In mice genetically manipulated to develop atherosclerosis, scientists at the University of Pennsylvania Medical Center have for the first time conclusively demonstrated that vitamin E confers potent protection from the disease. Atherosclerotic damage to cardiovascular tissues was limited by about 40 percent in at-risk mice receiving doses of the vitamin for only 16 weeks.
The researchers were also able to show that the benefit was due to the antioxidant action of vitamin E, not to other possible effects such as a reduction in blood cholesterol levels. This fact strongly suggests that free radicals do, in fact, play a central role in heart disease, a theory long proposed but never proven. A novel method recently developed by the same group for directly measuring oxidant stress in the body provided the data in support of the observations.
A report on the new findings appears in the October issue of Nature Medicine.
"This study offers powerful evidence for the efficacy of vitamin E as an antioxidant in atherosclerosis," says Garret A FitzGerald, MD, chairman of the department pharmacology and senior author on the report. "Significantly, it also shows that free-radical injury is functionally important in the development of cardiovascular disease."
The innovative measurement technique used in the study was developed in FitzGerald's laboratory in collaboration with Joshua Rokach, PhD, a chemist at the Florida Institute of Technology. It assesses the levels in blood or urine of certain biochemicals called isoprostanes. These isoprostanes are stable byproducts of free-radical catalyzed damage to lipids, or fatty molecules, found in tissues throughout the body, and they serve as quantitative markers for that damage.
The strain of mice used in the experiments has been genetically
engineered to lack the apoE gene, resulting in extremely high levels of
cholesterol and triglycerides in their blood. Atherosclerot
Contact: Franklin Hoke
University of Pennsylvania School of Medicine