260 VI. ACETIC, FORMIC, AND PROPIONIC ACIDS 



acetate. However, Kalnitsky^* reported that, in the presence of oxaloace- 

 tate, a marked accumulation of citrate in the fluoroacetate-poisoned kidney 

 took place, without the accumulation of acetate. Liebecq and Peters^^ 

 likewise found increased citrate without an accumulation of acetate when 

 fumarate was present. Elliott and Kalnitsky*^ reported that the inhibition 

 of acetate synthesis was reversed by oxaloacetate. It was suggested that 

 the inhibition of acetate is the result of the formation of fluorocitrate, 

 which inhibits citrate oxidation. 



As a parallel to the possible transformation of pyruvate to acetic acid, 

 one may cite the evidence of the formation of a closely related compound, 

 namely acetoacetate, from pyruvate'*'^ and from fatty acids as well, under 

 certain conditions. Embden and collaborators^^"^" found that acetone 

 bodies were formed when the livers of healthy dogs were perfused with 

 butyric, caproic, and isovaleric acids, and that the level of acetone pro- 

 duction was raised in the livers of phlorhizin-treated or depancreatized 

 dogs^^ when they were perfused with beef blood; acetone bodies were 

 increased in the livers of normal dogs following perfusion with beef and 

 dog blood.*^ Gorr and Wagner^' noted the presence of acetone bodies in 

 liver brei when pyruvate was added to the digest. According to Annau,^'' 

 the formation of acetoacetate from pyruvate is to be ascribed to the con- 

 densation of two pyruvate molecules, with subsequent decarboxylation and 

 oxidation. It has been shown that acetoacetate accumulates in amounts 

 up to 25-28% of the pyruvate oxidized,^^ when hver slices break down 

 pyruvate in the presence of malonate. Ammonium chloride also increases 

 the production of acetoacetic acid from pyruvate.^*-^^ 



Moreover, pyruvate is quantitatively converted to acetoacetate by the 

 washed-cell hver preparation of Lehninger.^*'" When fumarate was added 



'* G. Kalnitsky, /. Biol. Chem., 179, 1015-1025 (1949). 



« C. Liebecq and R. A. Peters, /. Physiol, 108 (Proc. Physiol. Soc.) IIP, June 1948; 

 Biochim. et Biophys. Acta, 3, 215-230 (1949). 



« W. B. Elliott and G. Kalnitsky, /. Biol. Chem., 186, 487-493 (1950). 



^^G. Embden and M. Oppenheim, Biochem. Z., 45, 186-206 (1912); 55, 335-340 

 (1913). 



^« G. Embden and A. Marx, Beitr. chem. Phijsiol. Pathol, 11, 318-322 (1908). 



^^ G. Embden and H. Engel, Beitr. chem. Physiol. Pathol, 11, 323-32G (1908). 



^° G. Embden, H. Salomon, and F. Schmidt, Beitr. chem. Physiol. Pathol, 8, 129-155 

 (1906). 



" G. Embden and L. Lattes, Beitr. chem. Physiol. Pathol, 11, 327-331 (1908). 



" G. Embden and F. Kalberlah, Beitr. chem. Physiol. Pathol, 8, 121-128 (1906). 



" G. Gorr and J. Wagner, Biochem. Z., S54, 5-7 (1932). 



^* E. Annau, Z. phijsiol Chem., 224, 141-149 (1934). 



" E. A. Evans, Jr., Biochem. J., 34, 829-837 (1940). 



^6 N. L. Edson, Biochem. J., 29, 2082-2094 (1935). 



" A. Lehninger, /. Biol. Chem., 165, 131-145 (1946). 



