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Dichloroacetate-induced peripheral neuropathy.

Peter W Stacpoole1, Christopher J Martyniuk2, Margaret O James3

  • 1Department of Medicine, College of Medicine, University of Florida, Gainesville, FL, United States; Department of Biochemistry and Molecular Biology, College of Medicine, University of Florida, Gainesville, FL, United States.

International Review of Neurobiology
|June 19, 2019
PubMed
Summary

Dichloroacetate (DCA) is an investigational drug that can cause peripheral neuropathy by increasing oxidative stress in Schwann cells. Antioxidants and muscarinic receptor antagonists may mitigate DCA-induced neurotoxicity.

Keywords:
Anti-oxidantsClinical trialDichloroacetateGlutathione-S-transferase zeta 1Metabolic diseaseMitochondriaOxidative damagePeripheral neuropathyTyrosine

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Area of Science:

  • Environmental toxicology
  • Biomedical science
  • Neuroscience

Background:

  • Dichloroacetate (DCA) is ubiquitous environmentally and used investigational drug.
  • DCA inhibits pyruvate dehydrogenase kinase (PDK), activating pyruvate dehydrogenase complex (PDC) and mitochondrial respiration.
  • Chronic DCA exposure can cause peripheral neuropathy, with Schwann cells implicated as a toxicological target.

Purpose of the Study:

  • Investigate the mechanism of DCA-induced peripheral neuropathy.
  • Explore potential therapeutic strategies for DCA neurotoxicity.

Main Methods:

  • Review of existing research on DCA's mechanism of action and toxicity.
  • Analysis of experimental data implicating Schwann cells and oxidative stress.
  • Consideration of preliminary findings in rodent models.

Main Results:

  • DCA activates PDC and mitochondrial respiration, potentially causing oxidative stress in Schwann cells.
  • DCA metabolism interferes with amino acid and heme synthesis, leading to reactive molecule accumulation.
  • Rodent models suggest antioxidants and muscarinic receptor antagonists may reduce DCA neurotoxicity.

Conclusions:

  • DCA-induced neurotoxicity may stem from uncompensated oxidative stress in Schwann cells.
  • Metabolic interference by DCA contributes to the accumulation of damaging reactive molecules.
  • Further research into antioxidants and muscarinic receptor antagonists is warranted for treating DCA peripheral neuropathy.