Prooxidant and Proinflammatory Potency of Air Pollution Particulate Matter (PM2.5-0.3) Produced in Rural, Urban, or Industrial Surroundings in Human Bronchial Epithelial Cells (BEAS-2B)
Prooxidant and Proinflammatory Potency of Air Pollution Particulate Matter (PM2.5-0.3) Produced in Rural, Urban, or Industrial Surroundings in Human Bronchial Epithelial Cells (BEAS-2B)
复制标题
DOI：
10.1021/tx200529v
复制
发表时间：
2012-04-01
影响因子：
4.1
通讯作者：
Garcon, Guillaume
中科院分区：
文献类型：
--
作者：
Dergham, Mona;Lepers, Capucine;Garcon, Guillaume
令人信服的证据表明，暴露于空气污染颗粒物（PM）会影响人类健康。然而，如何PM组合物与PM尺寸相互作用，造成不良的健康影响需要阐明。在这项研究中，我们也有兴趣在农村，城市或工业环境中产生的PM2.5-0.3样品的理化特性和毒理学终点，从而期望区分各自在体外对人体支气管上皮细胞（BEAS-2B）的不良健康影响。三个PM2.5-0.3样本的物理化学特征，特别是无机和有机成分，与各自的排放源密切相关。还参考剂量/反应关系;在三个PM2.5-0.3样品中，毒理学上最相关的暴露时间（即，24、48和72 h）和剂量（即，3.75μ g PM/cm（2）和15 μ g PM/cm（2））用于研究涉及PM诱导的肺毒性的潜在作用机制。吸附在三个PM2.5-0.3样品上的有机化学品（即，多环芳烃）能够诱导异生物质代谢酶的基因表达（即，细胞色素P4501 A1和1B 1，以及较小程度的NADPH-醌氧化还原酶-1）。此外，暴露于三种PM2.5-0.3样品的BEAS-2B细胞内的细胞内活性氧物质诱导氧化损伤（即，8-羟基-2 '-脱氧鸟苷形成、丙二醛产生和/或谷胱甘肽状态改变）。炎症介质的基因表达和/或蛋白质分泌也有统计学显著增加（即，特别是IL-6和IL-8）在BEAS-2B细胞暴露于三种PM2.5-0.3样品后的变化。两者合计，目前的研究结果表明，氧化损伤和炎症反应precancellation细胞毒性在空气污染PM2.5-0.3暴露的BEAS-2B细胞，并支持的想法，即PM的大小，组成和起源可以相互作用，以一种复杂的方式，以确定在体外对PM的反应。
Compelling evidence indicates that exposure to air pollution particulate matter (PM) affects human health. However, how PM composition interacts with PM-size to cause adverse health effects needs elucidation. In this study, we were also interested in the physicochemical characteristics and toxicological end points of PM2.5-0.3 samples produced in rural, urban, or industrial surroundings, thereby expecting to differentiate their respective in vitro adverse health effects in human bronchial epithelial cells (BEAS-2B). Physicochemical characteristics of the three PM2.5-0.3 samples, notably their inorganic and organic components, were closely related to their respective emission sources. Referring also to the dose/response relationships ;of the three PM2.5-0.3 samples, the most toxicologically relevant exposure times (i.e., 24, 48, and 72 h) and doses (i.e., 3.75 mu g PM/cm(2) and 15 mu g PM/cm(2)) to use to study the underlying mechanisms of action involved in PM-induced lung toxicity were chosen. Organic chemicals adsorbed on the three PM2.5-0.3 samples (i.e., polycyclic aromatic hydrocarbons) were able to induce the gene expression of xenobiotic-metabolizing enzymes (i.e., Cytochrome P4501A1 and 1B1, and, to a lesser extent, NADPH-quinone oxidoreductase-1). Moreover, intracellular reactive oxygen species within BEAS-2B cells exposed to the three PM2.5-0.3 samples induced oxidative damage (i.e., 8-hydroxy-2'-deoxyguanosine formation, malondialdehyde production and/or glutathione status alteration). There were also statistically significant increases of the gene expression and/or protein secretion of inflammatory mediators (i.e., notably IL-6 and IL-8) in BEAS-2B cells after their exposure to the three PM2.5-0.3 samples. Taken together, the present findings indicated that oxidative damage and inflammatory response preceeded cytotoxicity in air pollution PM2.5-0.3-exposed BEAS-2B cells and supported the idea that PM-size, composition, and origin could interact in a complex manner to determine the in vitro responsiveness to PM.