Acrylamide causes a peripehral neuropathy. The biochemical mechanism by which it does so is the subject of intense investigation. One of the principal hypotheses for this mechanism centers on acrylamide's ability to inhibit glycolysis. This study examines the effects of in vivo exposure to acrylamide on the enzymes of the nerve terminal particle, the synaptosome.
A method for measuring glycolytic enzyme inhibition in the synaptosome was developed. Acrylamide (500 mg/kg) was administered to rats intraperitoneally. Synaptosomes were prepared by the method of Dodd et al, and lysed by sonication. GAPDH activity and NSE concentration were measured. GAPDH inhibition measured in brain synaptosomes was similar to that measured in distal portions of peripheral nerve. One can infer from this data that NSE accumulates in the nerve terminal upon acrylamide exposure.
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