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xcision repair pathway. In other words, alcohol appears to contribute to genetic damage by impairing DNA repair processes.

Researchers tested the survival capabilities of Chinese hamster ovary A10 cells 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 (ADH), which is known to convert alcohol to acetaldehyde (AcHO). AcHO belongs to a class of compounds called aldehydes (such as formaldehyde, a disinfectant and preservative), and is well known as a highly reactive and toxic compound that can damage the cells of all living things. 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 specific genotoxicants used in the experiment were 1-methyl-3-nitro-1-nitrosoguanidine, ethyl methanesulfonate, 4-nitroquinoline-N-oxide, ICR 170, and mitomycin C. Also used was 6-thioguanine, which damages DNA but not directly. The non-DNA reactive compounds used were ouabain, cycloheximide, and colchicine. In addition, an inhibitor of ADH called 4-methylpyrazole was given to some of the A10 cells in order to establish if alcohol or its metabolite acetaldehyde was responsible for cell damage.

The major finding of this study is that alcohol causes an increase in the mutagenicity (the capacity to induce mutations) 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 that it is acetaldehyde itself that is causing the damage, but it could be other aldehydes as well. For example, acetaldehyde may interfere with the normal cellular mechanisms designed to inactivate endogenous aldehydes, thos
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14-Mar-2002


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