| Popis: |
Low density lipoprotein (LDL) from patients with coronary heart disease (CHD) caused 78-286% increase in accumulation of cholesterol in human aortic subendothelial cells compared to 2-17% caused by LDL from normal subjects. Ricin-Sepharose affinity chromatography was used to separate LDL into two subfractions, one sialic acid-rich (SAR) and the other sialic acid-poor (SAP). SAP-LDL from CHD patients caused 156-307% increase in accumulation of cellular cholesterol, whereas SAR-LDL from these patients caused only 14-21% increase. SAP-LDL from normal healthy subjects caused 50-86% increased accumulation, whereas their SAR-LDL induced only 2-12% increase. Carbohydrate analysis of SAP-LDL protein isolated from four CHD patients revealed mean values of 59, 25, 61, and 11 nmoles of N-acetyl glucosamine, galactose, mannose, and sialic acid per mg protein, respectively. Mean values for SAR-LDL protein from these patients were 59, 31, 77, and 24 nmol/mg protein, respectively. Analysis of SAP-LDL protein from four normal healthy subjects indicated respective mean values of 58, 29, 72, and 22 nmol/mg, whereas SAR-LDL protein from normals contained 59, 29, 72, and 29 nmol/mg. The carbohydrate content of LDL lipids represents about 25% of the total carbohydrate present in the lipoprotein. The mean values for SAP-LDL lipids from four CHD patients were about 2, 2, 18, 18, and 2 nmol/mg protein for N-acetyl galactosamine, N-acetyl glucosamine, galactose, glucose, and sialic acid, respectively. The mean values for SAR-LDL lipids from these patients were 3, 4, 34, 41, and 5 nmol/mg, respectively. Analysis of SAP-LDL lipids from four normal healthy subjects indicated respective mean values of 4, 6, 30, 31, and 3 nmol/mg, whereas SAR-LDL lipids from these subjects contained 6, 9, 41, 46, and 7 nmol/mg. These results suggest that the different biological properties of SAR-LDL and SAP-LDL are related to their different carbohydrate compositions. |
