Does pyruvate prevent acrylamide neurotoxicity? Implications for disease pathogenesis.
We used the prototype environmental neurotoxin, acrylamide monomer, to evaluate the hypothesis that neurotoxin-induced nerve fiber degeneration results from inactivation of axonal glycolytic enzymes. Treating intoxicated rats with sodium pyruvate, we hypothesized, would bypass the putative neurotoxin-induced blockade in glycolysis, thus ameliorating neurobehavioral and morphologic measures of neurotoxicity. After establishing that pyruvate itself did not affect behavior, we examined its effects on acrylamide-intoxicated animals. Pyruvate treatment had a significant effect on only one of eight neurobehavioral measures, though others showed similar trends. A morphologic observation of lumbar dorsal root ganglion cell bodies and peripheral nerves failed to show an effect of pyruvate. Those results suggested that inactivation of glycolytic enzymes alone is not a sufficient explanation of pathogenesis.[1]References
- Does pyruvate prevent acrylamide neurotoxicity? Implications for disease pathogenesis. Sterman, A.B., Panasci, D.J., Persons, W. Exp. Neurol. (1983) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg