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RECORD NUMBER: 19 OF 24

OLS Field Name OLS Field Data
Main Title Role of Neurotoxic Esterase (NTE) in the Prevention and Potentiation of Organophosphorus-Induced Delayed Neurotoxicity (OPIDN).
Author Pope, C. N. ; Tanaka, D. ; Padilla, S. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Neurotoxicology Div. ;Northeast Louisiana Univ., Monroe. School of Pharmacy. ;Michigan State Univ., East Lansing. Dept. of Anatomy.
Publisher 1993
Year Published 1993
Report Number EPA/600/J-94/032;
Stock Number PB94-137221
Additional Subjects Esterases ; Phosphorus organic compounds ; Nervous system ; Toxicity ; Drug interactions ; Enzyme inhibitors ; Phosphorylation ; Phenylmethylsulfonyl fluoride ; Reprints ;
Holdings
Library Call Number Additional Info Location Last
Modified
Checkout
Status
NTIS  PB94-137221 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 05/14/1994
Collation 12p
Abstract
The first step in the initiation of organophosphorus-induced delayed neuropathy (OPIDN) is proposed to be the phosphorylation of an enzyme found in the nervous system called neurotoxic esterase (neuropathy target esterase, NTE). It has been known for over twenty years that non-neuropathic inhibitors of NTE exist and can actually prevent OPIDN when given before a neuropathic organophosphate (OP). Within the last three years it has become evident that another outcome is possible following in vivo interaction between neuropathic and nonneuropathic NTE inhibitors. When administered after OP exposure, nonneuropathic inhibitors can intensify or potentiate signs of OPIDN in adult chickens. Additionally, whereas developing chickens are typically resistant to the effects of neuropathic OPs, resistant age groups will develop OPIDN when exposure to a neuropathic OP is followed by the non-neuropathic NTE inhibitor phenylmethylsulfonyl fluoride. As in the case of prevention, studies of the potentiation of OPIDN may yield insight into mechanisms involved in the pathogenesis of delayed neurotoxicity. A brief review of current knowledge regarding the role of NTE in both the prevention and potentiation of OPIDN is presented.