Record Display for the EPA National Library Catalog


OLS Field Name OLS Field Data
Main Title Triphenyl Phosphite: In vivo and In vitro Inhibition of Rat Neurotoxic Esterase (Journal Version).
Author Padilla, S. S. ; Grizzle, T. B. ; Lyerly, D. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. ;Northrop Services, Inc., Research Triangle Park, NC.
Publisher c1987
Year Published 1987
Report Number EPA/600/J-87/384;
Stock Number PB89-106819
Additional Subjects Toxic substances ; Toxicity ; Carboxylic ester hydrolases ; Spinal cord ; Brain ; Laboratory animals ; Enzyme inhibitors ; Phosphorus organic compounds ; Nerve degeneration ; Reprints ; Triphenyl phosphite ; Neurotoxic esterase ; Phosphorous acid/triphenyl ester
Library Call Number Additional Info Location Last
NTIS  PB89-106819 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 03/14/1989
Collation 9p
Organophosphorus compounds which, after acute administration, inhibit neurotoxic esterase (NTE) by > or = 65% and undergo a subsequent 'aging' reaction, produce a delayed neuropathy characterized by degeneration of large and long nerve fibers. The present studies examine in detail the NTE-inhibiting properties of triphenyl phosphite (TPP), a plasticizer which produces ataxia and degeneration of the spinal cord in animals. A neurotoxic dosing regimen (1184 mg/kg/week, sc, for 2 weeks) inhibited both brain and spinal cord NTE (< or = 40%) only marginally 4 and 48 hr postdosing. By contrast, TPP was shown in vitro to be a potent inhibitor of rat brain NTE relative to Mipafox or diisopropyl phosphorofluoridate. Preincubation of 10 micromolar TPP in buffer (37 deg C) resulted in a time-dependent loss of TPP's ability to inhibit NTE. In summary, TPP is a powerful NTE inhibitor in vitro, but only a marginal NTE inhibitor after in vivo administration. These results raise questions as to the causal events mediating TPP-induced neuropathy in the rat. (Copyright (c) 1987 Academic Press, Inc.)