Antioxidants, such as beta-carotene and Vitamin E, have been touted for their ability to protect against heart disease.
This protective effect is attributed to their ability to prevent the oxidation of bad cholesterol by free radicals - a process thought to contribute to the build-up of disease-causing fatty deposits on artery walls. But a new study, published in The Journal of Experimental Medicine, suggests that the heart-healthy effect of one antioxidant has little to do with cholesterol oxidation.
A group of researchers at the University of New South Wales in Australia, led by Roland Stocker, studied a cholesterol-lowering drug called Probucol (Lorelco) in laboratory rodents with vascular disease. Probucol reduces the risk of heart disease in humans, but is no longer prescribed in the US and Australia because of adverse side effects: a tendency to lower good cholesterol along with the bad and the potential to induce an irregular heartbeat. Probucol is still available in Canada and Europe.
In their new study, Stocker and his colleagues show that the protective effect of probucol has nothing to do with its ability to scavenge oxygen free radicals, as the free radical-busting part of the drug alone was ineffective in protecting animals against heart disease. Instead, a different part of the probucol molecule was doing the beneficial work.