THE ROLE OF COENZYME-A IN ACRYLAMIDE NEUROTOXICITY IN THE RAT.

Acrylamlde produces central-peripheral distal axonopathy. The mechanism of acrylamide-induced neuropathy is currently unknown, but has been postulated to occur through the inhibition of energy producing pathways within the nerve. Since coenzyme-A (CoA) is actively involved in neuronal energy production, the role of CoA in acrylamlde neurotoxicity was examined. The enzymatic function of CoA was not inhibited by acrylamide in vitro. CoA content of neural and non-neural tissues was elevated after a cumulative acrylamide dose of 250 mg/kg i.p. Animals demonstrated signs of neurotoxicity following a cumulative dose of acrylamide of 100 mg/kg i.p. Diet supplements which were designed to bypass putative energy blocks produced by acrylamide had no effect on either the onset or magnitude of acrylamide neurotoxicity. Acrylamide produced anticholinergic effects which were assessed by the ocular zingerone test. This test was found to be a simple, sensitive measure of neuronal alterations induced by acrylamide.