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Researchers identify how binge drinking may drive heart disease
Date:11/26/2008

mately 250 percent for 0.1 M acetaldehyde, and 700 percent for 25M acetaldehyde, when compared to controls.

When endothelial cells were subjected to a technique that shut down the genes that code for both P-selectin and TNFα prior to the addition of acetaldehyde, the ability of acetaldehyde to cause increased monocyte adhesion was reduced by 90 percent. These results argue strongly that acetaldehyde has its effects on monocytes primarily through these proteins.

Along with Cullen, the work was led in Rochester by Eileen Redmond, David Morrow, Sreenath Kundimi and Carol Miller-Graziano within in the Department of Surgery at the Medical Center. The work was supported in part by grants from the American Heart Association and the National Institutes of Health.

"Our study demonstrates for the first time that physiologically relevant concentrations of acetaldehyde can initiate several key steps involved in the monocyte recruitment cascade, specifically through P-selectin, CCR2 and TNFα," Cullen said. "We hypothesize that, following alcohol consumption, there is a delicate equilibrium between the effects of alcohol and its metabolite, acetaldehyde, on blood vessel walls. Further studies are underway to confirm that these actions of acetaldehyde underlie, in part, the detrimental effects of binge drinking on cardiovascular disease. "


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Contact: Greg Williams
Greg_Williams@urmc.rochester.edu
585-275-3676
University of Rochester Medical Center
Source:Eurekalert

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