Department of Environmental and Occupational Health, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15219-3130, USA.
Mol Nutr Food Res. 2011 Sep;55(9):1342-60. doi: 10.1002/mnfr.201100279.
Acrolein is a respiratory irritant that can be generated during cooking and is in environmental tobacco smoke. More plentiful in cigarette smoke than polycyclic aromatic hydrocarbons (PAH), acrolein can adduct tumor suppressor p53 (TP53) DNA and may contribute to TP53-mutations in lung cancer. Acrolein is also generated endogenously at sites of injury, and excessive breath levels (sufficient to activate metalloproteinases and increase mucin transcripts) have been detected in asthma and chronic obstructive pulmonary disease (COPD). Because of its reactivity with respiratory-lining fluid or cellular macromolecules, acrolein alters gene regulation, inflammation, mucociliary transport, and alveolar-capillary barrier integrity. In laboratory animals, acute exposures have lead to acute lung injury and pulmonary edema similar to that produced by smoke inhalation whereas lower concentrations have produced bronchial hyperreactivity, excessive mucus production, and alveolar enlargement. Susceptibility to acrolein exposure is associated with differential regulation of cell surface receptor, transcription factor, and ubiquitin-proteasome genes. Consequent to its pathophysiological impact, acrolein contributes to the morbidly and mortality associated with acute lung injury and COPD, and possibly asthma and lung cancer.
丙烯醛是一种呼吸刺激性物质，可在烹饪过程中产生，也存在于环境烟草烟雾中。丙烯醛在香烟烟雾中的含量比多环芳烃（PAH）多，可与肿瘤抑制因子 p53（TP53）DNA 加合物，并可能导致肺癌中 TP53 突变。丙烯醛也在内源性损伤部位产生，在哮喘和慢性阻塞性肺疾病（COPD）中检测到过量的呼吸水平（足以激活金属蛋白酶并增加粘蛋白转录本）。由于其与呼吸道衬里液或细胞大分子的反应性，丙烯醛改变了基因调控、炎症、黏液纤毛运输和肺泡-毛细血管屏障完整性。在实验动物中，急性暴露会导致类似于吸入烟雾引起的急性肺损伤和肺水肿，而较低浓度会导致支气管高反应性、过度黏液产生和肺泡扩大。对丙烯醛暴露的易感性与细胞表面受体、转录因子和泛素-蛋白酶体基因的差异调节有关。由于其病理生理影响，丙烯醛导致与急性肺损伤和 COPD 相关的发病率和死亡率增加，并可能与哮喘和肺癌有关。
