further revealed a reduction in MFN1 expression following exposure to CPA. In vitro experiments corroborated these observations, demonstrating that CPA induced mitochondrial fragmentation by downregulating SIRT1, PGC1-α, MFN1, and OPA1, increase reactive oxygen species, and inhibit testosterone synthesis in R2C cells. The administration of leflunomide was shown to mitigate the detrimental effects of CPA on PLCs. In conclusion, this research sheds new light on the deleterious effects of CPA on the reproductive development of prepubertal males.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117503"},"PeriodicalIF":6.2,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821558","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":"Integrated multi-omics analysis reveals the underlying molecular mechanism for the neurotoxicity of triclosan in zebrafish.","authors":"Shasha Zhao, Yuhang Ling, Baohua Zhang, Danting Wang, Limei Sun","doi":"10.1016/j.ecoenv.2024.117537","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117537","url":null,"abstract":"<p><p>Triclosan (TCS) is a primary broad-spectrum antibacterial agent commonly present in the environment. As a new type of environmental endocrine disruptor, it causes range of toxicities, including hepatotoxicity and reproductive toxicity. However, few research has examined the toxicity of long-term TCS-induced exposure in zebrafish at ambient concentrations, in contrast to the early life stage investigations. In the present study, we investigated the behavioral effects of TCS at environmental concentrations (300 μg/L) during constant exposure in zebrafish adults；An integrated transcriptomic and metabolomic analysis was performed to analyze the molecular mechanism underlying behavioral effects of TCS. Our results show that TCS exposure significantly induces behavioral disruptions such as anxiety-like behavior, memory problems, and altered social preferences. Histopathological investigations and neural ultrastructural observations demonstrated that TCS could induce variable levels of pyknosis and vacuolation in the cytoplasm of neurons as well as torn mitochondrial membranes, shrinkage and broken or absent cristae. Transcriptomics indicated that immune- and metabolism-related gene expression patterns were severely disturbed by TCS. Metabolomic analysis revealed 82 distinct metabolites in adult zebrafish exposed to TCS. Lipid metabolism, especially glycerophospholipid metabolism, and amino acid regulation pathways were co-enriched by multi-omics combinatorial analysis. Hence, this study highlights a number of biomarkers for the risk assessment of TCS against non-target organisms, offering a reference dataset for the behavioral toxicity of TCS to zebrafish, and strengthening the early warning, management, and control of TCS pollution.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"290 ","pages":"117537"},"PeriodicalIF":6.2,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821565","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":"Exploring the association between air pollution and the incidence of liver cancers.","authors":"Xin Wu, Xin Zhang, Xiaopeng Yu, Hongyuan Liang, Shaoshan Tang, Yao Wang","doi":"10.1016/j.ecoenv.2024.117437","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117437","url":null,"abstract":"<p><p>Liver cancer, namely hepatocellular carcinoma (HCC), is a major global health concern deeply influenced by environmental factors. Air pollutants emerged as significant contributors to its incidence. This review explores the association between air pollution-specifically particulate matter (PM2.5), industrial chemicals like vinyl chloride, and benzene-and the increased risk of liver cancer. Mechanistically, air pollutants may cause liver damage by inducing oxidative stress, inflammation, and genetic mutations, contributing to cancer development. Epidemiological evidence from cohort and geographic studies highlights a positive correlation between long-term exposure to air pollutants and elevated incidence and mortality of liver cancer. Furthermore, air pollution has been shown to worsen survival outcomes in liver cancer patients, particularly those diagnosed at early stages. The review emphasizes the need for stricter air quality regulations and relevant research for underlying mechanisms exposed to air pollution. Addressing air pollution exposure could be crucial for reducing liver cancer risks and improving public health outcomes.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"290 ","pages":"117437"},"PeriodicalIF":6.2,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821562","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":"Abcb1 is involved in the efflux of trivalent inorganic arsenic from brain microvascular endothelial cells.","authors":"Man Lv, Ziqiao Guan, Jia Cui, Xinbo Ma, Kunyu Zhang, Xinhua Shao, Meichen Zhang, Yanhui Gao, Yanmei Yang, Xiaona Liu","doi":"10.1016/j.ecoenv.2024.117515","DOIUrl":"https://doi.org/10.1016/j.ecoenv.2024.117515","url":null,"abstract":"<p><p>Arsenic (As) can penetrate brain tissue through the blood-brain barrier (BBB), and the ATP-binding cassette subfamily B member 1 (Abcb1) has been shown to facilitate the transport of inorganic arsenic (iAs) in animal liver, small intestine, and yeast. However, the relationship between Abcb1 and BBB has not been reported, and the mechanism of brain microvascular endothelial cells Abcb1 on the transport of iAs needs to be further studied. Increased arsenic levels were observed in mice exposed to 25 mg/L or 50 mg/L of sodium arsenite (NaAsO₂) in drinking water, and both arsenic uptake and efflux were detected in bEnd.3 cells treated with 16 μmol/L NaAsO₂. Elevated levels of Abcb1 protein were found in the NaAsO₂-exposed mouse brain microvascular endothelium and in NaAsO₂-treated bEnd.3 cells. Inhibition of Abcb1's efflux function significantly reduced the 2-hour arsenic efflux rate in bEnd.3 cells loaded arsenic. Conversely, overexpression of either Abcb1a or Abcb1b significantly increased the 2-hour arsenic efflux rate in these cells loaded arsenic. These findings suggest that Abcb1 may play a crucial role in mediating arsenic efflux from mouse brain microvascular endothelial cells.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"289 ","pages":"117515"},"PeriodicalIF":6.2,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821557","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}