The effect of vitamin B12 on the metabolism of formate and certain formate precursors by the rat

Abstract

The metabolism of sodium [C14]formate, DL-[3-C14]serine and L-[2-ring-C14]nistidine has been studied in vivo in young rats depleted of vitamin B12 by breeding from deficient mothers which were fed on a vitamin B12-low casein diet. The livers of rats fed on the deficient diet contained much less vitamin B12 than those of control animals and other internal organs were also depleted. The incorporation of serine and histidine into the mixed visceral proteins was not reduced by lack of vitamin B12. Administration of vitamin B12 to deficient rats increased the oxidation of formate to respiratory CO2 and decreased the urinary excretion of formate. The conversion of formate into both serine and methionine and that of serine and formate into choline methyl groups were markedly increased by vitamin B12. The utilization of histidine for the biosynthesis of serine, methionine and choline was not affected by the vitamin B12 deficiency. It is suggested that vitamin B12 is required for the interconversion of C1 compounds by oxidation-reduction, but not for their transfer at the same oxidation level. The possible physiological significance of this function is discussed.