Urinary excretion of formiminoglutamic acid (FIGLU) following an oral, intraperitoneal, intramuscular, or intravenous load with L-histidine-monohydro-chloride was markedly reduced in rats when fed on a riboflavin deficient diet for 11-30 days.
The assay of tetrahydrofolate-dependent enzyme activity of the liver revealed that there were a marked deeraase in the activity of N
5, 10 methylenetetrahydro-folate ieductase and a considerable decrease in that of N
5 methyltetrahydro-folate transferase of the liver from the riboflavin deficient rats.
Results of bioassay using
L. casei,
St. faecalis and
Pediococcus cerevisiae of folate compounds of the liver revealed a tendency toward relative increase in folato deriva-tives other than N
5 methyltetrahydrofolate in the liver of riboflavin deficient rats.
From these results it was assumed that a decreased activity in both the N
5, 10 methylenetetrahydrofolate reductase and N
5 methyltetrahydrofclate trans-ferase was induced by riboflavin deficiency, and then that the decrease in the activity of the both enzymes caused an accumulation of tetrahydrofolate com-pounds other than N
5 methyltetrahydrofolate, thus affording a relatively large amount of free tetrahydrofolate available for the formiminotransferase reaction, with a consequence of rapid conversion of FIGLU into glutamic acid.
Free methionine levels of the liver was not found to be increased but slightly decreased in riboflavin deficient rats as compared with those of control rats.
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