Abstract
Summary
When rats were fed a diet deficient in vitamin B12 and limiting in methionine, the 14CO2 production from L-histidine-2-14C was reduced in comparison with rats fed diets supplementd with vitamin B12 and/or methionine. In contrast, the production of 14CO2 from 5-14CH3-tetrahydrofolic acid was not altered by vitamin B12 deficiency or the level of dietary methionine. The T max for the oxidation of 5-14CH3-tetrahydrofolic acid to 14CO2 was delayed in vitamin B12 deficiency in comparison with normals, indicating that either an enzymatic reaction or transport into tissues becomes rate-limiting in the deficient state.
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