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DOI | 10.1186/s12989-014-0077-x |
Metal rich particulate matter impairs acetylcholine-mediated vasorelaxation of microvessels in mice | |
Cuevas, Azita K.1; Niu, Jingping2; Zhong, Mianhua1; Liberda, Eric N.1; Ghio, Andrew3; Qu, Qingshan1; Chen, Lung Chi1 | |
发表日期 | 2015-06-04 |
ISSN | 1743-8977 |
卷号 | 12 |
英文摘要 | Background: Exposure to PM2.5 (particulate matter <2.5 mu m) has been associated with changes in endothelial function. PM2.5 was collected from two Chinese cities, Jinchang (JC) and Zhangye (ZH), both with similar PM2.5 concentrations. However, JC had levels of nickel (Ni), selenium (Se), copper (Cu), and arsenic (As) that were 76, 25, 17, and 7 fold higher than that measured in ZH, respectively. We used this unique PM sample to delineate the chemical components that drive pulmonary and systemic effects and explore the mechanism(s) by which vascular dysfunction is caused. Methods: Male FVB/N mice received oropharyngeal aspiration of water or PM2.5 from JC, ZH or ZH spiked with one of the following elements at the same concentrations found in the JC PM (Ni = 4.76; As = 2.36; Se = 0.24; Cu = 2.43 mu g/mg) followed by evaluation of markers of pulmonary and systemic inflammation. Mesenteric arteries were isolated for gene expression or functional response to various agonists (Phenylephrine, Acetylcholine, and Sodium Nitroprusside) and inhibitors (L-NAME, Apocynin, and VAS2870) ex vivo. Results: Protein and total cell counts from lung lavage revealed significant pulmonary inflammation from ZH (p < 0.01) and JC and ZH + NiSO4 (p < 0.001) as compared to control and a significant decrease in mesenteric artery relaxation (p < 0.001) and this decrease is blunted in the presence of NADPH oxidase inhibitors. Significant increases in gene expression (TNF-alpha, IL-6, Nos3; p < 0.01; NOX4; p < 0.05) were observed in JC and ZH + NiSO4, as well as significantly higher concentrations of VEGF and IL-10 (p < 0.01, p < 0.001; respectively). Conclusions: Our results indicate that the specific toxicity observed in PM from JC is likely due to the nickel component in the PM. Further, since VAS2870 was the most successful inhibitor to return vessels to baseline relaxation values, NADPH Oxidase is implicated as the primary source of PM-induced O-2(center dot-). |
英文关键词 | Vascular function;Endothelial dysfunction;Nickel;Air pollution;Particulate matter;Endothelial nitric oxide;uncoupling;Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase |
语种 | 英语 |
WOS记录号 | WOS:000356037700001 |
来源期刊 | PARTICLE AND FIBRE TOXICOLOGY |
来源机构 | 美国环保署 |
文献类型 | 期刊论文 |
条目标识符 | http://gcip.llas.ac.cn/handle/2XKMVOVA/59000 |
作者单位 | 1.NYU, Sch Med, Dept Environm Med, Tuxedo Pk, NY 10987 USA; 2.Lanzhou Univ, Sch Publ Hlth, Lanzhou 730000, Peoples R China; 3.US EPA, NHEERL, Human Studies Div, Chapel Hill, NC USA |
推荐引用方式 GB/T 7714 | Cuevas, Azita K.,Niu, Jingping,Zhong, Mianhua,et al. Metal rich particulate matter impairs acetylcholine-mediated vasorelaxation of microvessels in mice[J]. 美国环保署,2015,12. |
APA | Cuevas, Azita K..,Niu, Jingping.,Zhong, Mianhua.,Liberda, Eric N..,Ghio, Andrew.,...&Chen, Lung Chi.(2015).Metal rich particulate matter impairs acetylcholine-mediated vasorelaxation of microvessels in mice.PARTICLE AND FIBRE TOXICOLOGY,12. |
MLA | Cuevas, Azita K.,et al."Metal rich particulate matter impairs acetylcholine-mediated vasorelaxation of microvessels in mice".PARTICLE AND FIBRE TOXICOLOGY 12(2015). |
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