Ambient fine particulate matter (PM2.5) poses great risk to human health worldwide. Pulmonary oxidative stress is considered to be a vital step in PM2.5 triggered adverse health effects. Many in vitro studies have demonstrated that PM2.5 could induce oxidative stress in lung epithelia or macrophages but few studies have explored the difference between these two types of cells when estimating PM2.5 caused pulmonary oxidative stress. In this study, we compared the oxidative stress intensity between lung epithelial cells (A549) and monocyte-macrophage cells (Raw264.7) after PM2.5 treatments and explored the major generation mechanism of ROS in both cell lines. We found that Raw264.7 was more sensitive to PM2.5-induced cytotoxicity than A549; however, PM2.5 caused much greater oxidative stress in A549 compared with in Raw264.7. Moreover, we found that production of ROS via xanthine oxidase and nitric oxide synthase was involved in oxidative stress in A549 cells, while NADPH oxidase and nitric oxide synthase were the major sources of ROS generation in Raw264.7 cells. These observations suggested that lung epithelial cell is a more sensitive cell when estimating PM2.5-induced pulmonary oxidative stress in vitro.
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This work was supported by the National Natural Science Foundation of China (31601192, 91643103), Zhejiang Provincial Natural Science Foundation of China (LY20H260004), special fund of the State Key Joint Laboratory of Environment Simulation and Pollution Control (16K04ESPCP) and Foundation of Zhejiang Chinese Medical University (2018ZJ07).
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Li, R., Wang, Y., Qiu, X. et al. Difference on oxidative stress in lung epithelial cells and macrophages induced by ambient fine particulate matter (PM2.5). Air Qual Atmos Health 13, 789–796 (2020). https://doi.org/10.1007/s11869-020-00835-5
- Air pollution
- Fine particulate matter
- Oxidative stress
- Lung epithelial cells