INCORPORATION OF "C INTO TISSUE 803 



of formation of labelled glycogen compensated by an increased cata- 

 bolism of almost inactive glycogen. An increased i*C content of the liver 

 glycogen after irradiation may, however, be due to a very different 

 reason as well, to a change in the sensitivity of ^^COg as an indicator 

 of ^^COg. If that to be the case, then if ^^COg formation from acetate is 

 slown down in the first phase of the experiment (during the first minutes), 

 the ^^COg content of the liver bicarbonate will be lower in the irradiated 

 animals than in the controls. Soon, however, the opposite will be the 

 case and thus a larger incorporation of ^^C into glycogen will be 

 observed. 



If it is not the specific activity of the carbon dioxide which is influenced 

 by irradiation, but it is the turnover rate of glycogen which is enhanced, 

 we should find in all phases of the experiment more ^^C in the glycogen 

 fraction. If, however, an increase in the ^^C content of the carbon dioxide 

 is responsible for the changed i^C uptake by the glycogen, we should ob- 

 serve an increased ^^C incorporation into glycogen in the first phase of 

 the experiment and a decreased one in the later phase. "Time experi- 

 ments" may thus supply important information about the metabolic 

 changes produced by irradiation. 



Much of the respiratory COg is the product of muscular metabolism. 

 Changes in the specific activity of carbon dioxide produced in an organ 

 with a minor contribution to the total COg production of the organism 

 may, therefore, not suffice to become clearly visible when comparing the 

 specific activities of CO2 of irradiated animals with that of controls. 

 Though such comparisons are of importance, they often are less revealing 

 than investigations into the effect of irradiation on the i^C content of 

 tissue fractions. 



We discussed above the possible effects of irradiation on the specific 

 activity of catabolic carbon dioxide. We shall now consider the result 

 of interference with the rate of formation of another product of acetate 

 metabolism with that of fatty acids. 



Part of the acetate carbon which reaches the liver is rapidly incor- 

 porated into the fatty acids of the liver of the mouse. After the lapse 

 of about 20 minutes the fatty acids show a maximum ^^C content, half 

 of that value being observed only after the lapse of further 40 minutes. 

 Many of the newly formed fatty acid molecules are soon leaving the liver 

 by catabolic processes or exodus and, as in the mean time the activity 

 level of the acetate and other fatty acid precursors is lowered, the 

 disappeared active fatty acid molecules are replaced by less active ones. 

 The marked decline in the activity level of acetate with time is, as 

 already mentioned, due to the fact that the injected labelled acetate is 

 rapidly metabolized, while the diluting non-radioactive endogenous 

 acetate due to incessant new-formation remains at a constant concentra- 

 tion level. 



51* 



