Abstract
IT has been suggested that vitamin B12-deficiency in man may produce a defect in folate utilization due to trapping of L. casei folate activity1. This suggestion has recently received support in the British literature2. The trapped folate is probably some form of N-5-methyltetrahydrofolic acid3. Donaldson and Keresztesy4 reported that N-5-methyltetrahydrofolic acid can be enzymatically oxidized to N-5,10-methylene-tetrahydrofolic acid in the presence of menadione (a synthetic preparation with vitamin K activity) as electron acceptor. This raised the possibility that supplying this electron acceptor might break the assumed block in folate utilization present in vitamin B12-deficieney.
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HERBERT, V., STREIFF, R., SULLIVAN, L. et al. Failure of Menadione to affect Folate Utilization in Vitamin B12-deficient Human Beings. Nature 201, 196–197 (1964). https://doi.org/10.1038/201196a0
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DOI: https://doi.org/10.1038/201196a0
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