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为了探讨石英、石棉对抗氧化酶活性的影响，利用改良Ｍｙｖｉｒｋ 法收集兔肺泡巨噬细胞进行体外培养，采用酶－ 底物反应形成有色物来测定巨噬细胞的细胞裂解液中谷胱甘肽过氧化物酶（ＧＳＨＰｘ）的酶活性。结果发现，随着粉尘浓度的增加，石英组和温石棉组巨噬细胞内的ＧＳＨＰｘ的酶活性相应降低，存在显著的剂量反应关系（Ｐ＜ ０．０１）。在不同的粉尘剂量组，温石棉组和石英组的ＧＳＨＰｘ 酶活性均显著低于二氧化钛组（Ｐ＜ ０．０５），温石棉组低于石英组，但未发现显著的统计学差异。石英组和温石棉组的巨噬细胞死亡率均随粉尘浓度的增加而增大，存在着剂量反应关系，且温石棉组的死亡率高于石英组。石英组、温石棉组巨噬细胞内ＧＳＨＰｘ 酶活性和巨噬细胞的死亡率之间的相关系数分别为－ ０．９３１８ 和－ ０．８９８４，而二氧化钛组只有－ ０．３６３７。这说明石英、温石棉均可致巨噬细胞内ＧＳＨＰｘ 酶活性呈剂量反应关系的降低，使得胞内自由基Ｈ２Ｏ２ 不能正常消除，促使脂质过氧化加重，损害细胞；且温石棉的效应强于石英。提示ＧＳＨＰｘ 酶活性的降低在石英、温石棉致病中具有一定的作用
In order to investigate the impact of quartz and asbestos on the activity of oxidative enzymes, rabbit alveolar macrophages were harvested by modified Myvirk method and cultured in vitro. Chromosomal glutathione peroxidation Enzyme (GSH Px) enzyme activity. The results showed that with the increase of dust concentration, the GSH-Px activity in macrophages of quartz group and chrysotile ascorbate group decreased correspondingly, and there was a significant dose-response relationship (P <0.01). In different dust dose groups, GSH-Px activity in chrysotile and quartz group was significantly lower than that in titanium dioxide group (P <0.05), and chrysotile group was lower than quartz group, but no significant statistical difference was found. Both the quartz group and the chrysotile group, the macrophage mortality rate increased with the increase of the dust concentration, and there was a dose-response relationship. The mortality rate in chrysotile was higher than that in quartz group. Correlation coefficients between GSH-Px activity in macrophages and macrophage mortality in quartz group and chrysotile asbestos group were -0.9318 and -0.8984, respectively, while those in titanium dioxide group were only -0.3637. This shows that quartz, chrysotile can cause macrophage GSH Px activity in a dose-response relationship decreased, so that intracellular free radicals can not be eliminated normally H2O2, prompting lipid peroxidation increased, damage cells; and the effect of chrysotile Stronger than quartz. Prompt reduction of GSH Px enzyme activity in quartz, chrysotile pathogenesis has a role