1968 Volume 94 Issue 4 Pages 417-430
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 N5, 10 methylenetetrahydro-folate ieductase and a considerable decrease in that of N5 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 N5 methyltetrahydrofolate in the liver of riboflavin deficient rats.
From these results it was assumed that a decreased activity in both the N5, 10 methylenetetrahydrofolate reductase and N5 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 N5 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.