Crotonaldehyde, a highly toxic α, β‐unsaturated aldehyde, is a ubiquitous hazardous pollutant. Because of its extreme toxicity and ubiquity in all types of smoke, most current research focuses on the lung toxicity of such air pollutants. However, the specific mechanism of pulmonary toxicity caused by crotonaldehyde remains unclear, especially after long‐term exposure to crotonaldehyde at low dose. Therefore, the aim of the present study is to determine whether crotonaldehyde‐induced oxidative damage and inflammation promote apoptosis in rats via the mitochondrial pathway using histopathology, immunohistochemistry, biochemistry analysis and Western blot analysis. The results show that crotonaldehyde elicited oxidative damage and inflammation in rats in a concentration‐dependent manner. Crotonaldehyde‐induced lung injury which was confirmed by H&E, Masson's trichrome staining and TUNEL. And crotonaldehyde‐induced lung cell apoptosis showed a concentration‐response relationship. Immunohistochemistry and Western blot results showed that apoptotic mitochondrial signaling pathway is abnormally activated in crotonaldehyde‐induced lung injury. Collectively, this study demonstrates that exposure of rats to crotonaldehyde induces lung injury by inducing apoptosis, which is related to oxidative damage and inflammation through mitochondrial pathway.

中文翻译：

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巴豆醛致肺损伤中线粒体信号通路调控肺细胞凋亡

巴豆醛是一种剧毒的 α, β-不饱和醛，是一种普遍存在的危险污染物。由于其极端毒性和普遍存在于所有类型的烟雾中，目前大多数研究都集中在此类空气污染物的肺毒性上。然而，巴豆醛引起肺毒性的具体机制尚不清楚，尤其是在长期接触低剂量巴豆醛后。因此，本研究的目的是通过组织病理学、免疫组织化学、生物化学分析和蛋白质印迹分析确定巴豆醛诱导的氧化损伤和炎症是否通过线粒体途径促进大鼠细胞凋亡。结果表明，巴豆醛以浓度依赖性方式引起大鼠的氧化损伤和炎症。H& 证实巴豆醛诱导的肺损伤 E，马森三色染色和 TUNEL。巴豆醛诱导的肺细胞凋亡呈浓度-反应关系。免疫组织化学和蛋白质印迹结果表明，在巴豆醛诱导的肺损伤中，凋亡线粒体信号通路异常激活。总的来说，这项研究表明，大鼠暴露于巴豆醛通过诱导细胞凋亡诱导肺损伤，这与通过线粒体途径的氧化损伤和炎症有关。