Abstract
In previous investigations it was shown that in folic acid deficiency there is a large increase in the urinary excretion of formimino-n-glutamic acid (l-6). This increase has been explained by recent enzymatic studies demonstrating that the first step in the metabolism of formimino+glutamic acid is the transfer of the formimino group to tetrahydrofolic acid (7-9). Formimino-n-glutamic acid is an intermediate in histidine metabolism (10, 11)) and the urinary excretion of this compound in folic acid deficiency can be increased by the administration of n-histidine (3). Experiments with N16-labeled histidine demonstrated that the urinary formimino-n-glutamic acid was derived from histidine (3). In the present work we have demonstrated that, in addition to formimino-n-glutamic acid, there is a large increase in the excretion of formic acid in the urine of folic acid-deficient rats; in contrast to the results with formiminoglutamic acid, this formic acid is not derived from histidine. Our current studies have been facilitated by the recent development of sensitive spectrophotometric methods for the determination of formic acid (12) and formiminoglutamic acid (13). EXPERIMENTAL
Highlights
In the present work we have demonstrated that, in addition to formimino-n-glutamic acid, there is a large increase in the excretion of formic acid in the urine of folic acid-deficient rats; in contrast to the results with formiminoglutamic acid, this formic acid is not derived from histidine
PossibleSources of Urinary Formic Acid in Folic Acid Desciency-The increased excretion of formiminoglutamic acid in folic acid-deficient rats can be explained by the demonstration that tetrahydrofolic acid is required for the further metabolism
To determine the Cl4 content of the formiminoglutamic acid, an aliquot of urine was subjected to alkaline hydrolysis [13] ; after acidification, the formic acid was distilled, and the neutralized distillate was assayed for radioactivity
Summary
In previous investigations it was shown that in folic acid deficiency there is a large increase in the urinary excretion of formimino-n-glutamic acid (l-6). In the present work we have demonstrated that, in addition to formimino-n-glutamic acid, there is a large increase in the excretion of formic acid in the urine of folic acid-deficient rats; in contrast to the results with formiminoglutamic acid, this formic acid is not derived from histidine. The excretion of formiminoglutamic acid (per 7 hour collection period) increased during the course of the deficiency from a normal value of 0.22 pmole On the 38th day, for example, the folic acid-deficient rats consumed an average of 3 gm. of food per rat (calculated histidine content [18], 100 pmoles per day), whereas the folic acid-supplemented rats consumed an average of 9 gm. of food per rat (calculated histidine content, 300 pmoles per day)
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