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Volume 3, Number 43 - March 22, 2002
Researchers Examine Alcohol, Cancer Link

 

    Alcohol could produce effects consistent with inhibiting a repair process that keeps normal body cells from being transformed into cancer cells, according to research released.
 
   "Epidemiological studies have shown that drinking alcohol is associated with an increased risk of tumors in the esophagus, mouth, larynx and liver," David B. Couch,  associate professor of pharmacology at the University of Mississippi and lead author of the study, told United Press International.
 
   "In the model system used, alcohol exposure could produce effects consistent with inhibition of the base excision repair pathway or one of the repair pathways of deoxyribonucleic acid -- there are several repair pathways -- base excision is just one of them."
 
   The study is found in the March issue of Alcoholism: Clinical & Experimental Research.
 
   Blood cells of alcoholics have a greater incidence of genetic damage but it has not been clear if alcohol itself is the cause, Couch said. 
 
   Couch, along with Richard A. Deitrich of University of Colorado Health Science Center in Denver, tested the survival capabilities of ovary A10 cells from Chinese hamsters by exposing them to alcohol, genotoxicants -- substances that can damage DNA through mutation or cancer -- and non-DNA reactive cytotoxic agents. A10 cells were chosen because they have been engineered to express alcohol dehydrogenase, which is known to convert alcohol to acetaldehyde or AcHo, the first product of alcohol metabolism. 
 
   Normally when people drink, alcohol is converted to AcHO in the liver, which is then rapidly metabolized to acetate, which is then further metabolized by tissues outside of the liver.
 
   "The major finding of this study is that alcohol causes an increase in the mutagenicity of agents that damage DNA," said Deitrich. "This is as a result of the metabolism of alcohol to acetaldehyde. In fact, it is clear that acetaldehyde is the major culprit in the effects noted here."
 
   The presumption is acetaldehyde itself causes the damage, but it could be other aldehydes as well. For example, it may interfere with the normal cellular mechanisms designed to inactivate endogenous aldehydes produced in normal cellular function or those produced as a result of alcohol's production of oxidative damage, Deitrich said. 
 
   "The concept of acetaldehyde being a mutagen is not a novel concept and the engineered cells produced a lot of acetaldehyde and these cells do not have the ability to inactivate the acetaldehyde unlike cells in the body," Boris Tabakoff, chairman of the department of pharmacology, University of Colorado School of Medicine in Denver, told UPI. "It would be more interesting to see if this happened under normal conditions in how we live and not in engineered cells to see if it has broader implications."
 
   "An interesting next step in the research might be to add cigarette smoke, which also contains acetaldehyde to the alcohol," he added.
 
   Couch acknowledged the study did not uncover new ground but sets up further research on DNA repair pathways and on the dose of acetaldehyde that causes damage. 
 
   "We speculate that alcohol in a limited dose does not impact on DNA repair and that it has a beneficial impact on lipids in the body, hence the studies on the beneficial effects of alcohol on the body," Qingyi Wei, a molecular epidemiologist, at the MD Anderson Cancer Center at the University of Texas in Houston, told UPI. 
   
   "Alcohol has been known to inhibit folate absorption and folate helps repair tissues from mutations -- that's why folate is needed both before and in the first weeks of pregnancy to reduce the risk of birth defects." 
 
   Folate is a B vitamin found in a variety of foods and added to many vitamin and mineral supplements as folic acid.
 
   Tabakoff said there is a line between the beneficial effects of alcohol and the damaging effects of alcohol on human health and he advised people to take no more than two drinks a day.
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Copyright 2002 by United Press International.
All rights reserved.
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