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矽肺发病机制中脂质过氧化作用的初探 被引量:2

PRELIMINARY EVALUATION ON LIPID PEROXIDATION IN THE PATHOGENIC MECHANISM OF SILICOSIS
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摘要 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。 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.
出处 《工业卫生与职业病》 CAS CSCD 1993年第6期341-343,共3页 Industrial Health and Occupational Diseases
基金 国家自然科学基金
关键词 矽肺 自由基 过氧化脂质 silicosis lipid Peroxidation free radical
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