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.

中文翻译：

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环境细颗粒物（PM2.5）对肺上皮细胞和巨噬细胞氧化应激的影响

环境细颗粒物 (PM2.5) 对全球人类健康构成巨大威胁。肺氧化应激被认为是 PM2.5 引发不良健康影响的重要步骤。许多体外研究表明，PM2.5 可以诱导肺上皮细胞或巨噬细胞的氧化应激，但在估计 PM2.5 引起肺氧化应激时，很少有研究探讨这两种细胞之间的差异。在这项研究中，我们比较了 PM2.5 处理后肺上皮细胞 (A549) 和单核巨噬细胞 (Raw264.7) 之间的氧化应激强度，并探讨了两种细胞系中 ROS 的主要生成机制。我们发现 Raw264.7 对 PM2.5 诱导的细胞毒性比 A549 更敏感；然而，与 Raw264.7 相比，PM2.5 在 A549 中引起了更大的氧化应激。而且，我们发现通过黄嘌呤氧化酶和一氧化氮合酶产生 ROS 参与了 A549 细胞的氧化应激，而 NADPH 氧化酶和一氧化氮合酶是 Raw264.7 细胞中产生 ROS 的主要来源。这些观察结果表明，在体外估计 PM2.5 诱导的肺氧化应激时，肺上皮细胞是一种更敏感的细胞。