Alcohol metabolism causes DNA damage that triggers breast, liver cancer
Washington, Sept 16 (ANI): A new study has found that alcohol metabolism causes DNA damage that may trigger breast and liver cancers.
Alcohol is known to be carcinogenic to humans in the upper aerodigestive tract, liver, colorectum, and the female breast.
Evidence suggests that acetaldehyde, the primary metabolite of alcohol, plays a major role in alcohol-related esophageal cancer.
Now, the new study using human cells has established linkages between alcohol metabolism and acetaldehyde-DNA damage that may have implications for breast and liver cancers.
When alcohol is metabolized in the human body, it is converted to acetaldehyde, a chemical that is structurally similar to formaldehyde. Acetaldehyde can cause DNA damage, trigger chromosomal abnormalities in cell culture studies, and act as an animal carcinogen.
"In most people, acetaldehyde is quickly converted to acetate, a relatively harmless substance, by an enzyme called aldehyde dehydrogenase 2 (ALDH2)," said Philip J. Brooks, program director in the Division of Metabolism and Health Effects at the National Institute on Alcohol Abuse and Alcoholism (NIAAA).
"However, approximately 30 percent of East Asians are unable to metabolise alcohol to acetate due to a genetic variant in the ALDH2 gene, and have a greatly elevated risk of esophageal cancer from alcohol drinking," he explained.
Brooks and his colleagues used human cells engineered to metabolise alcohol into acetaldehyde by the same enzyme - alcohol dehydrogenase 1B (ADH1B) - that is expressed in human liver and breast tissue.
They exposed these cells to alcohol at concentrations that would equate to levels found in the human body during social drinking.
"We found that the cells converted the alcohol into acetaldehyde, and that this resulted in increased levels of acetaldehyde-DNA damage," added Brooks.
The results will be published in the December 2011 issue of Alcoholism: Clinical and Experimental Research and are currently available at Early View. (ANI)
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