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Concise Publication Free access | 10.1172/JCI106994
Department of Medicine, New York University School of Medicine, New York 10016
The Molecular Disease Branch, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland 20014
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Department of Medicine, New York University School of Medicine, New York 10016
The Molecular Disease Branch, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland 20014
Find articles by Patriarca, P. in: JCI | PubMed | Google Scholar
Department of Medicine, New York University School of Medicine, New York 10016
The Molecular Disease Branch, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland 20014
Find articles by Pettis, P. in: JCI | PubMed | Google Scholar
Department of Medicine, New York University School of Medicine, New York 10016
The Molecular Disease Branch, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland 20014
Find articles by Stossel, T. in: JCI | PubMed | Google Scholar
Department of Medicine, New York University School of Medicine, New York 10016
The Molecular Disease Branch, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland 20014
Find articles by Mason, R. in: JCI | PubMed | Google Scholar
Department of Medicine, New York University School of Medicine, New York 10016
The Molecular Disease Branch, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland 20014
Find articles by Vaughan, M. in: JCI | PubMed | Google Scholar
Published July 1, 1972 - More info
Rabbit polymorphonuclear leukocytes ingesting paraffin oil particles stabilized with albumin, converted more lysolecithin-32P (added to the medium as an albumin complex) to cellular lecithin than did control cells.
Almost all of the increment in leukocyte lecithin-32P is found in association with the isolated phagocytic vacuoles.
About half of lecithin-32P of granulocytes incubated first with lysolecithin-32P and then reincubated with paraffin particles in a nonradioactive medium is transferred from a sedimentable (presumably membrane) fraction to the phagosomes. Isolated phagosomes or granules by themselves are capable of acylating lysolecithin. The main source of lysolecithin-32P for synthesis of cellular lecithin-32P, however, appears to be extracellular rather than lysolecithin-32P within the cytoplasm or the phagocytic vacuole. We interpret our findings therefore as indicating that lecithin-32P in the phagosomes derives chiefly from the outer membrane.