Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Oct;44:206-212.
doi: 10.1016/j.tiv.2017.07.009. Epub 2017 Jul 14.

The Vitamin B6 Paradox: Supplementation With High Concentrations of Pyridoxine Leads to Decreased Vitamin B6 Function

Affiliations

The Vitamin B6 Paradox: Supplementation With High Concentrations of Pyridoxine Leads to Decreased Vitamin B6 Function

Misha F Vrolijk et al. Toxicol In Vitro. .

Abstract

Vitamin B6 is a water-soluble vitamin that functions as a coenzyme in many reactions involved in amino acid, carbohydrates and lipid metabolism. Since 2014, >50 cases of sensory neuronal pain due to vitamin B6 supplementation were reported. Up to now, the mechanism of this toxicity is enigmatic and the contribution of the various B6 vitamers to this toxicity is largely unknown. In the present study, the neurotoxicity of the different forms of vitamin B6 is tested on SHSY5Y and CaCo-2 cells. Cells were exposed to pyridoxine, pyridoxamine, pyridoxal, pyridoxal-5-phosphate or pyridoxamine-5-phosphate for 24h, after which cell viability was measured using the MTT assay. The expression of Bax and caspase-8 was tested after the 24h exposure. The effect of the vitamers on two pyridoxal-5-phosphate dependent enzymes was also tested. Pyridoxine induced cell death in a concentration-dependent way in SHSY5Y cells. The other vitamers did not affect cell viability. Pyridoxine significantly increased the expression of Bax and caspase-8. Moreover, both pyridoxal-5-phosphate dependent enzymes were inhibited by pyridoxine. In conclusion, the present study indicates that the neuropathy observed after taking a relatively high dose of vitamin B6 supplements is due to pyridoxine. The inactive form pyridoxine competitively inhibits the active pyridoxal-5'-phosphate. Consequently, symptoms of vitamin B6 supplementation are similar to those of vitamin B6 deficiency.

Keywords: Neuropathy; Neurotoxic; Pyridoxine; Supplements; Vitamin B6.

Similar articles

See all similar articles

Cited by 8 articles

  • Neurology of Nutritional Deficiencies.
    Miller KL, Trifan G, Testai FD. Miller KL, et al. Curr Neurol Neurosci Rep. 2019 Nov 26;19(12):101. doi: 10.1007/s11910-019-1011-2. Curr Neurol Neurosci Rep. 2019. PMID: 31773293 Review.
  • Inborn Errors of Metabolism in Pediatric Epilepsy.
    Cosnahan AS, Campbell CT. Cosnahan AS, et al. J Pediatr Pharmacol Ther. 2019 Sep-Oct;24(5):398-405. doi: 10.5863/1551-6776-24.5.398. J Pediatr Pharmacol Ther. 2019. PMID: 31598103 Free PMC article. Review.
  • Peripheral nerve disease secondary to systemic conditions in children.
    Wilmshurst JM, Ouvrier RA, Ryan MM. Wilmshurst JM, et al. Ther Adv Neurol Disord. 2019 Aug 12;12:1756286419866367. doi: 10.1177/1756286419866367. eCollection 2019. Ther Adv Neurol Disord. 2019. PMID: 31447934 Free PMC article. Review.
  • The effectiveness of correcting abnormal metabolic profiles.
    Clayton PT. Clayton PT. J Inherit Metab Dis. 2020 Jan;43(1):2-13. doi: 10.1002/jimd.12139. Epub 2019 Jul 17. J Inherit Metab Dis. 2020. PMID: 31222759 Free PMC article.
  • PDXK mutations cause polyneuropathy responsive to pyridoxal 5'-phosphate supplementation.
    Chelban V, Wilson MP, Warman Chardon J, Vandrovcova J, Zanetti MN, Zamba-Papanicolaou E, Efthymiou S, Pope S, Conte MR, Abis G, Liu YT, Tribollet E, Haridy NA, Botía JA, Ryten M, Nicolaou P, Minaidou A, Christodoulou K, Kernohan KD, Eaton A, Osmond M, Ito Y, Bourque P, Jepson JEC, Bello O, Bremner F, Cordivari C, Reilly MM, Foiani M, Heslegrave A, Zetterberg H, Heales SJR, Wood NW, Rothman JE, Boycott KM, Mills PB, Clayton PT, Houlden H; Care4Rare Canada Consortium and the SYNaPS Study Group. Chelban V, et al. Ann Neurol. 2019 Aug;86(2):225-240. doi: 10.1002/ana.25524. Epub 2019 Jul 1. Ann Neurol. 2019. PMID: 31187503 Free PMC article.
See all "Cited by" articles

LinkOut - more resources

Feedback