LIKELY MEANS BY WHICH SMOKING CONTRIBUTES TO CLOGGED ARTERIES DISCOVERED BY EMORY RESEARCHERS

November 1997

Media Contacts: Sarah Goodwin, 404/727-3366 - sgoodwi@emory.edu
Kathi Ovnic, 404/727-9371 - covnic@emory.edu
http://www.emory.edu/WHSC/

SAN FRANCISCO -- The first study to propose a biochemical means by which cigarette smoke likely contributes to the development of deadly, artery-clogging plaque is being presented today by Emory University researcher Sampath Parthasarathy, Ph.D., at the annual meeting of The Oxygen Society.

Cigarette smoking has long been recognized as a risk factor for coronary artery disease, but until know, scientists have not known why this is so. One theory has held that cigarette smoke perhaps modifies, or oxidizes, low density lipoprotein (LDL, the "bad" cholesterol). According to the oxidation theory of atherosclerosis, oxidized LDL promotes atherosclerosis (Dr. Parthasarathy, together with Daniel Steinberg at the University of California, San Diego, first proposed the theory in 1989, a finding that spurred the current "antioxidant" craze). And according to a more recent theory, enzymes called peroxidases may turn antioxidants such as vitamin E into pro-oxidants that promote the oxidation of LDL and trigger arterial plaque formation.

Knowing that cigarette smoke actually contains some antioxidants, Dr. Parthasarathy and his Emory research team suspected that peroxidases might corrupt antioxidants in cigarette smoke, thus turning them into pro-oxidants. Indeed, when the researchers exposed human plasma to cigarette smoke extract (CSE) in the presence of plant and human peroxidases, they found evidence that cigarette smoke does indeed appear to act as a pro-oxidant to spur the development of atherosclerosis.

The team is reporting its findings at this week's meeting and has published data in a recent issue of FEBS Letters, a publication of the Federation of European Biochemical Societies.

"This is the first study suggesting that smoking may promote atherosclerosis by enhancing peroxidase-catalyzed lipid peroxidation," report Dr. Parthasarathy and colleagues in FEBS Letters. "The results presented in this study provide experimental support for the pro-oxidant effects of CSE in generating an oxidized LDL particle in the presence of peroxidases."

The team collected CSE from commercial cigarettes with class A filters. They exposed plasma from human donors to the CSE as well as a plant peroxidase (horseradish peroxidase) and a human peroxidase (myeloperoxidase, from human leukocytes).

Dr. Parthasarathy, senior author, is director of research and professor for the Department of Gynecology and Obstetrics and is also professor of Medicine at the Emory University School of Medicine; Nalini Santanam, Ph.D., is an Emory assistant professor of Gynecology and Obstetrics; Robert Sanchez and Sheldon Hendler are both from Vyrex Corporation of La Jolla, Calif.

The study was funded by Emory's Department of Gynecology and Obstetrics and the National Institutes of Health.

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