Maziere C, Conte M A, Dantin F, Maziere J C
Université de Picardie, Laboratoire de Biochimie, Hôpital Nord, Amiens, France.
Atherosclerosis. 1999 Mar;143(1):75-80. doi: 10.1016/s0021-9150(98)00277-9.
The effect of lipopolysaccharide (LPS, endotoxin) on low density lipoprotein (LDL) oxidative modification by copper ions, endothelial and smooth muscle cells was studied by determination of the level of lipid peroxidation products (thiobarbituric acid reactive substances or TBARS), the diene level and the electrophoretic mobility of the LDL particle. LPS 25-75 microg/ml induced a dose-dependent increase in LDL oxidation by copper ions, endothelial and smooth muscle cells. At 75 microg LPS/ml, the TBARS content was 1.9, 1.6, and 1.8-fold increased, respectively. The LDL degradation by J774 macrophage-like cells was concomitantly stimulated. Preincubation of the LDL particle with LPS induced a marked increase in the subsequent LDL oxidative modification either by copper ions or by endothelial and smooth muscle cells. In addition, pretreatment of endothelial and smooth muscle cells with LPS also induced an enhancement of LDL oxidative modification performed in the absence of LPS. This effect was accompanied by a parallel increase in superoxide anion release by the cells. These results point at one of the mechanisms involved in the described association between bacterial infection and acute myocardial infarction as well as coronary heart disease.
通过测定脂质过氧化产物(硫代巴比妥酸反应性物质或TBARS)水平、二烯水平和低密度脂蛋白(LDL)颗粒的电泳迁移率,研究了脂多糖(LPS,内毒素)对铜离子、内皮细胞和平滑肌细胞介导的低密度脂蛋白(LDL)氧化修饰的影响。25 - 75微克/毫升的LPS可诱导铜离子、内皮细胞和平滑肌细胞介导的LDL氧化呈剂量依赖性增加。在75微克LPS/毫升时,TBARS含量分别增加了1.9倍、1.6倍和1.8倍。J774巨噬细胞样细胞对LDL的降解也随之受到刺激。LDL颗粒与LPS预孵育后,随后无论是被铜离子、内皮细胞还是平滑肌细胞氧化修饰的程度都显著增加。此外,用LPS预处理内皮细胞和平滑肌细胞也会增强在无LPS情况下进行的LDL氧化修饰。这种效应伴随着细胞超氧阴离子释放的平行增加。这些结果指出了细菌感染与急性心肌梗死以及冠心病之间所述关联所涉及的一种机制。