Jajte J, Lao I, Wiśniewska-Knypl J M, Wrońska-Nofer T
Department of Biochemistry, Professor J Nofer Institute of Occupational Medicine, Lodz, Poland.
Br J Ind Med. 1988 Apr;45(4):239-45. doi: 10.1136/oem.45.4.239.
The dynamics of the biological response of pulmonary tissue to silica dust (silica earth from Piotrowice, Poland, recommended as a domestic reference fibrogenic standard) was studied in rats after single-shot intratracheal instillation of a suspension of 20 mg of the dust for one, three, and seven months. Silica dust provoked pronounced pulmonary fibrosis as inferred from increased collagen content together with pathomorphological alteration (silicotic nodules). The lung burden of silica dust affected the lysosomal subfraction as manifested by an increase in its protein content with concomitant stimulation (release and presumably induction) of beta-glucuronidase and cathepsin D and a transient (up to three months) stimulation of lipid peroxidation. Stimulation of activity of lysosomal enzymes and lipid peroxidation mediated by silica dust may reflect destructive metabolic processes resulting in the development of pulmonary fibrosis as the sign of a pathological repair mechanism. The extent of the effects brought about by silica earth testify that it may be recommended as a reference standard for evaluating the potential health hazard from industrial exposure to dusts containing SiO2.
在大鼠单次气管内注入20毫克来自波兰皮奥特罗维采的硅尘（推荐作为国内参考致纤维化标准的硅土）悬浮液后，对其肺部组织对硅尘的生物反应动力学进行了为期1个月、3个月和7个月的研究。从胶原蛋白含量增加以及病理形态学改变（矽结节）推断，硅尘引发了明显的肺纤维化。硅尘的肺负荷影响了溶酶体亚组分，表现为其蛋白质含量增加，同时β-葡萄糖醛酸酶和组织蛋白酶D受到刺激（释放并可能诱导），脂质过氧化受到短暂（长达3个月）刺激。硅尘介导的溶酶体酶活性和脂质过氧化的刺激可能反映了导致肺纤维化发展的破坏性代谢过程，这是病理修复机制的标志。硅土产生的影响程度证明，它可被推荐作为评估工业接触含二氧化硅粉尘潜在健康危害的参考标准。
