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.
D000178:Acrylamides / Q000633:toxicity*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D008297:Male; D009410:Nerve Degeneration / Q000187:drug effects; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control; D011773:Pyruvates / Q000627:therapeutic use*; D051381:Rats; D011919:Rats, Inbred Strains
D000178:Acrylamides; D011773:Pyruvates