The oxidation of acetone by a soil diphtheroid.

In recent months a series of papers have appeared, namely by Price and Rittenberg (1950), Plaut and Lardy (1950), and Sakami (1950), which indicate that acetone is utilized by mammalian tissue. Several metabolic pathways have been proposed for this oxidation. Plaut and Lardy (1950) concluded that acetone was directly incorporated into acetoacetate by a mechanism involving C02 fixation. Price and Rittenberg (1950) demonstrated the conversion of acetone to an acetylating agent by the mammalian organism. Sakami (1950) reported that when acetone labeled in the methyl groups with C14 was administered to rats, the labeled carbon appeared in the beta carbon of serine and the methyl carbon of choline and methionine. Similar labeling of these compounds occurred when C14 formate was administered to rats. This suggested to Sakami that the synthesis of labile methyl groups might occur over a pathway involving formate or a similar compound. His data are consistent with the hypothesis that there is a primary oxidative attack on acetone followed by a 2 and 1 carbon cleavage in which acetate and formate or some closely related compounds are formed. Rudney (1950) has observed that the administration of C-1 labeled propylene glycol to rats resulted in the appearance of C14 in the same compounds and in the same positions as when methyl labeled acetone was utilized. It appeared that the problem of acetone oxidation might be more readily attacked using microorganisms. In addition, it was conceived that the oxidation of acetone might proceed over a pathway involving acetol (CH3COCH20H) as an intermediate. Acetol then might undergo cleavage to yield acetaldehyde and a 1 carbon unit which could serve as a precursor of methyl groups. The following reactions illustrate the postulated pathway for acetone oxidation.