Pyridoxine (vitamin B6) neurotoxicity: enhancement by protein‐deficient diet

  title={Pyridoxine (vitamin B6) neurotoxicity: enhancement by protein‐deficient diet},
  author={Seymour Levine and Arthur M. Saltzman},
  journal={Journal of Applied Toxicology},
Large doses of pyridoxine cause injury to the primary sensory neurons in trigeminal and dorsal root ganglia of animals and patients subjected to megavitamin therapy. The increased hazard to subjects with reduced renal excretory function has been explored previously. In the present work, the neurotoxicity of pyridoxine for rats was found to be increased by dietary protein deficiency. A mere 3 or 7 days of pretreatment with either of two protein‐deficient diets were sufficient to accelerate and… 

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.

B6-responsive disorders: A model of vitamin dependency

  • P. Clayton
  • Biology, Medicine
    Journal of Inherited Metabolic Disease
  • 2005
Pyridoxal phosphate is the cofactor for over 100 enzyme-catalysed reactions in the body, including many involved in the synthesis or catabolism of neurotransmitters, and in other infants with inborn errors of metabolism B6 treatment can be extremely beneficial.

Pyridoxine-induced sensory ataxic neuronopathy and neuropathy: revisited

Consumption of high dose pyridoxine can cause sensory neuronopathy and axonal sensorimotor polyneuropathy, leading to sensory ataxia which may not be reversible.

Improvement of pyridoxine-induced peripheral neuropathy by Cichorium intybus hydroalcoholic extract through GABAergic system

The results showed beneficial effects of CE on pyridoxine-induced peripheral neuropathy and modulating of the GABAergic system mediated by TNF-α may be involved in the anti-neurotoxic effect of CE.

Role of Vitamin B6 Deficiency in the Nitrogen Balance of Streptozotocin-Diabetic Rats

Pyridoxine-deficient diabetic rats treated with insulin suffered important changes in the utilization of dietary proteins, as observed by nitrogen balance and enzyme activity studies.

Effects of pyridoxamine (K-163) on glucose intolerance and obesity in high-fat diet C57BL/6J mice.



Pyridoxine Megavitaminosis: An Analysis of the Early Changes Induced with Massive Doses of Vitamin B6 in Rat Primary Sensory Neurons

These findings identify the probable target site for pyridoxine toxicity, and establish a simple animal model for studying not only sensory denervation, but also the axonal reaction and secondary degeneration of nerve cell bodies and processes.

Pyridoxine (vitamin B6) toxicity: enhancement by uremia in rats.

  • S. LevineA. Saltzman
  • Medicine, Biology
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • 2002

Dose‐dependent expression of neuronopathy after experimental pyridoxine intoxication

Multiple factors including rate of administration, differential neuronal vulnerability, and species susceptibility have bearing on the final expression of pyridoxine neurotoxicity.

High-dose pyridoxine as an 'anti-stress' strategy.

High intakes of pyridoxine may have the potential to improve prognosis in many individuals and reduction of homocysteine levels should contribute to this benefit, consistent with recent epidemiology correlating plasma PLP levels with risk for vascular events and overall survival.

Neurotoxicity of pyridoxine analogs is related to coenzyme structure.

Using morphometry and a model system of dorsal root ganglion neurons in culture, it is found that several analogs of pyridoxine were neurotoxic in vitro and several hypotheses that link coenzyme function to toxic effect are described.

Pyridoxine neuropathy in rats

Qualitative histologic techniques found axonal degeneration of sensory system fibers and that the fibers derived from the ventral root were spared, and found no early decrease in oxygen consumption of nerve, suggesting that impaired oxidative metabolism was not the primary event.

Update on interconversions of vitamin B-6 with its coenzyme.

Both kinase and oxidase involved in B-6 metabolism are potential targets for pharmacologic agents and the evolutionary retention of homologous portions of pyridoxal kinase in humans as well as bacteria are emphasized.

Effects of Two Weeks of Feed Restriction on Some Common Toxicologic Parameters in Sprague-Dawley Rats

Changes in the mildly and moderately restricted groups were considered adaptive and innocuous since feed restriction of this degree has historically been associated with increased longevity and decreased disease incidence in chronic studies.

Carbohydrate diet prolongs survival of rats with acute uremia after bilateral nephrectomy.

Feeding pure sucrose cubes in the diet was more effective for prolonging survival than specialized commercial diets, highly palatable and useable in conventional pellet feeders, and carried the dietary approach to its limit.

Mechanisms of Toxic Injury in the Peripheral Nervous System: Neuropathologic Considerations

Two examples of toxic neuropathy are discussed, where demyelination noted in young animals is coincident with toxin-induced interference of cholesterol synthesis by Schwann cells.