Nita Wong ’21

Nearly 85 years after the end of Prohibition, alcohol remains a controversial topic. While the excessive consumption of alcohol may disrupt communication pathways within the brain and damage the heart, liver, and pancreas, consumption in moderation can protect the heart from coronary disease. While the biochemical basis of the latter correlation has long remained a mystery, a recent study conducted by researchers at the University of São Paulo’s Biomedical Institute (ICB-USP) in Brazil has opened doors in understanding the rationale behind the cardiovascular benefits of moderate alcohol intake.

Under the leadership of Dr. Cintia Bagne Ueta of the Department of Anatomy at ICB-USP and in partnership with members of the Department of Chemical and Systems Biology at Stanford University, researchers structured their model system using ex vivo mouse hearts kept alive by an artificial system. These mice were divided into five groups. One group acted as the control and received neither treatment nor intervention. The second group was subjected to ischemia and reperfusion – a period of lack of oxygen followed by a flood of nutrients and oxygen that conventionally results in the loss of 50 percent of heart cells. Hearts in the third group were also subjected to ischemia and reperfusion; however, prior to this treatment, they were exposed to 50 μM ethanol – the dosage of which was correlated to the corresponding mouse’s mass – for 10 minutes. Hearts in the fourth group were both treated with alcohol and exposed to a drug that inhibits the activity of ALDH2 – a mitochondrial enzyme the researchers had hypothesized to play a crucial role on the cardioprotective effects of alcohol – prior to undergoing ischemia and reperfusion. Hearts in the fifth group, which originated from mice with a mutation that reduces ALDH2’s activity by 20 percent, also received the alcohol treatment before undergoing ischemia and reperfusion.

The scientists uncovered several trends of potential significance. Firstly, they discovered that the hearts in group three had lost 30 percent less cells than and doubled the ALDH2 activity as those in group two. Secondly, they found that when ALDH2 activity was inhibited (i.e. groups four and five), cell death increased to 80 percent and 70 percent, respectively. The researchers concluded that ALDH2 not only contributes to the body’s elimination of the toxic byproducts of alcohol breakdown, but also plays a role in the body’s cardioprotective mechanism that protects heart cells against stress.

References

1. C. Ueta, et. al., Cardioprotection induced by a brief exposure to acetaldehyde: role of aldehyde dehydrogenase 2. Cardiovascular Research 114, 1006-1015 (2018). doi: 10.1093/cvr/cvy070.  
2. Image retrieved from: https://www.pexels.com/photo/rock-glass-with-liquid-and-ice-162571/