DALLAS - November 24, 1998 - In laboratory tests vitamin E prevented the early stages of plaque formation by preventing white blood cells from sticking to cells that line the artery wall - another weapon in the antioxidant's attack on heart disease, according to research at UT Southwestern Medical Center at Dallas.
The study, the first to examine how vitamin E-enrichment of these white plaque-producing cells -- called monocytes -- affects adhesion to the cells that line arteries, was published in the November 24 edition of Circulation: Journal of the American Heart Association.
"This beneficial effect of vitamin E further strengthens its role as an adjunctive therapy in the management of atherosclerosis," said lead author Dr. Ishwarlal Jialal, a professor of pathology and internal medicine at UT Southwestern.
Scientists, including the UT Southwestern researchers, had already established that vitamin E can reduce susceptibility to atherosclerosis, or hardening of the arteries, because it inhibits the oxidation of low-density lipoprotein (LDL), or "bad" cholesterol. Two years ago, work by Jialal and Dr. Sridevi Devaraj, an instructor of pathology at UT Southwestern, showed the first intracellular effect of vitamin E - that it suppressed the function of monocytes.
The monocyte is the critical cell in early plaque development. An early stage of artery-clogging plaque involves the attachment of the monocyte to human endothelial cells - the artery wall. Preventing this step could be another important target in the treatment of atherosclerosis, said Jialal, who is also a senior investigator in the Center for Human Nutrition at UT Southwestern.
The laboratory study examined the effect that vitamin E had on the monocyte's ability to bind itself to endothelial cells.
"These and other studies support the concept that the possible beneficial
effects of vitamin E supplementation in reducing coronary-artery disease can be a
Contact: Bridgette Rose McNeill
UT Southwestern Medical Center