Epidemiologic studies have suggested that elevated concentrations of particulate matter (PM) are strongly associated with an increased risk of developing cardiovascular diseases, including arrhythmia. However, the cellular and molecular mechanisms by which PM exposure causes arrhythmia and the component that is mainly responsible for this adverse effect remains to be established. In this study, the arrhythmogenicity of mobilized organic matter from two different types of PM collected during summer (SPM) and winter (WPM) seasons in the Seoul metropolitan area was evaluated. In addition, differential effects between polycyclic aromatic hydrocarbons (PAHs) and oxygenated PAHs (oxy-PAHs) on the induction of electrophysiological instability were examined. We extracted the bioavailable organic contents of ambient PM, measuring 10 μm or less in diameter, collected from the Seoul metropolitan area using a high-volume air sampler. Significant alterations in all factors tested for association with electrophysiological instability, such as intracellular Ca2+ levels, reactive oxygen species (ROS) generation, and mRNA levels of the Ca2+-regulating proteins, sarcoplasmic reticulum Ca2+ATPase (SERCA2a), Ca2+/calmodulin-dependent protein kinase II (CaMK II), and ryanodine receptor 2 (RyR2) were observed in cardiomyocytes treated with PM. Moreover, the alterations were higher in WPM-treated cardiomyocytes than in SPM-treated cardiomyocytes. Three-fold more oxy-PAH concentrations were observed in WPM than SPM. As expected, electrophysiological instability was induced higher in oxy-PAHs (9,10-anthraquinone, AQ or 7,12-benz(a) anthraquinone, BAQ)-treated cardiomyocytes than in PAHs (anthracene, ANT or benz(a) anthracene, BaA)-treated cardiomyocytes; oxy-PAHs infusion of cells mediated by aryl hydrocarbon receptor (AhR) was faster than PAHs infusion. In addition, ROS formation and expression of calcium-related genes were markedly more altered in cells treated with oxy-PAHs compared to those treated with PAHs. The concentrations of oxy-PAHs in PM were found to be higher in winter than in summer, which might lead to greater electrophysiological instability through the ROS generation and disruption of calcium regulation.

中文翻译：

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来自周围颗粒物的氧化多环芳烃会诱导心肌细胞的电生理不稳定。

流行病学研究表明，颗粒物（PM）浓度升高与发生心血管疾病（包括心律不齐）的风险增加密切相关。然而，PM暴露引起心律不齐的细胞和分子机制以及主要负责这种不良反应的成分尚待确定。在这项研究中，评估了首尔市区夏季（SPM）和冬季（WPM）两种季节收集的两种不同类型PM中动员有机物的心律失常性。此外，检查了多环芳烃（PAHs）和氧化的PAHs（oxy-PAHs）在诱导电生理不稳定方面的不同作用。我们提取了直径为10μm或更小的周围PM的生物可利用有机物含量，使用大容量空气采样器从首尔市区收集。与电生理不稳定相关的所有测试因素的显着变化，例如细胞内Ca2 +水平，活性氧（ROS）生成以及Ca2 +调节蛋白，肌浆网Ca2 + ATPase（SERCA2a），Ca2 + /钙调蛋白依赖性mRNA水平在用PM处理的心肌细胞中观察到蛋白激酶II（CaMK II）和ryanodine受体2（RyR2）。此外，WPM处理过的心肌细胞中的变化高于SPM处理过的心肌细胞中的变化。在WPM中，观察到的氧PAH浓度是SPM的三倍。不出所料，经氧-PAHs（9,10-蒽醌，AQ或7,12-benz（a）蒽醌，BAQ）处理的心肌细胞比PAHs（蒽，ANT或苯并（a）蒽（BaA）处理的心肌细胞; 芳烃受体（AhR）介导的氧-PAHs输注比PAHs输注更快。此外，与用PAHs处理的细胞相比，用oxy-PAHs处理的细胞中ROS的形成和钙相关基因的表达变化更大。人们发现，冬季PM中的氧-PAHs浓度要高于夏季，这可能通过产生ROS和破坏钙调节作用而导致更大的电生理不稳定。