It has been postulated that the activities of certain enzymes may be markers of a genetic predisposition to alcoholism. We previously showed that low fluoride-stimulated platelet adenylate cyclase (AC) activity, and an increased sensitivity of platelet monoamine oxidase (MAO) to in vitro inhibition by ethanol, effectively discriminated alcoholic and non-alcoholic individuals. We have now examined the heritability of platelet fluoride-stimulated AC activity in families with alcoholic members, and have found familial transmission, with a major gene effect, for this enzyme activity. The major gene was transmitted as a Mendelian co-dominant. Transmission of basal AC activity was more complex. The findings are compatible with the possibility that fluoride-stimulated AC activity, which is transmitted as a single major gene in families of alcoholics, could represent a trait marker for a predisposition to alcoholism. In addition to G/sa, future studies will quantitate AC with the use of antibodies raised against specific peptides. The studies described will help to determine whether the observed differences in platelet enzyme activities between alcoholics and non-alcoholics are genetically based, and may be a marker for a predisposition to alcoholism, or are a consequence of ethanol consumption.
