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. A new study using human cells has established linkages between alcohol metabolism and acetaldehyde-DNA damage that may have implications for breast and liver cancers.
Results will be published in the December 2011 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
"Although the link between drinking alcohol and certain types of cancers was first established in the 1980s," said Philip J. Brooks, program director in the Division of Metabolism and Health Effects at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), "the existence of such a relationship did not prove that alcohol itself caused the cancers. More recent evidence, however, has confirmed that alcohol - or more specifically, ethanol - is carcinogenic to humans at several sites in the body." Brooks, who is the corresponding author for the study, carried out this research while he was an investigator in the NIAAA Laboratory of Neurogenetics, part of the Division of Intramural Clinical and Biological Research.
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 Brooks. "However, approximately 30 percent of East Asians are unable to metabolize alcohol to acetate due to a genetic variant in the ALDH2 gene, and have a greatly elevated risk of esophageal cancer from alcohol drinking. This helped researchers establish the carcinogenicity of acetaldehyde in humans and its role in alcohol-related esophageal cancer."
Continue Reading: eurekalert.org
Results will be published in the December 2011 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
"Although the link between drinking alcohol and certain types of cancers was first established in the 1980s," said Philip J. Brooks, program director in the Division of Metabolism and Health Effects at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), "the existence of such a relationship did not prove that alcohol itself caused the cancers. More recent evidence, however, has confirmed that alcohol - or more specifically, ethanol - is carcinogenic to humans at several sites in the body." Brooks, who is the corresponding author for the study, carried out this research while he was an investigator in the NIAAA Laboratory of Neurogenetics, part of the Division of Intramural Clinical and Biological Research.
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 Brooks. "However, approximately 30 percent of East Asians are unable to metabolize alcohol to acetate due to a genetic variant in the ALDH2 gene, and have a greatly elevated risk of esophageal cancer from alcohol drinking. This helped researchers establish the carcinogenicity of acetaldehyde in humans and its role in alcohol-related esophageal cancer."
Continue Reading: eurekalert.org
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