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The molecular perspective: alcohol.

Alcohol is a substance fraught with contradictions. It is a dangerously toxic solvent, yet it has been produced and consumed since the dawn of civilization. A glass of wine or a cocktail will complement any meal and smooth out the tensions of the day, but a few more drinks will inhibit reaction times, making the consumer the major threat currently on the road. A drink or two each day will reduce the risk for heart disease, a fact vividly shown in the unexpectedly low incidence of heart disease in the French in spite of a steady diet of rich foods. More heavy drinking, however, leads to myriad and widespread health problems, including cancer. Alcohol is detoxified in the human body in two enzymatic steps (Fig. 1). First, alcohol is oxidized to acetaldehyde by the enzyme alcohol dehydrogenase. However, acetaldehyde is even more toxic than alcohol, so it is quickly oxidized to acetate by a second enzyme, aldehyde dehydrogenase. Both of these enzymes use the cofactor nicotinamide adenine dinucleotide (NAD) to provide the oxidizing power needed for these transformations. The need for the special redox talents of NAD places an important limit on the amount of alcohol that may be detoxified. Liver cells contain a limited supply of NAD, so these enzymes can act only as fast as it is recycled. This typically limits the detoxification rate to about one drink per hour—any additional alcohol stays in the circulation until the enzymes can get around to it. Human cells build a collection of variants of these two enzymes. Six separate genes for alcohol dehydrogenase are found in the human genome, and several of these show multiple alleles. To further complicate the matter, active complexes may be formed in many cases by mixing two different types into one dimeric structure. This leads to a wide range of activities of the different forms, both in their detoxification of alcohol and their transformations of similar substrates. For instance, a particularly active form of alcohol dehydrogenase is common in people from the Pacific Rim. This might be a good thing, except that many of these individuals also carry an inactive form of aldehyde dehydrogenase, and thus they cannot metabolize the acetaldehyde that is so efficiently formed. These people are highly sensitive to alcohol, suffering from severe side effects of acetaldehyde poisoning when they drink alcoholic beverages. The strongest linkage of alcohol consumption with cancer is, quite expectedly, with cancers of the mouth, pharynx, larynx, and esophagus. The mechanisms of carcinogenesis are still a matter of study and debate, but two probable mechanisms involve the enzymes of alcohol detoxification. The acetaldehyde formed in the first step may be a major culprit. Acetaldehyde is a reactive compound that forms covalent complexes with proteins and DNA, and thus may act as a mutagen. Alcohol abuse also