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Free access | 10.1172/JCI106198
Lipid Research Laboratory, Department of Medicine B, Hadassah University Hospital, Hebrew University-Hadassah Medical School, Jerusalem, Israel
Department of Experimental Medicine and Cancer Research, Hebrew University-Hadassah Medical School, Jerusalem, Israel
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Lipid Research Laboratory, Department of Medicine B, Hadassah University Hospital, Hebrew University-Hadassah Medical School, Jerusalem, Israel
Department of Experimental Medicine and Cancer Research, Hebrew University-Hadassah Medical School, Jerusalem, Israel
Find articles by Stein, Y. in: PubMed | Google Scholar
Lipid Research Laboratory, Department of Medicine B, Hadassah University Hospital, Hebrew University-Hadassah Medical School, Jerusalem, Israel
Department of Experimental Medicine and Cancer Research, Hebrew University-Hadassah Medical School, Jerusalem, Israel
Find articles by Stein, O. in: PubMed | Google Scholar
Published December 1, 1969 - More info
The role of phospholipases in the regulation of the changing phospholipid composition of normal human aortae with age was studied. Portions of grossly and histologically lesion-free ascending aortae from 16 females and 29 males obtained at autopsy, were analyzed for deoxyribonucleic acid (DNA), phospholipid, and cholesterol content and phospholipid composition. Enzymic activity toward four substrates, lecithin (LE), phosphatidyl ethanolamine, lysolecithin, and sphingomyelin (SP), was determined on portions of the same homogenate. By regression analysis for correlation between all determinations and age the following results were obtained: (a) total phospholipids and choleserol increased linearly with age; (b) the increase in sphingomyelin accounted for about 70% of the phospholipid increment; (c) hydrolysis of lecithin and phosphatidyl ethanolamine increased markedly with age, that of lysolecithin only moderately; (d) hydrolysis of sphingomyelin decreased with age; and (e) an inverse relation between the SP/LE ratio and age and sphingomyelinase/lecithinase activity and age was obtained. These results were interpreted to indicate that a causal relation exists between the fall in sphingomyelinase activity, both absolute and relative to lecithinase activity, and the accumulation of sphingomyelin with age.