Chappey B, Beyssen B, Foos E, Ledru F, Guermonprez J L, Gaux J C, Myara I
Laboratoire de Biochimie Appliquée, Faculté des Sciences Pharmaceutiques et Biologiques, Châtenay-Malabry, France.
Arterioscler Thromb Vasc Biol. 1998 Jun;18(6):876-83. doi: 10.1161/01.atv.18.6.876.
We recently showed that sialic acid content of LDL was not a marker of early cardiovascular disease (Arterioscler Thromb Vasc Biol. 1995;15:334-339). Here, we investigated this parameter in patients with advanced coronary artery disease (CAD). We first examined 100 patients having undergone coronary angiography. The distribution of LDL sialic acid values was very similar in subjects with no coronary stenosis (31.3+/-3.7 nmol/mg LDL protein, mean+/-SD) and those with > or = 75% stenosis in at least one main coronary artery or > or = 50% stenosis in at least two main coronary arteries (32.1+/-5.5 nmol/mg LDL protein). In contrast, LDL sialic acid content was significantly increased in patients with both coronary stenosis and peripheral arterial atherosclerotic lesions compared with those with either no lesion or only one or the other type of lesion. We then examined LDL sialic acid content in 20 patients with acute myocardial infarction. LDL sialic acid content was significantly higher (35.9+/-3.2 nmol/mg LDL protein) than that in the CAD(-) control group. These data suggest that LDL sialic acid content increases with the extension of atherosclerosis and its progression to acute complications. To explain the discordance with Orekhov and coworkers (Atherosclerosis. 1991;86:153-161), who showed that LDL sialic acid content in patients with advanced CAD was lower than that in healthy subjects, we studied the time courses of sialic acid, TBARS, and vitamin E levels in LDL dialyzed in different experimental conditions. A continuous decrease in both sialic acid and vitamin E levels and an increase in TBARS levels were observed in LDL samples containing less than 1 mmol/L EDTA, the intensity and rapidity of which varied with the EDTA concentration in the buffer. Our data support the idea that desialylation may result from in vitro peroxidation of LDL.
我们最近的研究表明，低密度脂蛋白（LDL）的唾液酸含量并非早期心血管疾病的标志物（《动脉硬化、血栓形成和血管生物学》。1995年；15:334 - 339）。在此，我们对晚期冠状动脉疾病（CAD）患者的这一参数进行了研究。我们首先检查了100例接受冠状动脉造影的患者。在无冠状动脉狭窄的受试者（31.3±3.7 nmol/mg LDL蛋白，均值±标准差）与至少一条主要冠状动脉狭窄≥75%或至少两条主要冠状动脉狭窄≥50%的受试者（32.1±5.5 nmol/mg LDL蛋白）中，LDL唾液酸值的分布非常相似。相比之下，与无病变或仅有一种或另一种病变类型的患者相比，同时患有冠状动脉狭窄和外周动脉粥样硬化病变的患者LDL唾液酸含量显著升高。然后我们检查了20例急性心肌梗死患者的LDL唾液酸含量。LDL唾液酸含量显著高于CAD（ - ）对照组（35.9±3.2 nmol/mg LDL蛋白）。这些数据表明，LDL唾液酸含量随着动脉粥样硬化的扩展及其进展为急性并发症而增加。为了解释与奥列霍夫及其同事（《动脉粥样硬化》。1991年；86:153 - 161）研究结果的不一致，他们发现晚期CAD患者的LDL唾液酸含量低于健康受试者，我们研究了在不同实验条件下透析的LDL中唾液酸、硫代巴比妥酸反应物（TBARS）和维生素E水平的时间进程。在含有低于1 mmol/L乙二胺四乙酸（EDTA）的LDL样本中，观察到唾液酸和维生素E水平持续下降以及TBARS水平升高，其强度和速度随缓冲液中EDTA浓度而变化。我们的数据支持这样一种观点，即去唾液酸化可能是由LDL的体外过氧化作用导致的。
