Shiotsuka R N, Yermakoff J K, Osheroff M R, Drew R T
J Toxicol Environ Health. 1986;17(2-3):297-310. doi: 10.1080/15287398609530824.
The biologic interactions of potentially fibrogenic agents commonly occurring as environmental pollutants remain to be rigorously characterized. Two agents that produce pulmonary fibrosis were selected for this study. Separate groups of male Sprague-Dawley rats were intratracheally instilled with 0, 2, 12, and 50 mg silica and then either sham-exposed or exposed to 0.8 ppm ozone 6 h/d, 5 d/w, for 37 exposure days. Interaction was not detected between silica and ozone in the development of pulmonary fibrosis as determined by quantitative biochemical indices (hydroxyproline and lysyl oxidase) or by histopathologic examination of the lungs. Thus, environmentally relevant levels of ozone appear unlikely to affect the progression of a concurrent silicotic lesion.
作为环境污染物常见的潜在致纤维化因子的生物相互作用仍有待严格表征。本研究选择了两种可导致肺纤维化的因子。将雄性Sprague-Dawley大鼠分成不同组，经气管内分别注入0、2、12和50 mg二氧化硅，然后进行假暴露或每天6小时、每周5天暴露于0.8 ppm臭氧，共暴露37天。通过定量生化指标（羟脯氨酸和赖氨酰氧化酶）或肺部组织病理学检查确定，在肺纤维化的发展过程中未检测到二氧化硅和臭氧之间存在相互作用。因此，与环境相关水平的臭氧似乎不太可能影响同时存在的矽肺病变的进展。
