The cardioprotective effects of alcohol have been known about for at least 20 years, though the mechanism behind it has been poorly understood.
New research by the University of São Paulo reveals that it may be associated with activation of ALDH2 (aldehyde dehydrogenase-2), a mitochondrial enzyme that helps rid the organism of the toxic byproducts of alcohol digestion.
Julio Cesar Batista Ferreira, the study’s principal investigator, said: ‘Our data suggest moderate exposure to ethanol causes minor stress in heart cells but not enough to kill them. Intracellular signalling is reorganised as a result, and heart cells eventually create a biochemical memory to protect against stress, also known as preconditioning. When the cells are submitted to a higher level of stress, they know how to deal with it.’
To study the cardioprotective effects of alcohol at the cellular level, the researchers simulated a condition similar to myocardial infarction (heart attack) in mouse hearts kept alive artificially.
Mice were divided into groups to explore the mechanisms underlying the observed protective effect. The hearts in the control group suffered no damage and received no treatment or intervention. The hearts in the second group were submitted to ischemia and reperfusion, losing approximately 50 per cent of their cells as a result.
In the third group, before inducing the ischemic injury, the researchers exposed the hearts extracted from male mice to ethanol for ten minutes, at a dose equivalent to two cans of beer or two glasses of wine for an average man. The dose was adjusted according to each animal’s mass.
The hearts were washed for ten minutes to remove surplus alcohol, and the flow of oxygen and nutrients was then interrupted. An analysis performed approximately one hour after reperfusion showed that only 30 per cent of the cells had died. In other words, the damage was reduced by almost 60 per cent following exposure to alcohol.
The results of the study have been published in the journal Cardiovascular Research.