Kurasawa K
Department of Hygiene, Shinshu University School of Medicine.
Sangyo Igaku. 1988 Mar;30(2):121-33. doi: 10.1539/joh1959.30.121.
Ethanol-treated and ethanol-nontreated rats were exposed to 0, 500, 1,000, 2,000, 4,000 and 8,000 ppm of trichloroethylene for 2 h in order to evaluate the metabolic (metabolic rate of styrene) and morphologic changes in the lung. The exposure resulted in dose-dependent decrease of styrene metabolism. By MPA (Maclura pomifera agglutinin) stain it was revealed by light microscopy that trichloroethylene caused a highly selective damage to nonciliated bronchiolar epithelial (Clara) cells, which were characterized by flattened cells. The ratios of the length of apical surface (a) to the length of the base (b) of Clara cells analyzed morphometrically decreased dependent on trichloroethylene dose. Electron microscopy showed that the bronchiolar luminal surface was covered by flattened and dilated endoplasmic reticulum and that destruction of mitochondrial crista and disappearance of secretory granules were dependent on increase in trichloroethylene concentration. Time-course studies conducted with exposure of 8,000 ppm of trichloroethylene to ethanol-treated rats demonstrated that maximal Clara cell damage occurred between 8 and 22 h after exposure, and that the cells appeared to be virtually identical to these of the control by 4 wk after exposure. Ethanol ingestion slightly increased Clara cell damage induced by trichloroethylene.
为了评估肺中的代谢（苯乙烯代谢率）和形态学变化，将经乙醇处理和未经乙醇处理的大鼠暴露于浓度为0、500、1000、2000、4000和8000 ppm的三氯乙烯中2小时。该暴露导致苯乙烯代谢呈剂量依赖性下降。通过MPA（桑科柘属凝集素）染色，光镜检查显示三氯乙烯对无纤毛细支气管上皮（克拉拉）细胞造成高度选择性损伤，这些细胞的特征是细胞扁平。通过形态计量学分析，克拉拉细胞顶端表面长度（a）与基部长度（b）的比值随三氯乙烯剂量的增加而降低。电子显微镜显示，细支气管腔表面覆盖着扁平且扩张的内质网，线粒体嵴的破坏和分泌颗粒的消失取决于三氯乙烯浓度的增加。对暴露于8000 ppm三氯乙烯的乙醇处理大鼠进行的时间进程研究表明，最大的克拉拉细胞损伤发生在暴露后8至22小时之间，并且在暴露后4周时，这些细胞似乎与对照组的细胞几乎相同。摄入乙醇会略微增加三氯乙烯诱导的克拉拉细胞损伤。
