Sialic Acid Content of LDL in Coronary Artery Disease: No Evidence of Desialylation in Subjects With Coronary Stenosis and Increased Levels in Subjects With Extensive Atherosclerosis and Acute Myocardial Infarction

Relation Between Desialylation and In Vitro Peroxidation

From Laboratoire de Biochimie Appliquée, Faculté des Sciences Pharmaceutiques et Biologiques, Châtenay-Malabry, France (B.C., I.M.); and Laboratoire de Biochimie (B.C., E.F., I.M.), INSERM U-430 (I.M.), Département de Radiologie Vasculaire (B.B., J.C.G.), and Département de Cardiologie (F.L., J.L.G.), Hôpital Broussais, Paris, France.

Correspondence to Dr B. Chappey, Laboratoire de Biochimie Appliquée, Tour D4, 2ème étage, Faculté de Pharmacie, Paris Sud, 5 rue Jean-Baptiste Clément, 92296 Châtenay-Malabry, France.

Abstract—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 75% stenosis in at least one main coronary artery 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.

Key Words: low-density lipoprotein • sialic acid • coronary artery disease • angiography • peroxidation

This article has been cited by other articles:

				H. Eguchi, Y. Ikeda, T. Ookawara, S. Koyota, N. Fujiwara, K. Honke, P. G. Wang, N. Taniguchi, and K. Suzuki Modification of oligosaccharides by reactive oxygen species decreases sialyl lewis x-mediated cell adhesion Glycobiology, November 1, 2005; 15(11): 1094 - 1101. [Abstract] [Full Text] [PDF]

				B. Poirier, O. Michel, R. Bazin, J. Bariety, J. Chevalier, I. Myara, and A.-T. Gaston Conjugated dienes: a critical trait of lipoprotein oxidizability in renal fibrosis Nephrol. Dial. Transplant., August 1, 2001; 16(8): 1598 - 1606. [Abstract] [Full Text] [PDF]

				N. Lindbohm, H. Gylling, and T. A. Miettinen Sialic acid content of low density lipoprotein and its relation to lipid concentrations and metabolism of low density lipoprotein and cholesterol J. Lipid Res., July 1, 2000; 41(7): 1110 - 1117. [Abstract] [Full Text]