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通过体外试验鉴定与燃烧产生的烟尘表面化学和颗粒结构相关的毒性参数。

Identification of Toxicity Parameters Associated with Combustion Produced Soot Surface Chemistry and Particle Structure by in Vitro Assays.

作者信息

Al Housseiny Heba, Singh Madhu, Emile Shaneeka, Nicoleau Marvin, Wal Randy L Vander, Silveyra Patricia

机构信息

Biobehavioral Laboratory, School of Nursing, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

John and Willie Leone Family Department of Energy and Mineral Engineering, The Pennsylvania State University, University Park, PA 16801, USA.

出版信息

Biomedicines. 2020 Sep 11;8(9):345. doi: 10.3390/biomedicines8090345.

Abstract

Air pollution has become the world's single biggest environmental health risk of the past decade, causing millions of yearly deaths worldwide. One of the dominant air pollutants is fine particulate matter (PM), which is a product of combustion. Exposure to PM has been associated with decreased lung function, impaired immunity, and exacerbations of lung disease. Accumulating evidence suggests that many of the adverse health effects of PM exposure are associated with lung inflammation and oxidative stress. While the physical structure and surface chemistry of PM are surrogate measures of particle oxidative potential, little is known about their contributions to negative health effects. In this study, we used functionalized carbon black particles as surrogates for atmospherically aged combustion-formed soot to assess the effects of PM surface chemistry in lung cells. We exposed the BEAS-2B lung epithelial cell line to different soot at a range of concentrations and assessed cell viability, inflammation, and oxidative stress. Our results indicate that exposure to soot with varying particle surface composition results in differential cell viability rates, the expression of pro-inflammatory and oxidative stress genes, and protein carbonylation. We conclude that particle surface chemistry, specifically oxygen content, in soot modulates lung cell inflammatory and oxidative stress responses.

摘要

空气污染已成为过去十年全球最大的单一环境健康风险,每年在全球造成数百万例死亡。主要空气污染物之一是细颗粒物(PM),它是燃烧的产物。接触PM与肺功能下降、免疫力受损以及肺部疾病恶化有关。越来越多的证据表明,接触PM对健康的许多不利影响与肺部炎症和氧化应激有关。虽然PM的物理结构和表面化学是颗粒氧化潜力的替代指标,但对于它们对负面健康影响的作用知之甚少。在本研究中,我们使用功能化炭黑颗粒作为大气老化燃烧形成的烟尘的替代物,以评估PM表面化学在肺细胞中的作用。我们将BEAS-2B肺上皮细胞系暴露于不同浓度的烟尘中,并评估细胞活力、炎症和氧化应激。我们的结果表明,暴露于具有不同颗粒表面组成的烟尘会导致不同的细胞活力率、促炎和氧化应激基因的表达以及蛋白质羰基化。我们得出结论,烟尘中的颗粒表面化学,特别是氧含量,调节肺细胞的炎症和氧化应激反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c633/7555766/6e16a980cb19/biomedicines-08-00345-g001.jpg

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