| Abstrakt: |
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. |
