Accumulation of surfactant phospholipids in lipid pneumonia induced with methylnaphthalene.

Abstract

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.

• Authors: T Taki, T Nakazima, Y Emi, Y Konishi, A Hayashi, M Matsumoto
• Journal: Lipids (Lipids) Vol. 21 Issue 9 Pg. 548-52 (Sep 1986) ISSN: 0024-4201 [Print] United States
• PMID: 3762327 (Publication Type: Journal Article)

Chemical References

• Cholesterol Esters
• Fatty Acids
• Naphthalenes
• Phospholipids
• Pulmonary Surfactants
• Triglycerides
• Cholesterol

Topics

• Animals
• Cholesterol (metabolism)
• Cholesterol Esters (metabolism)
• Chromatography, Gas
• Chromatography, High Pressure Liquid
• Fatty Acids (analysis)
• Female
• Mass Spectrometry
• Mice
• Naphthalenes
• Phospholipids (metabolism)
• Pneumonia, Aspiration (metabolism)
• Pneumonia, Lipid (chemically induced, metabolism)
• Pulmonary Surfactants (metabolism)
• Triglycerides (metabolism)