Toxic neurofilamentous axonopathies and fast anterograde axonal transport. IV. In vitro analysis of transport following acrylamide and 2,5-hexanedione.
Recent investigations into the mechanisms of neurotoxicity of acrylamide and gamma-diketones have demonstrated reductions in the delivery of radiolabelled proteins to the distal axon. To differentiate a toxicant-induced compromise in the capacity of the fast anterograde axonal transport system from a neuron cell body processing effect, selective exposure of either the L5 dorsal root ganglion or sciatic nerve to 0.7 mM acrylamide (ACR) or 4 mM 2,5-hexanedione (2,5-HD) was performed during in vitro transport. Nerve exposure to ACR decreased the quantity of transport by 32%, 2,5-HD reduced the quantity by 44%. Ganglion exposure produced no significant changes. We conclude that both toxicants penetrate the nerve barriers and act directly and/or indirectly on the axonal transport mechanisms to cause the reductions in transport.
Sickles
D W
DW
Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta 30912-2000.
D020106:Acrylamide; D000178:Acrylamides / Q000633:toxicity*; D000818:Animals; D006588:Hexanones / Q000633:toxicity*; D007382:Intermediate Filaments / Q000187:drug effects*; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism; D010525:Peripheral Nerves / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012183:Retrograde Degeneration / Q000187:drug effects*
D000178:Acrylamides; D006588:Hexanones; D009419:Nerve Tissue Proteins; D020106:Acrylamide; C011269:2,5-hexanedione