DALLAS - April 9, 1999 - Furthering evidence of the importance of vitamin E, researchers at UT Southwestern Medical Center at Dallas have identified the pathway that may allow the vitamin to block the trigger of arterial plaque formation at the molecular level.
As an antioxidant, vitamin E prevents the oxidation of low-density lipoproteins (LDL), the so-called "bad" cholesterol that contributes to heart disease. But research by Dr. Ishwarlal Jialal, professor of pathology and internal medicine, and Dr. Sridevi Devaraj, pathology instructor at UT Southwestern, also has found it to be a powerful player on the molecular level. Their latest work, published in the April 8th issue of Arteriosclerosis, Thrombosis and Vascular Biology, establishes for the first time that vitamin E inhibits the activity of an enyzme, 5-lipoxygenase, which is key to the initiation of plaque formation.
"Mounting evidence suggests that plaque formation is an inflammatory process," Devaraj said. This enzyme, 5-lipozygenase, produces a substance that stimulates the release of the protein interleukin-1beta (IL-1beta), which promotes plaque formation. Studies have shown it stimulates adhesion of white blood cells or monocytes to the arterial lining, promotes uptake of cholesterol by the cells and stimulates smooth-muscle-cell proliferation. Also, increased levels of IL-1beta have been observed in the coronary arteries of patients with heart disease and have been shown to correlate with the severity of the plaque.
"This is the first study showing that vitamin E has a novel biological anti-inflammatory effect on this crucial enzyme in cells that is more than just an antioxidant effect," Jialal said. "This pioneering work sheds more light on the possible prevention of heart disease with this antioxidant supplement, by decreasing not only oxidation of bad cholesterol but also by having important effects on cell function in the plaque."