Inter-individual differences in pharmacokinetics of vitamin B6: A possible explanation of different sensitivity to its neuropathic effects

@article{Vrolijk2020InterindividualDI,
  title={Inter-individual differences in pharmacokinetics of vitamin B6: A possible explanation of different sensitivity to its neuropathic effects},
  author={Misha F Vrolijk and Geja J. Hageman and Sonja van de Koppel and Florence van Hunsel and Aalt Bast},
  journal={PharmaNutrition},
  year={2020},
  volume={12},
  pages={100188}
}

Vitamin B-6-Induced Neuropathy: Exploring the Mechanisms of Pyridoxine Toxicity

It is concluded that PDXK inhibition and consequently disrupted GABA neurotransmission is the most plausible mechanism of toxicity.

Physiological and Biochemical Markers of the Sex-Specific Sensitivity to Epileptogenic Factors, Delayed Consequences of Seizures and Their Response to Vitamins B1 and B6 in a Rat Model

The findings on the sex differences in sensitivity to epileptogenic factors, action of vitamins B1/B6 and associated biochemical events have medical implications.

Physiological and Biochemical Markers of the Gender-specific Sensitivity to Epileptogenic Factors, Delayed Consequences of Seizures and Their Response to Vitamins B1 and B6 in a Rat Model of Epilepsy

The findings on the gender differences in sensitivity to epileptogenic factors, action of vitamins B1/B6 and associated biochemical events have medical implications.

The Pharmacokinetics of Doxycycline in Channel Catfish (Ictalurus punctatus) Following Intravenous and Oral Administrations

This study provides future studies with a framework for determining the BA of doxycycline in channel catfish in the development of a new formulation and provides information on the appropriate use of DC in aquaculture.

References

SHOWING 1-10 OF 31 REFERENCES

Pharmacokinetic Properties of the Plasma B6 Vitamers after Single and Chronic Oral Pyridoxine Mega Doses

Data from pharmacokinetic studies provide insight into vitamin B, metabolism after single and chronic pyridoxine administration and aspartate aminotransferase activities in RBC shows a significant decrease after the high oral PN administration.

The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function.

Liquid chromatographic studies of vitamin B6 metabolism in man.

Plasma content of B6 vitamers and its relationship to hepatic vitamin B6 metabolism.

The results suggest that orally ingested pyridoxine is rapidly metabolized in liver and its products are released into the circulation in the form of pyrsidoxal-P, pyrIDoxal, and pyriridoxic acid, the principal B6 vitamer in plasma.

Relation of short-term pyridoxine-HCl supplementation to plasma vitamin B-6 vitamers and amino acid concentrations in young women.

Altered plasma amino acid profiles and increased plasma urea concentrations in response to supplementation suggested accelerated protein and/or amino acid metabolism.

Measurement of plasma B6 vitamer profiles in children with inborn errors of vitamin B6 metabolism using an LC-MS/MS method

It is shown that patients with inborn errors of B6 metabolism such as pyridox(am)ine 5’-phosphate oxidase (PNPO) deficiency have characteristic B6 profiles which allow them to be differentiated from each other and control populations, even when on treatment with B6.

Association of plasma B-6 vitamers with systemic markers of inflammation before and after pyridoxine treatment in patients with stable angina pectoris.

The results suggest that the acute phase and activated cellular immunity are associated with increased cellular uptake and catabolism of vitamin B-6, respectively.

Plasma vitamin B6 vitamers before and after oral vitamin B6 treatment: a randomized placebo-controlled study.

Vitamin B( 6) treatment has an immediate effect on the concentrations and the forms of B(6) vitamers present in plasma, and the changes remain the same during prolonged treatment.

Markedly increased circulating pyridoxal-5'-phosphate levels in hypophosphatasia. Alkaline phosphatase acts in vitamin B6 metabolism.

These findings identify increased circulating PLP concentration as a marker for hypophosphatasia and provide further evidence that tissue nonspecific AP acts in vitamin B6 metabolism.