Hydroxyl radical production and lung injury in the rat following silica or titanium dioxide instillation in vivo.
Hydroxyl radical production and lung injury in the rat following silica or titanium dioxide instillation in vivo.
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DOI：
10.1165/ajrcmb.12.2.7865220
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发表时间：
1995-02
影响因子：
6.4
通讯作者：
R. Schapira;A. Ghio;R. Effros;J. Morrisey;U. Almagro;C. Dawson;A. Hacker
中科院分区：
文献类型：
--
作者：
R. Schapira;A. Ghio;R. Effros;J. Morrisey;U. Almagro;C. Dawson;A. Hacker
羟基自由基（.OH）是一种高活性氧自由基，被认为是暴露于二氧化硅和硅酸盐后肺损伤的原因。尽管有证据表明二氧化硅在体外产生.OH，但以前没有证据表明暴露于非纤维状矿物氧化物粉尘后体内产生.OH。我们测试了这一假设，即向大鼠肺部滴注二氧化硅与体内更大的.OH产生和急性肺部炎症相关，相对于毒性较低的非硅酸盐颗粒二氧化钛的滴注。使用水杨酸钠作为.OH捕集器测量粉尘滴注后肺中.OH的产生。暴露于粉尘7天后，大鼠腹腔注射水杨酸盐，分离肺，测定水杨酸盐羟基化产物（2，3-和2，5-二羟基苯甲酸），反映.OH。与注入二氧化钛的肺相比，暴露于二氧化硅的肺中的2，3-二羟基苯甲酸显著更多。此外，在体内将二氧化硅滴入大鼠肺部与更大的急性炎症反应相关。我们得出结论，在体内暴露后，二氧化硅刺激更大的.OH生产相对于毒性较小的颗粒，二氧化钛。OH生成的这些差异对应于急性肺部炎症的差异。
The hydroxyl radical (.OH) is a highly reactive oxygen free radical that has been implicated as a cause of lung injury following exposure to silica and silicates. Despite evidence that silica generates .OH in vitro, there has been no previous demonstration of in vivo production of .OH after exposure to nonfibrous mineral oxide dusts. We tested the hypothesis that instillation of silica into rat lungs is associated with greater .OH production and acute lung inflammation in vivo relative to the instillation of a less toxic nonsilicate particle, titanium dioxide. The production of .OH in the lungs following dust instillation was measured using sodium salicylate as an .OH trap. Seven days after dust exposure, the rats were given intraperitoneal salicylate, the lungs isolated, and salicylate hydroxylation products (2,3- and 2,5-dihydroxybenzoic acid), reflecting .OH, were measured. There was significantly more 2,3-dihydroxybenzoic acid in silica-exposed lungs compared with lungs instilled with titanium dioxide. In addition, the instillation of silica into rat lungs in vivo was associated with a greater acute inflammatory response. We conclude that following in vivo exposure, silica stimulates greater .OH production relative to the less toxic particle, titanium dioxide. These differences in .OH generation correspond to disparities in acute lung inflammation.