Pyridoxine-induced toxicity in rats: a stereological quantification of the sensory neuropathy

@article{Perry2004PyridoxineinducedTI,
  title={Pyridoxine-induced toxicity in rats: a stereological quantification of the sensory neuropathy},
  author={Tracyann Perry and Ananda Weerasuriya and Peter R. Mouton and Harold W. Holloway and Nigel H. Greig},
  journal={Experimental Neurology},
  year={2004},
  volume={190},
  pages={133-144}
}

Pyridoxine induced neuropathy by subcutaneous administration in dogs

This study confirmed the possibility of producing a pyridoxine-induced sensory neuropathy model in dogs with short-term administration and confirmed that this subcutaneous administration method did not cause systemic toxicity and effectively induced sensory Neuropathy.

Neuropathological changes in dorsal root ganglia induced by pyridoxine in dogs

The results suggest that PDX-induced neuropathy is reversible in dogs; thus, dogs can be considered a good experimental model for research on neuropathy.

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.

Glutamate Carboxypeptidase II Inhibition Behaviorally and Physiologically Improves Pyridoxine-Induced Neuropathy in Rats

I inhibition of GCP II may be beneficial against the peripheral sensory neuropathy caused by pyridoxine, including normalization of hot plate reaction time, foot fault improvements and increased open field distance travelled.

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.

Evidence of GLP-1-mediated neuroprotection in an animal model of pyridoxine-induced peripheral sensory neuropathy

High-dosage pyridoxine-induced auditory neuropathy and protection with coffee in mice.

It is demonstrated that high-dose pyridoxine administration can be used to produce a new mouse model for AN, and coffee or trigonelline as a main active compound of coffee extract can potentially facilitate recovery from pyrIDoxine-induced auditory neuropathy.

Toxic neuropathy

The study of toxic neuropathy is enhancing knowledge of the mechanisms of neurotoxicity but also the neurobiology of peripheral neuropathy in general; and is likely to reveal avenues for therapeutics.

Pyridoxine-induced sensory ataxic ganglionopathy: a case report and literature review

A case of 54-year-old, right-handed man presented for insidious, progressive numbness and imbalance for 12 years, which suggested the presence of severe, generalized, and non-lengthdependent sensory neuronopathy/ganglionopathy is reported.

SP, CGRP changes in pyridoxine induced neuropathic dogs with nerve growth factor gene therapy

It is reasoned that NGF gene therapy in pyridoxine induced neuropathic dogs does not induce neuropathic pain with this dosage, even with increasing the expression of CGRP.
...

References

SHOWING 1-10 OF 34 REFERENCES

Pyridoxine-Induced Neuropathy in Rats: A Sensory Neuropathy That Responds to 4-Methylcatechol

This study proves that it is possible to induce a nonlethal, exclusively sensory, reversible neuropathy by intoxicating rats with large amounts of pyridoxine, and proposes that this model be used as an additional model for preclinical studies of neuroprotective drugs.

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.

Pyridoxine megavitaminosis produces degeneration of peripheral sensory neurons (sensory neuronopathy) in the dog.

It is apparent that the peripheral neuropathy previously attributed to pyridoxine actually represents a toxic, peripheral sensory neuronopathy, and may reflect the selective permeability of blood vessels in the peripheral ganglia.

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 neuropathy: Correlation of functional tests and neuropathology in beagle dogs treated with large doses of vitamin B6

The neurologic examination revealed the early changes of neuropathy induced in the beagle dog by administration of excessive amounts of vitamin B6, while electrodiagnostics and microscopic neuropathology were indicators of more advanced stages of toxic neuropathy and disclosed selective lesions in individuals whose gait appeared to be unremarkable.

Alteration of neuronal cytoskeletal organization in dorsal root ganglia associated with pyridoxine neurotoxicity

The results indicate that an early morphological correlate of pyridoxine neurotoxicity is the accumulation of NF with MT-NF dissociation in the unipolar process of the DRG in the absence of extensive vacuolization, and that the observed cytoskeletal disruption may be related to an increased rate of NF protein synthesis together with mechanical obstruction of transport phenomena.

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.

Subacute toxicity of pyridoxine hydrochloride in the beagle dog.

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.