Tertov V V, Orekhov A N, Sobenin I A, Morrisett J D, Gotto A M, Guevara J G
Institute of Experimental Cardiology, Russian Cardiology Research Center, Moscow.
J Lipid Res. 1993 Mar;34(3):365-75.
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.
与正常受试者的低密度脂蛋白（LDL）导致人主动脉内皮下细胞胆固醇蓄积增加2%-17%相比，冠心病（CHD）患者的LDL可使胆固醇蓄积增加78%-286%。采用蓖麻毒蛋白-琼脂糖亲和色谱法将LDL分离为两个亚组分，一个富含唾液酸（SAR），另一个唾液酸含量低（SAP）。冠心病患者的SAP-LDL可使细胞胆固醇蓄积增加156%-307%，而这些患者的SAR-LDL仅使胆固醇蓄积增加14%-21%。正常健康受试者的SAP-LDL可使胆固醇蓄积增加50%-86%，而其SAR-LDL仅诱导增加2%-12%。对从4例冠心病患者分离的SAP-LDL蛋白进行碳水化合物分析，结果显示每毫克蛋白中N-乙酰葡糖胺、半乳糖、甘露糖和唾液酸的平均值分别为59、25、61和11纳摩尔。这些患者的SAR-LDL蛋白的平均值分别为59、31、77和24纳摩尔/毫克蛋白。对4例正常健康受试者的SAP-LDL蛋白分析表明，其平均值分别为58、29、72和22纳摩尔/毫克，而正常受试者的SAR-LDL蛋白含有59、29、72和29纳摩尔/毫克。LDL脂质中的碳水化合物含量约占脂蛋白中总碳水化合物的25%。4例冠心病患者的SAP-LDL脂质中，N-乙酰半乳糖胺、N-乙酰葡糖胺、半乳糖、葡萄糖和唾液酸的平均值分别约为2、2、18、18和2纳摩尔/毫克蛋白。这些患者的SAR-LDL脂质的平均值分别为3、4、34、41和5纳摩尔/毫克。对4例正常健康受试者的SAP-LDL脂质分析表明，其平均值分别为4、6、30、31和3纳摩尔/毫克，而这些受试者的SAR-LDL脂质含有6、9、41、46和7纳摩尔/毫克。这些结果表明，SAR-LDL和SAP-LDL不同的生物学特性与其不同的碳水化合物组成有关。
