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. 1971 Sep;50(9):1901–1909. doi: 10.1172/JCI106682

Conversion of vitamin B6 compounds to active forms in the red blood cell

Barbara B Anderson 1, Catherine E Fulford-Jones 1, J Anthony Child 1, Michael E J Beard 1, Christopher J T Bateman 1
PMCID: PMC292116  PMID: 5567559

Abstract

In studies with pyridoxine and other B6 compounds in blood, the active forms pyridoxal and pyridoxal phosphate were measured by differential assays using Lactobacillus casei. Red cell uptake of tritiated pyridoxine was also measured. A new metabolic pathway for conversion of pyridoxine to active forms was demonstrated in red cells.

In vivo studies in normal subjects suggested that pyridoxine was taken up by red cells where it was converted to pyridoxal phosphate and then pyridoxal, followed by gradual release of a proportion of pyridoxal into plasma. In vitro incubation of pyridoxine with blood confirmed this observation.

Increasing amounts of pyridoxine were taken up and converted as the amount added to blood was increased, and only very small numbers of red cells were needed to convert appreciable amounts. Conversion was markedly inhibited at temperatures lower than 37°C, and stopped altogether at - 20°C.

Release of pyridoxal into plasma was always directly proportional to the amount of pyridoxal formed and to the volume of plasma present. That pyridoxal phosphate was not released into plasma was demonstrated in stored blood, for pyridoxine was converted mainly only as far as pyridoxal phosphate, probably due to inactivation of the phosphatase. Pyridoxal phosphate remained in the red cells.

Pyridoxine was converted when incubated with washed red cells in saline or phosphate buffer suspension (0.08 M). In saline suspension, pyridoxal formed but was not released in the absence of plasma. In phosphate buffer suspension, pyridoxal phosphate was formed but was not changed to pyridoxal, probably due to inactivation of phosphatase by excess phosphate.

Pyridoxamine was converted to active forms in red cells less efficiently. Pyridoxal entered red cells rapidly, equilibrating between plasma and cells within 1 min in the same ratio as pyridoxal formed inside red cells. Pyridoxal phosphate did not enter red cells in whole blood but did so readily in washed cells in saline.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Anderson B. B., Peart M. B., Fulford-Jones C. E. The measurement of serum pyridoxal by a microbiological assay using Lactobacillus casei. J Clin Pathol. 1970 Apr;23(3):232–242. doi: 10.1136/jcp.23.3.232. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Baker H., Frank O., Thomson A. D., Feingold S. Vitamin distribution in red blood cells, plasma, and other body fluids. Am J Clin Nutr. 1969 Nov;22(11):1469–1475. doi: 10.1093/ajcn/22.11.1469. [DOI] [PubMed] [Google Scholar]
  3. Beutler E. Effect of flavin compounds on glutathione reductase activity: in vivo and in vitro studies. J Clin Invest. 1969 Oct;48(10):1957–1966. doi: 10.1172/JCI106162. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Chanutin A., Curnish R. R. Effect of organic and inorganic phosphates on the oxygen equilibrium of human erythrocytes. Arch Biochem Biophys. 1967 Jul;121(1):96–102. doi: 10.1016/0003-9861(67)90013-6. [DOI] [PubMed] [Google Scholar]
  5. Hamfelt A. Pyridoxal kinase activity in blood cells. Clin Chim Acta. 1967 Apr;16(1):7–18. doi: 10.1016/0009-8981(67)90263-x. [DOI] [PubMed] [Google Scholar]
  6. Hines J. D., Cowan D. H. Studies on the pathogenesis of alcohol-induced sideroblastic bone-marrow abnormalities. N Engl J Med. 1970 Aug 27;283(9):441–446. doi: 10.1056/NEJM197008272830901. [DOI] [PubMed] [Google Scholar]
  7. Hines J. D., Love D. S. Determination of serum and blood pyridoxal phosphate concentrations with purified rabbit skeletal muscle apophosphorylase b. J Lab Clin Med. 1969 Feb;73(2):343–349. [PubMed] [Google Scholar]
  8. Lee K. W., Abelson D. M., Kwon Y. O. Nicotinic acid-6-14C metabolism in man. Am J Clin Nutr. 1968 Mar;21(3):223–225. doi: 10.1093/ajcn/21.3.223. [DOI] [PubMed] [Google Scholar]
  9. MCCORMICK D. B., GREGORY M. E., SNELL E. E. Pyridoxal phosphokinases. I. Assay, distribution, I. Assay, distribution, purification, and properties. J Biol Chem. 1961 Jul;236:2076–2084. [PubMed] [Google Scholar]
  10. PREISS J., HANDLER P. Biosynthesis of diphosphopyridine nucleotide. I. Identification of intermediates. J Biol Chem. 1958 Aug;233(2):488–492. [PubMed] [Google Scholar]
  11. Paniker N. V., Beutler E. Effect of normal metabolites on the oxygen-hemoglobin equilibrium. Proc Soc Exp Biol Med. 1970 Nov;135(2):389–391. doi: 10.3181/00379727-135-35058. [DOI] [PubMed] [Google Scholar]
  12. Polansky M. M., Murphy E. W. Vitamin B6 components in fruits and nuts. J Am Diet Assoc. 1966 Feb;48(2):109–111. [PubMed] [Google Scholar]
  13. Polansky M. M. Vitamin B6 components in fresh and dried vegetables. J Am Diet Assoc. 1969 Feb;54(2):118–121. [PubMed] [Google Scholar]
  14. WADA H., MORISUE T., SAKAMOTO Y., ICHIHARA K. Quantitative determination of pyridoxal-phosphate by apotryptophanase of Escherichia coli. J Vitaminol (Kyoto) 1957 Sep 10;3(3):183–188. doi: 10.5925/jnsv1954.3.183. [DOI] [PubMed] [Google Scholar]
  15. Yamada K., Tsuji M. Transport of vitamin B6 in human erythrocytes. J Vitaminol (Kyoto) 1968 Dec 10;14(4):282–294. doi: 10.5925/jnsv1954.14.282. [DOI] [PubMed] [Google Scholar]

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