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目前对矽肺的发病机理,有种见解认为,Sio_2粉尘被吞噬细胞胞饮后发生分子水平的作用,是由于 Sio_2催化脂质过氧化反应引起的。体外试验证明石英粉尘与豚鼠肺泡巨噬细胞在37°(下孵育一小时,可使肺泡巨噬细胞的过氧化反应增强。对大鼠肺组织的脂质过氧化具有一定的剂量——效应关系,表现为双向性。而脂质过氧化在矽肺纤维化过程中的作用,报导不尽相同。尚无结论。本研究经体内试验,观察 Sio_2粉尘作用下,大鼠肺组织与血清过氧化脂质水平的变
Currently on the pathogenesis of silicosis, there is a perception that Sio_2 dust is phagocytic cells to drink after the molecular level of the role, due to lipid peroxidation caused by Sio_2 reaction. In vitro experiments show that quartz dust and guinea pig alveolar macrophages at 37 ° (for one hour under the alveolar macrophages peroxidation can be enhanced on rat lung tissue lipid peroxidation has a dose-effect relationship , The performance of the two-way.The role of lipid peroxidation in the process of silicosis, the report is not the same.No conclusion.In this study, in vivo experiments observed Sio_2 dust, lung tissue and serum lipid peroxidation The level of quality change