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Heppleston等人认为:游离二氧化硅表面的羟基可与巨噬细胞溶酶体膜的磷脂和蛋白质形成氢键,从而引起溶酶体膜破裂,溶菌酶释放和细胞自溶;死亡的巨噬细胞释放出H因子,导致了矽肺的形成。由于溶菌酶能将自身细胞破坏,引起肺部纤维化,为此,溶菌酶活性测定,对评价粉尘致纤维化能力具有一定意义。本实验采用大白鼠气管注入法进行了锑尘对溶菌酶动态改变的初步观察。
Heppleston et al. Argue that hydroxyl groups on the surface of free silica can form hydrogen bonds with the phospholipids and proteins of the lysosomal membrane of macrophages, leading to rupture of lysosomal membranes, release of lysozyme and autolysis of cells; dead macrophages The release of factor H, resulting in the formation of silicosis. Because lysozyme can destroy its own cells, causing pulmonary fibrosis, for this, the determination of lysozyme activity, to evaluate the ability of dust induced fibrosis has some significance. In this experiment, tracheal injection of rat antimony dust dynamic changes of lysozyme preliminary observation.