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目的：探讨矽尘致肺泡巨噬细胞损伤过程中是否存在着氧化损伤机制。方法：对矽尘作用于肺泡巨噬细胞产生的 Ｏ２和 Ｈ２Ｏ２进行原位显示、定量测定并做相关分析；以 ＡＴＰａｓｅ作为膜功能酶改变的反映；在亚细胞水平观察细胞形态结构。结果：细胞形态结构受损程度、膜ＡＴＰａｓｅ的活性与矽生致肺泡巨噬细胞早期产生的氧自由基活性直接相关。结论：（ｌ）首次将原位显示氧自由基技术应用于矽尘致肺泡巨噬细胞损伤机制研究，发现氧自由基的产生及其介导的进一步的自由基连锁反应是砂尘损伤肺泡巨噬细胞的机制之一，提示应用抗氧化剂减弱矽生所致的损伤，以预防肺成纤维细胞增殖，给临床用药提供了理论参考；（２）形态学方法定位显示氧自由基比自由基总体测定技术更能直观具体地阐明细胞损伤状况。为矽肺发病机制的研究提供了又一项实验技术。
OBJECTIVE: To investigate whether oxidative damage exists during the injury of alveolar macrophages induced by silica dust. Methods: O2 and H2O2 generated by the exposure of silica dust to alveolar macrophages were in situ displayed, quantitatively analyzed and correlated. ATPase was used as a marker of membrane functional enzyme changes. Morphology and structure were observed at subcellular level. Results: The degree of cell morphology and structure damage, membrane ATPase activity and silicon-induced alveolar macrophages early generation of oxygen free radical activity is directly related. Conclusion: (1) For the first time, the in situ display of oxygen free radical technology was applied to the study of the mechanism of alveolar macrophage injury induced by silica dust. It was found that the generation of oxygen free radicals and the further free radical chain reaction mediated by them are sand-dust damage alveolar macrophages Suggesting that the use of antioxidants to weaken the damage caused by silica, in order to prevent the proliferation of lung fibroblasts, to provide a theoretical reference for clinical use; (2) Morphological methods showed that oxygen free radicals than the total free radical Determination of technology can be more intuitive and specific description of cell damage. For the study of pathogenesis of silicosis provides another experimental technique.