Department of Pediatrics, University of Texas Medical Branch, 301 University Blvd., Galveston, Texas 77555-0369.
Environ Toxicol. 2014 Aug;29(8):908-15. doi: 10.1002/tox.21818. Epub 2012 Oct 10.
Increases in asthma worldwide have been associated epidemiologically with expanding urban air pollution. The mechanistic relationship between airway hyper-responsiveness, inflammation, and ambient airborne triggers remains ambiguous. Acrolein, a ubiquitous aldehyde pollutant, is a product of incomplete combustion reactions. Acrolein is abundant in cigarette smoke, effluent from industrial smokestacks, diesel exhaust, and even hot oil cooking vapors. Acrolein is a potent airway irritant and can induce airway hyper-responsiveness and inflammation in the lungs of animal models. In the present study, we utilized the mast cell analog, RBL-2H3, to interrogate the responses of cells relevant to airway inflammation and allergic responses as a model for the induction of asthma-like conditions upon exposure to acrolein. We hypothesized that acrolein would induce oxidative stress and degranulation in airway mast cells. Our results indicate that acrolein at 1 ppm initiated degranulation and promoted the generation of reactive oxygen species (ROS). Introduction of antioxidants to the system significantly reduced both ROS generation and degranulation. At higher levels of exposure (above 100 ppm), RBL-2H3 cells displayed signs of severe toxicity. This experimental data indicates acrolein can induce an allergic inflammation in mast cell lines, and the initiation of degranulation was moderated by the application of antioxidants.
全球范围内哮喘发病率的增加与不断扩大的城市空气污染有关。气道高反应性、炎症和环境空气触发因素之间的机制关系仍不清楚。丙烯醛是一种普遍存在的醛类污染物，是不完全燃烧反应的产物。丙烯醛在香烟烟雾、工业烟囱废气、柴油尾气甚至热油烹饪蒸气中都很丰富。丙烯醛是一种强烈的气道刺激物，可在动物模型的肺部引起气道高反应性和炎症。在本研究中，我们利用肥大细胞类似物 RBL-2H3 来研究与气道炎症和过敏反应相关的细胞反应，作为暴露于丙烯醛时诱导类似哮喘条件的模型。我们假设丙烯醛会在气道肥大细胞中诱导氧化应激和脱颗粒。我们的结果表明，1 ppm 的丙烯醛引发脱颗粒并促进活性氧 (ROS) 的生成。将抗氧化剂引入系统可显著减少 ROS 的产生和脱颗粒。在更高的暴露水平（高于 100 ppm）下，RBL-2H3 细胞显示出严重毒性的迹象。这些实验数据表明，丙烯醛可在肥大细胞系中诱导过敏炎症，而脱颗粒的起始可通过应用抗氧化剂来调节。
