Abstract
The amidine carbon atom (C-Z) of L-histidine is known to be an efficient metabolic precursor of single carbon units. Following the administration of n-histidine-2-Cr4, the radioactivity has been found in CO2 and urea, in carbons 2 and 8 of purines, in the hydroxymethyl group of serine, and in choline, and creatine (l-4). The major pathway of histidine degradation which involves deamination to urocanic acid and finally, cleavage of the ring to formiminoglutamic acid (5-7) has been assumed to be the sole means of liberation of this carbon atom for “1 carbon metabolism.” The liberation of the single carbon unit can be accomplished by transfer of the formimino group to tetrahydrofolic acid. The formimino moiety is ultimately transformed into the formyl group of Nr”-formyltetrahydrofolic acid (8, 9). Folic acid or vitamin Bit-deficient rats excrete large amounts of formiminoglutamic acid in the urine (10, 11). In the more recent study (ll), the basal diet employed was limiting in the sulfur amino acids (9% casein). The addition of excess methionine to the diet, in the absence of either folic acid or vitamin Br2, significantly reduces urinary formiminoglutamic acid (11). The studies reported in this paper were prompted by this finding and were designed to clarify the nature of this effect. These studies show that radioactive COz (derived from carbon 2 of histidine) is greatly increased following the administration of excess methionine to the deficient animal. Furthermore, the evidence presented is consistent with the view that methionine does not divert histidine metabolism from the urocanic acid pathway, but exerts its influence at the level of formiminoglutamic acid.
Highlights
It was of primary interest to determine whether or not the action of methionine in reducing the excretion of formiminoglutamic acid was associated with the release of carbon 2 of histidine as a "C-l unit." The urine from a folic acid- and a vitamin B12deficient rat, both of which had been fed their respective diets for 5 weeks after weaning, was collected for 18 hours
Since the fate of carbon 2 of histidine is so radically altered by a "preinjection" of methionine, it can be assumed that rats which had ingested larger amounts of the diet containing excess methionine just before radioactive histidine injection would convert more of the carbon 2 to CO2
It is concluded that methionine influences histidine metabolism by increasing the utilization of formiminoglutamic acid in folic acid and vitamin B12-deficient rats
Summary
Diets used [11] were modified to contain 0.2% added n-histidine monohydrochloride and 100 pg of vitamin B1z per kg. Male rats of the Sprague-Dawley strain were fed the experimental diets after weaning. Labeled radioactive L-histidine-Cl4 (0.21 PC per pmole) was purchased from Schwarz Laboratories; L-histidine-. 2-Cl4 (3.56 PC per pmole), sodium formate-Cl4 and L-serine-/3-. Urocanic acid were formed enzymatically from their respective histidines [12] without dilution of specific activity. They were purified by fractionation on Dowex l-acetate columns with gra-
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