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Acrylamide (ACR) appears to be a contaminant generated during the preparation of certain foods. Although the polymer is nonneurotoxic, exposure of human and laboratory animals to monomeric ACR produces ataxia, skeletal muscle weakness, and weight loss. Early morphological studies indicated that this neurotoxic syndrome was associated with nerve damage characterized by multifocal paranodal swelling of preterminal distal myelinated axons. These swellings contained an abundance of tubulovesicular profiles, neurofilaments, and degenerating mitochondria and, as ACR intoxication progressed, axonal regions below these swellings degenerated. However axonopathy developed only during low-dose / long term exposure conditions. Axon degeneration did not play an important role in the expression of ACR neurotoxicity. Axon degeneration might be abundant in the central nervous system (CNS) of rats exposed at this higher ACR dose rate. High-dose ACR intoxication produced primarily CNS nerve damage.
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