ISOTOPE TECHNIQUE 



live reactions occur continuously. During life, the effects of these 

 degradative processes are nullified by synthetic reactions which re-form 

 as much tissue constituents per unit time as are destroyed by the auto- 

 lytic reactions; at death, the synthetic reactions, which in general are 

 coupled to oxidative reactions, cease and we observe the effects of 

 degradative processes alone. The mechanisms by which the cell 

 regulates these reactions are completely unknown. Since these reac- 

 tion rates can only be investigated in the intact animal, the only method 

 at present available which can be used is the isotope technique. It 

 can safely be assumed that the determination of these reaction rates 

 will occupy the attention of many investigatois in the coming years. 



There are several published researches which illustrate the 

 method by which the isotope technique may be applied to the study 

 of the conversion of one compound to another in the intact animal. 

 It was known from feeding experiments with immature rats that, 

 while phenylalanine was an essential component of the diet, tyrosine 

 was not (29). From the chemical similarity of these amino acids, it 

 was suspected that phenylalanine could be oxidized to tyrosine. Fur- 

 thermore, in tyrosinosis, tlie feeding of either tyrosine or phenylalanine 

 results in excretion of /^-hydroxyphenylpyruvic acid (22). It should 

 be recognized, however, that this latter piece of evidence is not as 

 definitive as it appears. The fact that the feeding of a compound to 

 an animal results in the excretion of an excess of another related com- 

 pound cannot be taken as positive proof that the first compound has 

 been converted to the second, even if, as in some cases, a stoichiometric 

 relationship appears to exist between the amounts of these substances. 

 It is well known that the feeding of mineral oil to rats results in an 

 enhanced excretion of fecal steroids. This is certainly not the result 

 of the conversion of these hydrocarbons to cholesterol but is due to 

 interference by the mineral oil with the reabsorption of cholesterol by 

 the intestinal tract. Further, the addition of glycine to the diet 

 results, in the next 24 hours, in an added excretion of nitrogen in the 

 urine equivalent to that of the added glycine. The conclusion that 

 this extra urinary nitrogen is derived from the dietary glycine would 

 not be correct. We have fed u> luunans small quantities of glycine 

 labeled with N'^ (ab(jut 10 mg. per kilo weight) and have foimd that 

 only about 33% of the labeled glycine nitrogen appears in the urine 

 in the next 24 hours. E\'en after 3 days only al)Out 50% has been 



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