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Neurotoxic esterase and neurotoxicity.
Department of Neuroscience, Yeshiva University, Bronx, New York, 1986 Aug; :1-2
The relationship between the neuropathy target esterase (NTE) to organophosphorus (OP) compound interaction and the fate of retrograde transport of iodine-125 labeled tetanus-toxin was studied in hen sciatic nerve following a single subcutaneous injection of either a neurotoxic OP compound, a nonneurotoxic OP compound, or paraoxon (311455). In order to induce central peripheral distal axonopathy in these hens, a greater than 80 percent phosphorylation and subsequent intramolecular rearrangement of NTE in the nerve fiber were required. A progressive decrement of retrograde axonal transport in sensory and motor fibers that culminated, days later, in axon degeneration, was caused by suprathreshold biochemical reaction a few hours after dosing. Seven days after neurotoxic OP dosing the maximum transport deficit was reached; this was prior to the onset of nerve fiber degeneration and clinical signs of neuropathy. No effect on axon transport, nerve fiber integrity or clinical status was caused by nonneurotoxic OP. Paraoxon did not inhibit NTE and did not cause either deficit in retrograde transport or neuropathy. The author conclude that alterations in retrograde axonal transport may be important in the pathogenesis of nerve fiber degeneration in this and related toxic neuropathies.
NIOSH-Grant; Neurotoxic-effects; Organo-phosphorus-compounds; Nervous-system-disorders; Enzyme-activity
Neuroscience Albert Einstein College of Med 1300 Morris Park Ave Bronx, N Y 10461
Final Grant Report
NTIS Accession No.
Neurotoxic Disorders; Neurotoxic-effects
Department of Neuroscience, Yeshiva University, Bronx, New York
Yeshiva University, New York, New York
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