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New Insights About 'Good Cholesterol'

Enzyme Acts As Antioxidant

New research gives a clearer understanding of how so-called "good cholesterol" helps prevent heart disease and may one day lead to treatments, according to Canadian chemists. The scientists say they have determined that a particular enzyme bound to the "good" high-density lipoprotein, or HDL, acts as a powerful antioxidant within blood vessels.

The findings will appear in the American Chemical Society (ACS) peer-reviewed journal Biochemistry. ACS Web publication of the paper will be on April 27 and the research will be in the journal's May 11 print edition. ACS is the world's largest scientific society.

For years, epidemiological studies have shown higher blood levels of HDL reduce coronary artery disease. Recent studies show HDL may help ward off heart disease by preventing oxidative modifications of low-density lipoprotein (LDL) that lead to the formation of artery- clogging plaques. University of Ottawa Heart Institute biochemist Daniel L. Sparks, Ph.D., now says HDL's antioxidant ability is partly due to an attached enzyme called lecithin-cholesterol acyltransferase (LCAT).

"We have shown that LCAT has the ability to both eliminate and prevent the formation of oxidized lipids in plasma lipoproteins," claims Sparks. LCAT's role was previously thought to be limited to promoting cholesterol transport and clearance. While the mechanism for LCAT's antioxidant actions is still under investigation, Sparks maintains "the antioxidant activity is not short-lived as with vitamins C or E, since LCAT appears able to regenerate itself and efficiently maintain its ability to prevent oxidation."

Oxidative damage is thought to be involved in many diseases, including the biggest killers -- heart disease and cancer. Sparks thinks it may be possible to develop ways to enhance the antioxidant activity of LCAT in the body, and says his research has begun focusing on such efforts.


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Contact: Charmayne Marsh
y_marsh@acs.org
202-872-4445
American Chemical Society
27-Apr-1999


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