IXCOlll'ORATIOX OF LAB. ACETATE CARBON (C) IXTO TISSUE EliACTIOXS 413 



undor the action of the dinitro-compound the formation in or intrusion 

 of fatty acids or their precursors into the muscle should be slowed down, 

 we would obtain a lower ^*C content in the D.P.P. injected mice. A lower 

 J^C incorporation can, however, be tlu> result not only of a depressed 



Brain 

 Tolal tissue 



»; 



mm. 



Broin 

 Total fats 



mm. 



Fig. 4. Effect of dinitro-cyclo-pentylphenol on the incorporation 

 of i*C into total fats (b) and total tissue (a) of the brain of the mouse, 



i^C injected as CHg^COONa. 



formation rate of fats and other labelled components, but also of an en- 

 hanced dilution of the labelled acetate or its transportation products by 

 endogenous inactive compounds. 



Assuming the half-life time of the average fatty acid molecule in the 

 mouse to bel8 days, the metabolism of 1 gm fatty acids present in the 

 muscles of a 20 gm mouse will lead to the formation of about 1 millimol en- 

 dogenous (at the start inactive, later slightly active) acetic acid. In this 

 calculation only the carcass fatty acids are considered (4). Tf under the 

 eff(H't of the D.P.P. the carcass fatty acids should be catabolized at 

 an enhanced rate, for example, twice as rapidly as in the controls (inac- 

 tivation of pyruvate is leading to the accumulation of acetate as well), 

 the dilution of the active muscle acetate and its transformation products 



