Liu Zhiyuan, Xu Pengfei, Gong Fuxu, Tan Yizhe, Han Jie, Tian Lei, Yan Jun, Li Kang, Xi Zhuge, Liu Xiaohua
Tianjin University of Sport, Tianjin 301617, China; Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China.
Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China.
Sci Total Environ. 2022 Feb 1;806(Pt 2):150630. doi: 10.1016/j.scitotenv.2021.150630. Epub 2021 Sep 28.
Ozone (O) exposure not only causes lung injury and lung inflammation but also changes blood composition. Previous studies have mainly focused on inflammatory processes and metabolic diseases caused by acute or chronic ozone exposure. However, the effect of ozone on lipid expression profiles remains unclear. This study aimed to investigate the lipidomic changes in lung tissue and serum of rats after ozone exposure for three months and explore the lipid metabolic pathway involved in an ozone-induced injury. Based on the non-targeted lipidomic analysis platform of the UPLC Orbitrap mass spectrometry system, we found that sub-chronic exposure to ozone significantly changed the characteristics of lipid metabolism in lungs and serum of rats. First, the variation in sphingomyelin (SM) and triglyceride (TG) levels in the lung and serum after O exposure are shown. SM decreased in both tissues, while TG decreased in the lungs and increased in the serum. Further, the effect of ozone on glycerophospholipids in the lung and serum was completely different. Phosphatidylethanolamine (PE), phosphatidylserine (PS), and phosphatidylinositol (PI) were the major glycerophospholipids whose levels were altered in the lung, while phosphatidylglycerol (PG), phosphatidic acid (PA), and phosphatidylcholine (PC) levels changed dramatically in the serum. Third, after O exposure, the level of monogalactosyldiacylglycerol (MGDG), mainly MGDG (43, 11), a saccharolipid, declined significantly and uniquely in the serum. These results suggested that sub-chronic O exposure may play a role in the development of several diseases through perturbation of lipidomic profiles in the lungs and blood. In addition, changes in the lipids of the lung and blood may induce or exacerbate respiratory diseases.
臭氧（O）暴露不仅会导致肺损伤和肺部炎症，还会改变血液成分。先前的研究主要集中在急性或慢性臭氧暴露引起的炎症过程和代谢疾病上。然而，臭氧对脂质表达谱的影响仍不清楚。本研究旨在调查臭氧暴露三个月后大鼠肺组织和血清中的脂质组学变化，并探索参与臭氧诱导损伤的脂质代谢途径。基于超高效液相色谱-轨道阱质谱系统的非靶向脂质组学分析平台，我们发现亚慢性臭氧暴露显著改变了大鼠肺和血清中的脂质代谢特征。首先，展示了臭氧暴露后肺和血清中鞘磷脂（SM）和甘油三酯（TG）水平的变化。两种组织中的SM均下降，而肺中的TG下降，血清中的TG上升。此外，臭氧对肺和血清中甘油磷脂的影响完全不同。磷脂酰乙醇胺（PE）、磷脂酰丝氨酸（PS）和磷脂酰肌醇（PI）是肺中水平发生改变的主要甘油磷脂，而血清中磷脂酰甘油（PG）、磷脂酸（PA）和磷脂酰胆碱（PC）水平变化显著。第三，臭氧暴露后，主要为单半乳糖基二酰基甘油（MGDG）（43, 11）的糖脂单半乳糖基二酰基甘油（MGDG）在血清中的水平显著且独特地下降。这些结果表明，亚慢性臭氧暴露可能通过干扰肺和血液中的脂质组学谱在多种疾病的发生发展中起作用。此外，肺和血液中脂质的变化可能诱发或加重呼吸系统疾病。
