Can methionine and zinc prevent the embryopathic effects of alcohol?

Alcoholism is a major and world-wide health problem. A characteristic pattern of congenital defects, known as the fetal alcohol syndrome, has been detected in the offspring of mothers who are chronic alcoholics. The mechanism underlying the teratogenic effects of ethanol is not known. An important hypothesis is that ethanol becomes teratogenic by inducing maternal/fetal nutritional deficiencies. Nutrients affected by ethanol consumption include methionine and zinc. Epidemiological and experimental studies have shown that zinc deficiency is associated with both fetal growth retardation and developmental defects. Furthermore, the ethanol metabolizing enzyme, alcohol dehydrogenase, is a zinc metalloenzyme. Zinc deficiency decreases alcohol dehydrogenase activity and thus slows down elimination of ethanol. Methionine, an essential amino acid, is a lipotrope, as well as a universal methyl donor. It is involved in hepatic detoxification. Studies on the effects of methionine and zinc might lead to appropriate therapeutic intervention in pregnancies of alcoholic mothers who are at a risk of giving birth to an impaired offspring. Furthermore, the results of such investigations will provide a better understanding of the mechanism of action of ethanol on the embryo.