Taki T, Nakazima T, Emi Y, Konishi Y, Hayashi A, Matsumoto M
Lipids. 1986 Sep;21(9):548-52. doi: 10.1007/BF02534050.
Lipid analyses were carried out on the lungs of female B6C3F1 mice treated with methylnaphthalene. Cholesteryl ester, which could not be detected in lungs of control animals, was present in lungs of treated animals. Cholesterol and dipalmitoylglycerophosphocholine (DPPC) content was increased about five times in lungs of treated mice compared with control mice, and the content of a minor phospholipid was increased six times. The latter phospholipid was purified by high performance liquid chromatography and identified as phosphatidylglycerol by thin layer chromatography and by fast atom bombardment-mass spectrometry. Both DPPC and phosphatidylglycerol are known to be pneumonal surfactants produced from type II pneumocytes. Therefore, the accumulation of these lipids in lung tissue was assumed to be caused by the proliferation of type II cells induced by the administration of methylnaphthalene. The results provide important information concerning the underlying mechanism of endogenous lipid pneumonia in mice.
对用甲基萘处理的雌性B6C3F1小鼠的肺进行了脂质分析。在对照动物的肺中未检测到的胆固醇酯存在于处理过的动物的肺中。与对照小鼠相比,处理过的小鼠肺中的胆固醇和二棕榈酰甘油磷酸胆碱(DPPC)含量增加了约五倍,一种次要磷脂的含量增加了六倍。后一种磷脂通过高效液相色谱法纯化,并通过薄层色谱法和快原子轰击质谱法鉴定为磷脂酰甘油。已知DPPC和磷脂酰甘油都是由II型肺细胞产生的肺表面活性剂。因此,这些脂质在肺组织中的积累被认为是由甲基萘给药诱导的II型细胞增殖引起的。这些结果提供了有关小鼠内源性脂质肺炎潜在机制的重要信息。