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Neurotoxic Esterase and Neurotoxicity.

PB89129605

Publication Date	1986
Personal Author	Spencer, P. S.
Page Count	4
Abstract	The relationship of the interaction of neuropathy target esterase (NTE) and organophosphorus (OP) compounds to 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 or a nonneurotoxic OP compound, e.g. 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 concludes that alterations in retrograde axonal transport may be important in the pathogenesis of nerve fiber degeneration in this and related toxic neuropathies.
Keywords	Phosphorus organic compounds Esterases Toxicity Nerve degeneration Peripheral nerve diseases Chickens Nerve fibers Axoplasmis flow Neurotoxic esterase CAS 311-45-5
Source Agency	National Institute for Occupational Safety and Health
NTIS Subject Category	57Y - Toxicology 57P - Pest Control
Corporate Authors	Yeshiva Univ., New York.; National Inst. for Occupational Safety and Health, Cincinnati, OH.
Supplemental Notes	Sponsored by National Inst. for Occupational Safety and Health, Cincinnati, OH.
Document Type	Technical Report
Title Note	Final rept.,
NTIS Issue Number	198906

Neurotoxic Esterase and Neurotoxicity.

Neurotoxic Esterase and Neurotoxicity.
PB89129605

Publication Date	1986
Personal Author	Spencer, P. S.
Page Count	4
Abstract	The relationship of the interaction of neuropathy target esterase (NTE) and organophosphorus (OP) compounds to 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 or a nonneurotoxic OP compound, e.g. 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 concludes that alterations in retrograde axonal transport may be important in the pathogenesis of nerve fiber degeneration in this and related toxic neuropathies.
Keywords	Phosphorus organic compounds Esterases Toxicity Nerve degeneration Peripheral nerve diseases Chickens Nerve fibers Axoplasmis flow Neurotoxic esterase CAS 311-45-5
Source Agency	National Institute for Occupational Safety and Health
NTIS Subject Category	57Y - Toxicology 57P - Pest Control
Corporate Authors	Yeshiva Univ., New York.; National Inst. for Occupational Safety and Health, Cincinnati, OH.
Supplemental Notes	Sponsored by National Inst. for Occupational Safety and Health, Cincinnati, OH.
Document Type	Technical Report
Title Note	Final rept.,
NTIS Issue Number	198906