Scott J E, Forkert P G, Oulton M, Rasmusson M G, Temple S, Fraser M O, Whitefield S
Department of Anatomy, Dalhousie University, Halifax, Nova Scotia, Canada.
Exp Mol Pathol. 1988 Aug;49(1):141-50. doi: 10.1016/0014-4800(88)90028-7.
Trichloroethylene (TCE) is a common organic solvent in use as a dry cleaning agent as well as an inhalant anesthetic. Nevertheless the effects of this material on the pulmonary surfactant which prevents alveolar collapse at maximal expiration is not known. Therefore, we have examined the effect of TCE on the intra- and extracellular surfactant pools and the activity of phospholipase A2, an enzyme which controls the remodeling of phosphatidylcholine to dipalmitoylphosphatidylcholine, the primary constituent of the pulmonary surfactant. Male CD-1 mice were treated ip with 2500 or 3000 mg/kg TCE. Twenty-four hours later mice were anesthetized and the lungs lavaged. Mice were then killed, the lungs perfused and excised, and subcellular fractions including lamellar bodies prepared. Some lungs were prepared for ultrastructural examination. Phospholipase A2 was assayed in all subcellular fractions. Phospholipid was assayed in the lavage (extracellular surfactant) and the lamellar bodies (intracellular surfactant). TCE (2500 mg/kg) caused selective exfoliation of Clara cells. However, only the dose of 3000 mg/kg TCE produced a significant decrease in the intracellular surfactant phospholipid. Minimal changes occurred in the phospholipid profiles. Phospholipase A2 specific activity was significantly decreased at both dosages within the lung microsomal fraction. In addition after treatment with 3000 mg/kg TCE the enzyme activity in the lamellar body fraction was significantly increased. These data suggest that inhalation of TCE may damage the enzymes which are responsible for synthesizing the pulmonary surfactant resulting in lower amounts of surfactant being stored and available for secretion into the alveolus.
三氯乙烯（TCE）是一种常用的有机溶剂，用作干洗剂和吸入性麻醉剂。然而，这种物质对在最大呼气时防止肺泡塌陷的肺表面活性物质的影响尚不清楚。因此，我们研究了TCE对细胞内和细胞外表面活性物质池以及磷脂酶A2活性的影响，磷脂酶A2是一种控制磷脂酰胆碱重塑为二棕榈酰磷脂酰胆碱（肺表面活性物质的主要成分）的酶。雄性CD-1小鼠腹腔注射2500或3000mg/kg TCE。24小时后，将小鼠麻醉并进行肺灌洗。然后处死小鼠，灌注并切除肺，制备包括板层小体在内的亚细胞组分。一些肺用于超微结构检查。在所有亚细胞组分中测定磷脂酶A2。在灌洗液（细胞外表面活性物质）和板层小体（细胞内表面活性物质）中测定磷脂。2500mg/kg的TCE导致克拉拉细胞选择性脱落。然而，只有3000mg/kg的TCE剂量使细胞内表面活性物质磷脂显著减少。磷脂谱变化极小。在两个剂量下，肺微粒体组分中的磷脂酶A2比活性均显著降低。此外，用3000mg/kg TCE处理后，板层小体组分中的酶活性显著增加。这些数据表明，吸入TCE可能会损害负责合成肺表面活性物质的酶，导致储存的表面活性物质减少，且可供分泌到肺泡中的量也减少。
