INCORPORATION OF "C IXTO TISSUE 801 



tion being soon exhausted or almost exhausted while endogenous ^^COg 

 is constantly produced, the specific activity of the respiratory carbon 

 dioxide is bound to decrease markedly with time in the later phase of the 

 experiment. 



After the lapse of 50 minutes, the specific activity of the exhaled 

 carbon dioxide is only half of the value observed after the lapse of 20 

 minutes. 



If the injected labelled carbon compound is metabolized at a less 

 rapid rate than acetate or if we interfere with the normal metabolic 

 rate of acetate in the early phase of the experiment, the increase in the 

 i^COg content of the respiratory carbon dioxide will take place at a 

 slower rate, than in that of normally metabolizing acetate and so will 

 the decrease in the specific activity occurring in the later stage of the 

 experiment. This is the case when the slower metabolizing labelled 

 succinate is administered to rats. Figure 1 w^iich is plotted by making 

 use of the data of Gould and assoc.^^) demonstrates the change in specific 

 activity of the expiratory carbon dioxide following injection of labelled 

 acetate and succinate respectively. The results obtained by the above 

 mentioned authors, clearly demonstrate the lower metabolic rate of 

 succinate. The velocity constant of the conversion of acetate carboxyl 

 carbon and succinate carboxyl carbon into carbon dioxide is found by 

 the above mentioned authors to be 0.043 min~^ and 0.028 min~i re- 

 spectively. 



If the irradiation influences the metabolic rate of acetate the produced 

 change will reflect itself in a change in the slope of the time-specific 

 activity curve of the exhaled carbon dioxide, as the amount of ^^COg 

 contributed to the COg exhaled in the time unit will now differ from 

 that contributed by the controls. Catabolic changes in which labelled 

 acetate does not participate, or participates to a minor extent only, 

 may also influence the slope of the time-specific activity curves of exhaled 

 carbon dioxide. The amount of ^^COg to which a given quantity of ^^COg 

 is to be admixed, will now be different. The change in the time-specific 

 activity curves will reflect itself in activity figures for all tissue fractions 

 into which COg is incorporated. A metabolic interference which leads 

 to an increase in the ^^COg content of the liver CO2 (bicarbonate), so far 

 as it does not influence glycogen turnover, will result in higher activity 

 figures of glycogen. In this statement we disregard possible differences 

 in the i^C incorporation due to the fact that some ^*C enters glycogen 

 by another w^ay than through circulating COg. 



An increased ^^C content of the liver glycogen after irradiation may 

 be due to an increased turnover rate of glycogen. If this leads to 



^1^ R. G. Gould, F. M. Sinex, I. N. Rosenberg, A. K. Solomon and A. B. 

 Hastings, J. Biol. Chem. 177, 295 (1949). 



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