FORMATION OF ETHYL ACETATE IN FERMENTATION WITH BREWER'S YEAST: IV. METABOLISM OF ACETYL-COENZYME A

During fermentation with Saccharomyces cerevisiae, esters are formed from alcohols and acyl-CoA. The formation of ethyl acetate thus depends on the availability of acetyl-CoA, which is formed partly by activating acetic acid (requiring ATP) and partly by oxidative decarboxylation of pyruvic acid (requiring lipoic acid and thiamine pyrophosphate participation). Formation of ethyl acetate is stimulated by addition of small quantities of DNP (2,4-dinitrophenol), an effect which is enhanced by addition of lipoic acid and counteracted by sodium arsenite (an inhibitor to lipoic acid). These results show that oxidative decarboxylation of pyruvic acid is an important contributive factor to anaerobic formation of acetyl-CoA by Sacch. cerevisiae. Formation of ethyl butyrate from butyric acid is inhibited by DNP in all concentrations; butyrate must first be activated to butyryl-CoA (requiring ATP). Formation of ethyl acetate is inhibited by higher concentrations of DNP, owing to diminished oxidation to acetate in different states, to inhibition of formation of coenzyme A from pantothenic acid (requiring ATP) or to the enzymatic pattern of the cells becoming changed; all these factors may play some part. Formation of esters is stimulated when other reactions requiring acetyl-CoA are inhibited, e.g., the citric acid cycle and carboxylation of acetyl-CoA to malonyl-CoA, which can be achieved by making the medium biotin-free. Malonic acid is also an inhibitor of the citric acid cycle and interacts in lipid synthesis.