A Study of the Metabolism of 4-Amino-5-Imidazolecarboxamide (AIC) in Folic Acid Deficiency in Rats

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IT is well known that folic acid deficiency is an important and fairly common cause of macrocytic anemia. At the present time, clinical states of folic acid deficiency can be studied by two laboratory methods. One method involves direct determination of the concentration of folic acid in the serum, by bacteriologic and other technics that are cumbersome and not fully reliable. The other method involves determination of the urinary excretion of formiminoglutamic acid (figlu), a metabolite of the amino acid, histidine, which requires folic acid for its catabolism. This latter method lacks the desired specificity for detecting folic acid deficiency, and it has been reported1 that the test is often positive also in B12 deficiency and in chronic disease of the liver.

The well-known role of folic acid in converting the compound, 4-amino-5-imidazolecarboxamide (AIC), into the corresponding purine derivative (Fig. 1) suggested the possibility that this naturally occurring purine precursor might provide yet another valuable tool in the study of folic acid deficiency. Various investigators2, 3 have shown that AIC is converted into the purine moiety of nucleic acids in experimental animals and also in man. In the absence of folic acid, this conversion does not occur, and it was shown many years ago that in bacterial cultures treated with sulfonamides (folic acid antagonists) AIC accumulated in significant amounts.4 Little information is available on the fate of AIC in well-defined folic acid deficiency in experimental animals or in man. Accordingly, our investigation was undertaken to study the fate of AIC. . .



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