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

  title={Pyridoxine-Induced Neuropathy in Rats: A Sensory Neuropathy That Responds to 4-Methylcatechol},
  author={Noelle Callizot and J. M. Warter and Philippe Poindron},
  journal={Neurobiology of Disease},
Sensory neuropathies are frequently associated with diabetes or with antimitotic treatments in humans suffering from cancer, and are in this case the most important limitation to the use of antimitotic drugs. For this reason, there is a need to establish and validate animal models of sensory neuropathies that could be routinely used, together with the already known models, for studying and evaluating the effects of putative neuroprotective compounds. In the present study, we prove by behavioral… 

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.

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.

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.

Fenugreek seed extract treats peripheral neuropathy in pyridoxine induced neuropathic mice

Findings of the present study demonstrate that treatment with fenugreek seed extract can potentially facilitate healing from pyridoxine induced peripheral neuropathy in mice.

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.

Enhancement of Cutaneous Nerve Regeneration by 4-Methylcatechol in Resiniferatoxin-Induced Neuropathy

Results indicate that 4MC promoted regeneration of unmyelinated nerves in experimental RTX-induced neuropathy and enhanced function.

Neuropathology of Skin Denervation in Acrylamide-Induced Neuropathy

The findings establish the pathological consequences of acrylamide neurotoxicity in cutaneous sensory nerves with far-reaching implications of providing an animal system to study "dying-back" pathology of nociceptive nerves and forming the ultrastructural foundation for interpreting the pathology of cutaneous nerve degeneration in skin biopsies.

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.

Dose-dependent effects of glutamate in pyridoxine-induced neuropathy.



Neurotrophin-3 Administration Attenuates Deficits of Pyridoxine-Induced Large-Fiber Sensory Neuropathy

Coadministration of the neurotrophic factor neurotrophin-3 (NT-3; 5–20 mg · kg−1 · d−1, s.c.) during chronic pyridoxine treatment largely attenuated the behavioral and electrophysiological sequelae associated with pyrIDoxine toxicity, and NT-3 administration prevented degeneration of sensory fibers in the dorsal column of the spinal cord.

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.

Effects of 4-methylcatechol, a stimulator of endogenous nerve growth factor synthesis, on experimental acrylamide-induced neuropathy in rats.

It is suggested that 4-MC can prevent the progression of ACR-induced neuropathy and decreased NGF levels may be involved in the pathogenesis ofACR neuropathy.

A catechol derivative (4-methylcatechol) accelerates the recovery from experimental acrylamide-induced neuropathy.

It is suggested that 4-MC can accelerate the recovery process clinically, electrophysiologically, biochemically and neuropathologically in promoting recovery from experimental ACR neuropathy in rats.

Sensory neuropathy from pyridoxine abuse. A new megavitamin syndrome.

It is indicated that consumption of large doses of pyridoxine can cause sensory neuropathy or neuronopathy syndromes and that safe guidelines should be established for the use of this widely abused vitamin.

Acute sensory neuropathy‐neuronopathy from pyridoxine overdose

Two patients who developed an acute, profound, and permanent sensory deficit after treatment with massive doses of parenteral pyridoxine are reported, who had transient autonomic dysfunction, mild weakness, nystagmus, lethargy, and respiratory depression.

Peripheral Neuropathy in Rats Produced by Acrylamide

In animals with severe clinical abnormalities, motor nerve conduction velocity in the fibr supplying the small muscles of the hind paw was reduced to approximately 80% of the control value, and histological evidence of regeneration of nerve fibres was found.

Peripheral neuropathy from taxol and cisplatin combination chemotherapy: Clinical and electrophysiological studies

It is concluded that sensory–motor neuropathy is a frequent dose‐dependent toxicity of combined cisplatin and taxol use and is likely to become the major dose‐limiting toxicity of taxol–cisplatin combination chemotherapy when higher doses of these agents are administered with granulocyte‐colony stimulating factor.