NORMOLIPIDEMIC XANTHELASMA PALPEBRARUM - LIPID-COMPOSITION, CHOLESTEROL-METABOLISM IN MONOCYTE-DERIVED MACROPHAGES, AND PLASMA-LIPID PEROXIDATION

Citation
R. Bergman et al., NORMOLIPIDEMIC XANTHELASMA PALPEBRARUM - LIPID-COMPOSITION, CHOLESTEROL-METABOLISM IN MONOCYTE-DERIVED MACROPHAGES, AND PLASMA-LIPID PEROXIDATION, Acta dermato-venereologica, 76(2), 1996, pp. 107-110
Citations number
27
Categorie Soggetti
Dermatology & Venereal Diseases
Journal title
ISSN journal
00015555
Volume
76
Issue
2
Year of publication
1996
Pages
107 - 110
Database
ISI
SICI code
0001-5555(1996)76:2<107:NXP-LC>2.0.ZU;2-P
Abstract
The lipid compositions of 8 normolipidemic xanthelasma palpebrarum (XP ) lesions were analyzed using thin-layer chromatography, with the adja cent uninvolved skin used as control. The lesions were found to be com posed predominantly of cholesterol, mostly cholesteryl ester, whereas in the control specimens phospholipids predominated. The degradation r ates of I-125-low-density lipoprotein (LDL), oxidized LDL, and acetyl LDL, and the rates of intracellular cholesterol synthesis from 1,2-C-1 4-acetate, in blood monocyte-derived macrophages (MDM) from 3 normolip idemic patients, were similar to those of MDM from 3 normal control su bjects. The mean levels of lipid peroxides and conjugated dienes under basal conditions, as well as following the addition of a free radical -generating compound (2,2'-azobis-2-amidinopropane hydrochloride) to t he plasma of 14 normolipidemic XP patients were significantly higher t han those of 14 age- and sex-matched normal controls. We conclude that the predominant lipid accumulated in normolipidemic XP lesions is cho lesteryl ester, but there is no evidence for intrinsic cellular choles terol metabolism derangement in blood MDM from patients which could ac count for this. Since macrophage cholesterol accumulation can also res ult from enhanced uptake of increased levels of oxidized LDL, the incr eased plasma lipid peroxidation (derived from oxidized LDL) might lead to accumulation of cholesterol in macrophages and formation of foam c ells via this mechanism.