Electrophysiologic deficits in peripheral nerve as a discriminator of early hexacarbon neurotoxicity.
To determine the extent of neurotoxicity of parenterally administered hexacarbons, male Sprague-Dawley rats were given either n-hexane or 2,5-hexanedione for 35 consecutive days. Electrophysiologic measurements showed a lengthening of the sciatic and sural nerve action potentials (slower conduction velocities) and increased refractory periods. These effects correlated with a shift in the nerve membrane sensitivity to potassium-induced depolarization. A similar effect can be induced by ouabain, an Na+, K+-ATPase inhibitor. These effects were seen with both n-hexane and 2,5-hexane-dione. Although the treated animals gained weight more slowly than controls, they showed no loss of motor function when tested behaviorally, and there were no signs of histopathology in the peripheral nerves. These results show that hexacarbons produce a neurotoxicity that can be demonstrated by changes in nerve excitability, prior to overt behavioral neurotoxicity. Furthermore, these electrophysiologic changes may be related to a hexacarbon-induced disruption of nerve-membrane ATPase activity.
D000818:Animals; D006586:Hexanes / Q000633:toxicity*; D006588:Hexanones / Q000633:toxicity*; D007659:Ketones / Q000633:toxicity*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009431:Neural Conduction / Q000187:drug effects; D010525:Peripheral Nerves / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012032:Refractory Period, Electrophysiological / Q000187:drug effects
D006586:Hexanes; D006588:Hexanones; D007659:Ketones; C026385:n-hexane; C011269:2,5-hexanedione