BACKGROUND: The free-radical oxidation of low-density lipoprotein (LDL) cholesterol is an early step in the development of coronary artery disease. Oxidized LDL attracts white blood cells, which engulf LDL and then become lodged in the walls of arteries. These white blood cells release free radicals, which damage the blood vessels and set the stage for coronary artery disease.
RESEARCH: Researchers studied how oxidized LDL, vitamin E, and two synthetic antioxidants (BHT and probucol) affected endothelial cells. These cells normally line blood vessels, but they also "migrate" to heal microscopic artery damage, such as after balloon angioplasty. In these cell studies, the researchers used two types of oxidized LDL. In one, LDL oxidation was induced artificially with copper, a common experimental technique. In the other, LDL oxidation was initiated by white blood cells, which more closely resembles how LDL actually becomes oxidized in blood vessels.
RESULTS: Both types of oxidized LDL inhibited the migration of endothelial cells, demonstrating that oxidized LDL interferes with the normal healing of blood vessels. However, vitamin E preserved the normal migration of endothelial cells after the white blood cell-induced oxidation of LDL but not after copper-induced oxidation. Since the two synthetic antioxidants did not provide a benefit, the researchers concluded that vitamin E maintained the normal function of endothelial cells by stabilizing their membranes (walls), not through an antioxidant effect.
IMPLICATIONS: This study describes a new mechanism by which vitamin E may enhance normal healing processes within blood vessels. Based on this study, oxidized LDL interferes with normal endothelial cell migration, but vitamin E may help maintain normal endothelial cell function.
van Aalst JA, Burmeister W, Fox PL, et al. Alpha-tocopherol preserves endothelial cell migration in the presence of cell-oxidized low-density lipoprotein by inhibiting changes in cell membrane fluidity. Journal of Vascular Surgery, 2004;39:229-237.
For the original abstract, visit: