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Vitamin B6: pyridoxine hydrochloride vs. pyridoxal 5’-phosphate?
Neuropathy | Last Active: Nov 11 3:38pm | Replies (13)Comment receiving replies
Hello again, Debbie. I'm guessing, as it's been since last night since I posed my question (pyridoxine vs. pyridoxal) and five hours since you posted the only response that the question of the possibility of two effectively distinct forms of B6 (as you summed up so perfectly: one "good" form and one "bad" form) is a question many people have not heard before. If that's true, it just deepens my perplexity. –Ray (@ray666)
Replies to "Hello again, Debbie. I'm guessing, as it's been since last night since I posed my question..."
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Here's the answer...
The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function
Misha F Vrolijk 1, Antoon Opperhuizen 2, Eugène H J M Jansen 3, Geja J Hageman 4, Aalt Bast 4, Guido R M M Haenen 4
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PMID: 28716455 DOI: 10.1016/j.tiv.2017.07.009
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.