Mechanisms of acrylamide (79061) axonopathy are discussed. The basic processes by which axonal integrity is maintained are reviewed. Acrylamide neuropathy is considered. Studies have shown that the underlying lesion induced by acrylamide involves distal retrograde degeneration of long and large axons. This has indicated that acrylamide neuropathy belongs to the class of central/peripheral distal axonopathies, a relatively common nervous system response found in a large variety of unrelated toxic/metabolic states. The effects of acrylamide on axonal transport are considered. Studies have shown that single doses of acrylamide induce profound changes in axonal transport, and that if exposure is repeated over the course of a few weeks, functional signs of neuropathy appear. These transport defects precede by many days the appearance of morphologic or functional signs of axonal pathology. It has been suggested that alterations in axon/perikaryal interaction may be the basic process occurring in acrylamide induced axonopathy. The authors conclude that acrylamide induced axonopathy may be the result of at least two lesions: a relatively non specific lesion involving inhibition of glycolytic enzyme activity or a lesion resulting from the interaction of acrylamide with sulfhydryl, amino, or hydroxyl moieties associated with axon components; or inhibition of perikaryal mediated axon repair and maintenance mechanisms due to a direct perikaryon effect or to retrograde axonal transport alterations.
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