Phosphocholine-induced energy source shift alleviates mitochondrial dysfunction in lung cells caused by geospecific PM2.5 components

• 成果类型: Article
• 署名作者: Song, Yuanyuan; Zhang, Yanhao; Zhu, Lin; Chen, Yanyan; Chen, Yi-Jie; Zhu, Zhitong; Feng, Jieqing; Qi, Zenghua; Yu, Jian Zhen; Yang, Zhu; Cai, Zongwei
• 署名单位: Hong Kong Baptist University; Guangdong University of Technology; Hong Kong University of Science & Technology; Hong Kong Baptist University
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-12382
• DOI: 10.1073/pnas.2317574121
• 发表日期: 2024-03-25
• 关键词: polycyclic aromatic-hydrocarbons; airborne particulate matter; polyaromatic hydrocarbons; CHINA; guangzhou; derivatives; exposure; taiyuan; urban; city

摘要

Fine particulate matter (PM2.5) is globally recognized for its adverse implications on human health. Yet, remain limited the individual contribution of particular PM2.5 components to its toxicity, especially considering regional disparities. Moreover, prevention solutions for PM2.5- associated health effects are scarce. In the present study, we comprehensively characterized and compared the primary PM2.5 constituents and their altered metabolites from two locations: Taiyuan and Guangzhou. Analysis of year - long PM2.5 samples revealed 84 major components, encompassing organic carbon, elemental carbon, ions, metals, and organic chemicals. PM2.5 from Taiyuan exhibited higher contamination, associated health risks, dithiothreitol activity, and cytotoxicities than Guangzhou's counterpart. Applying metabolomics, BEAS-2B lung cells exposed to PM2.5 from both cities were screened for significant alterations. A correlation analysis revealed the metabolites altered by PM2.5 and the critical toxic PM2.5 components in both regions. Among the PM2.5-down-regulated metabolites, phosphocholine emerged as a promising intervention for PM2.5 cytotoxicities. Its supplementation effectively attenuated PM2.5-induced energy metabolism disorder and cell death via activating fatty acid oxidation and inhibiting Phospho1 expression. The highlighted toxic chemicals displayed combined toxicities, potentially counteracted by phosphocholine. Our study offered a promising functional metabolite to alleviate PM2.5-induced cellular disorder and provided insights into the geo-based variability in toxic PM2.5 components.