Roles for Replicative Deactivation in Yeast-Ethanol Fermentations

Mechanisms for the high potency of ethanol in inducing cell replicative deactivation are discussed. It is concluded that ethanol per se is not the effector but that acetaldehyde is the actual causative agent, acetaldehyde being the metabolic intermediate prior to ethanol in the glycolytic pathway. The minimum concentration of acetaldehyde is thus related to that of ethanol via an equilibrium reaction catalyzed by alcohol dehydrogenase. During active metabolism the level of acetaldehyde may be higher due to imbalances in the cellular redox balance and to differences between the rates of production and consumption of acetaldehyde.