In support of the above, homocysteine appears to facilitate and methionine to reduce de novo DNA synthesis. This was measured by the ability of deoxyuridine to suppress thymidine-3H uptake into DNA in human bone marrow cultures. The homocysteine effect in B12-deficient marrow supports the possibility that there is in man an additional B12-independent pathway for regeneration of THFA by methylation of homocysteine to form methionine.
In B12 deficiency, inadequate DNA synthesis seems due in large measure to a block of tetrahydrofolic acid (THFA) regeneration from 5-methyl THFA (via homocysteine transmethylation).
Vitamin B12 and folate play an integral role in DNA synthesis and thus are essential to cell division and proper functioning of virtually all tissues in the body.
Among possible explanations for the methionine effect is end-product inhibition of the homocysteine transmethylase reaction, resulting in further accumulation of 5-methyl THFA. Homocysteine transmethylation may play an important role in the regulation of THFA availability and de novo DNA synthesis.