矽肺发病机制中脂质过氧化作用的初探

本文利用扫描电镜观察石英对肺泡巨噬细胞(AM)损伤的形态改变,观察到:向AM培养液中加入超氧化物歧化酶(SOD),石英对AM的损伤可以得到明显保护。表明石英对AM的损伤过程中有SOD作用底物自由基——超氧阴离子(O_2~÷)参与。在此基础上进行体内实验,给大鼠气管注入石英的同时,投予SOD,观察肺纤维化改变,结果与对照组比较纤维化程度未见明显差异。作者认为矽肺发病机制中存在脂质过氧化过程,引致脂质过氧化反应的自由基的来源,可能是石英自身产生的,也可能是石英诱导AM产生的。后者不容忽视,它可能是构成AM自身与肺组织损伤的一个或相加因素。但在石英引致的肺纤维化过程中,脂质过氧化反应恐不是石英致纤维化的唯一因素。

PRELIMINARY EVALUATION ON LIPID PEROXIDATION IN THE PATHOGENIC MECHANISM OF SILICOSIS

The morphological findings of alveolar macrophages (AM) damage induced by quartz were observed with scanning electron microscope.However,the damage could be inhibited through adding superoxide dismutase(SOD).This indicated that the free radical, Peroxide anion (O2-) of the substrate of SOD might beinvolved in the damage due to quartz.A further observation of the fibrotic reaction was performed with simultaneous administration of quartz and SOD by intratracheal injection in rats, but no obvious difference was noted compared with the controls.The author believed that tie free radical related to liPid Peroxidation in the Pathogenic mechanism of silicosis might originate from quartz itself or from quartz-irritated AM.The latter could not be overlooked since it might constitute single or additive factors in the occurance of the damage of AM and lung tissue.In spite of this, the liPid Perxidation might not be the unique factor in the fibrogenesis due to quartz.