580 BIOTIN 

 CO 



/ \ 



NH NH NH2 NH, 



CH CH -~> CH CH 



CH2 CH2-(CH2)4-COOH CH, CHj- (CH2)4-COOH 



of C^^ by C^^ was observed. Thus, the ureido carbonyl group is apparently 

 not transferred during carbon dioxide fixation. ^^ 



Fixation of carbon dioxide in mammalian tissues and in microorganisms 

 under the influence of biotin has been clearly demonstrated.^^"^^ In the 

 presence of biotin, L. arabinosus fixed C^* from bicarbonate into cellular 

 aspartic acid. However, no fixation was observed when the medium con- 

 tained less than 0.05 m7 biotin per milliliter or when aspartic acid or an 

 antibiotin was added. Biotin analogs having antimetabolite properties in- 

 hibited the fixation of carbon dioxide when added simultaneously with 

 biotin to cells grown on a low-biotin medium. They had little influence on 

 the carbon dioxide fixing capacity of cells grown in the presence of biotin.-^ 



Oxybiotin is inherently less effective than biotin for carbon dioxide fixa- 

 tion even at neutral pH.^' 



Intraperitoneal injection of NallCOs containing C'' into normal and 

 biotin-deficient rats resulted in a larger C^^ fixation into adenine, goianine, 

 arginine, aspartic acid, citric acid, and bone carbonate of the control ani- 

 mals than into the corresponding compounds of the biotin-deficient animals. 

 The presence of C^^ in bone citrate indicates that this citrate is in dynamic 

 equilibrium with other tissue citrate. "The small fixation is probably due 

 to the fact that the major portion of the isotopic citrate formed would be 

 immediately oxidized via the citric acid cycle. "^^ 



The biotin-deficient rat exhibits lower carbon dioxide fixation into tissue 

 arginine than normal controls. The Krebs-Henseleit cycle^* involves urea 

 formation through the intermediate of arginine, and this again passes 

 through the overall step of carbon dioxide fixation via ornithine — > citrul- 

 line."'* The synthesis of citiiiUine from ornithine is significantly decreased in 

 the liver homogenates of biotin-deficient rats. The impaired synthesis by the 

 deficient liver may be increased by the addition in vitro of a heated residue 



" H. A. Lardy, R. L. Potter, and R. H. Burris, /. Biol. Chem. 179, 721 (1949). 



3» P. R. MacLeod and H. A. Lardy, J. Biol. Chem. 179, 733 (1949). 



31 P. R. MacLeod, S. Grisolia, P. P. Cohen, and H. A. Lardy, J. Biol. Chem. 180, 



1003 (1949). 

 « R. L. Potter and C. A. Elvehjem, J. Biol. Chem. 183, 587 (1950). 

 " H. A. Krebs and K. Ilenseleit, Hoppe-Scyler's Z. physiol. Chem. 210, 33 (1932). 

 »< S. Grisolia and P. P. Cohen, /. Biol. Chem. 176, 929 (1948). 



