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Departments of Biochemistry and Microbiology, North Carolina State University, Raleigh, NC 27650 and Department of Pathology, Rex Hospital, Raleigh, NC 27603
Weanling male mice fed rac-1(3)-palmitoyl glycerol at levels of 30 mmoles/100 g of diet or higher develop, within a few days, a severe pulmonary inflammation characterized by marked infiltration of the interstitium by macrophages and a few polymorphonuclear leukocytes. This results in severe vascular stasis, alveolar collapse and death of the animal. Adult mice and weanling rats also show the syndrome, but only at higher levels of palmitoyl glycerol. Neither the position of palmitate on the glycerol nor the level of myo-inositol in the diet affects the toxicity of palmitoyl glycerol. Supplementation of the diet with small amounts of linoleate or oleate prevents the toxicity although oleate is less effective than linoleate. There are no differences between mice fed linoleate and those that were not in: the rate of absorption of palmitoyl glycerol, oxidative phosphorylation by liver or heat mitochondria, excretion of carbon dioxide and tissue distribution of radioactivity following gavage of rac-1(3)-[1-14C]palmitoyl glycerol.
KEY WORDS: toxicity saturated fat pneumonitis lung palmitoyl glycerol macrophages
1 Contribution from the Department of Biochemistry, School of Agriculture and Life Sciences and School of Physical and Mathematical Sciences. Paper No. 6396 of the Journal Series of the North Carolina Agricultural Research Service, Raleigh, NC 27650. This investigation was supported in part by Public Health Service Research Grant AM-02483 from the National Institute of Arthritis and Metabolic Diseases and Grant DAAG29-78-G-0006 from the United States Army Research Office.
2 Present address: Department of Biochemistry, University of Wisconsin, Madison, WI 53706.
3 To whom reprint requests should be sent.
Manuscript received 21 April 1980.