http://www.sciam.com/article.cfm?id=novel-...t-attack-damage

'An alcohol-busting enzyme may help prevent heart attack damage, according to a new study in Science. Researchers report that aldehyde dehydrogenase 2 (ALDH2), an enzyme important for processing alcohol in the human body, clears harmful toxins produced in cells when blood flow is blocked in the heart—and a new drug can switch it on.

Red wine has long been toted as a preventive measure against cardiac disease. In fact, heart cells exposed to ethanol in the laboratory actually recover better when researchers temporarily stop the flow of oxygenated blood to them. The study published today suggests that ALDH2 may contribute to wine's beneficial effects. The enzyme, activated as cells work to clear alcohol, also eliminates toxic by-products from the breakdown of fats in cells during a heart attack—thereby reducing damage to this vital organ.

During a cardiac event, blood flow to the heart ceases. Free radicals (highly reactive molecules released during energy production) accumulate in cells struggling through oxygen deprivation, damaging critical fats and proteins and increasing the chance of premature cell death. ALDH2 may help heart cells survive this onslaught by repairing some of the damaged fats, according to the study. Although not all cardiac damage is avoided, "any time you can save cells, you have a better chance of recovery," says study co-author Thomas Hurley, a biochemist at Indiana University School of Medicine in Indianapolis.

Researchers, aware that alcohol triggers the protective effects of ALDH2 during a heart attack, searched for drug alternatives that could switch on the enzyme. The synthetic compound aldA1 was found to directly bind ALDH2, enhancing its activity and reducing cardiac damage by 60 percent when injected directly into the hearts of live healthy rats five minutes before blood flow blockage was induced. Although these results are promising, adapting this therapy for intravenous or oral use in humans will be a challenge, cautions Michael Sack, a cardiologist at the National Heart, Lung and Blood Institute in Bethesda, Md., who did not participate in the study.

The researchers remain optimistic about the newly identified drug, however, arguing that it could help patients in east Asia where 40 percent of the population has nonfunctional ALDH2 due to a gene mutation. Aside from enhancing ALDH2 activity two-fold in normal rat hearts, aldA1 can actually restore full function to the mutant form of the enzyme, Hurley notes.' [...]