Abstract
When rats were made folate deficient and given diphenylhydantoin (DPH), it was found that there were an increase in formation of 14CO2 from urocanate-2-14C and histidine-2-14C by liver slices, a decrease in urinary formiminoglutamic acid (FIGLU) after urocanate load, and an increase in the incorporation of formate-14C into serine by liver slices. These results suggested that utilization of single carbon from FIGLU and formate via folate pathway proceeded more effectively in folate deficient rats when DPH had been administered.