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dc.contributor.authorVrolijk, Misha F
dc.contributor.authorOpperhuizen, Antoon
dc.contributor.authorJansen, Eugène H J M
dc.contributor.authorHageman, Geja J
dc.contributor.authorBast, Aalt
dc.contributor.authorHaenen, Guido R M M
dc.date.accessioned2018-01-04T11:55:50Z
dc.date.available2018-01-04T11:55:50Z
dc.date.issued2017-10
dc.identifier.citationThe vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function. 2017, 44:206-212 Toxicol In Vitroen
dc.identifier.issn1879-3177
dc.identifier.pmid28716455
dc.identifier.doi10.1016/j.tiv.2017.07.009
dc.identifier.urihttp://hdl.handle.net/10029/621021
dc.description.abstractVitamin 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.
dc.language.isoenen
dc.rightsArchived with thanks to Toxicology in vitro : an international journal published in association with BIBRAen
dc.titleThe vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function.en
dc.typeArticleen
dc.identifier.journalToxicol in Vitro 2017, 44:206-12en
html.description.abstractVitamin 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.


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