School of Public Health, the key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Guizhou Medical University, Guiyang, 550025, People's Republic of China.
College of Life Science and Oceanography, Shenzhen University, Shenzhen, 518060, People's Republic of China.
Biol Trace Elem Res. 2023 Aug;201(8):3882-3902. doi: 10.1007/s12011-022-03466-2. Epub 2022 Nov 5.
Chronic arsenic poisoning is a global health problem that affects millions of people, and studies have found that long-term ingestion of arsenic-containing compounds can lead to lung damage, but the exact mechanism is unknown. In this study, Sprague-Dawley (SD) rats were used as the research object, and the proteomic analysis method based on sequential window acquisition of all theoretical fragment ions (SWATH) was used to detect the changes in the expression levels of related proteins in the lung tissue of arsenic-exposed rats, and to explore the mechanism of arsenic compound-induced lung injury. The results showed that arsenic exposure resulted in the abnormal expression of collagen type III and proteins involved in metabolic, immune, and cellular processes, leading to the dysfunction of important pathways associated with these proteins, resulting in lung injury. It suggested that the underlying mechanism of arsenic-induced lung injury may be related to oxidative stress, immune injury, cell junction, and collagen type III. This result provides a new research idea for revealing the mechanism of lung injury caused by arsenic exposure.
慢性砷中毒是一个全球性的健康问题，影响着数以百万计的人，研究发现，长期摄入含砷化合物会导致肺损伤，但具体机制尚不清楚。本研究以 Sprague-Dawley（SD）大鼠为研究对象，采用基于序贯窗口采集所有理论碎片离子（SWATH）的蛋白质组学分析方法，检测砷暴露大鼠肺组织中相关蛋白表达水平的变化，探讨砷化合物诱导肺损伤的机制。结果表明，砷暴露导致 III 型胶原和参与代谢、免疫和细胞过程的蛋白异常表达，导致与这些蛋白相关的重要途径功能障碍，从而导致肺损伤。这表明砷诱导肺损伤的潜在机制可能与氧化应激、免疫损伤、细胞连接和 III 型胶原有关。该结果为揭示砷暴露引起的肺损伤机制提供了新的研究思路。
