Main Title |
Neuropathy Target Esterase Inhibition by Organophosphorus Esters in Human Neuroblastoma Cells. |
Author |
Ehrich, M. ;
Correll, L. ;
Veronesi, B. ;
|
CORP Author |
Virginia-Maryland Regional Coll. of Veterinary Medicine, Blacksburg, VA.;Health Effects Research Lab., Research Triangle Park, NC. Neurotoxicology Div. |
Publisher |
cJul 94 |
Year Published |
1994 |
Report Number |
EPA/600/J-94/521; |
Stock Number |
PB95-148839 |
Additional Subjects |
Organophosphorus compounds ;
Esters ;
Nervous system diseases ;
Esterases ;
Enzyme inhibitors ;
Toxicology ;
Cultured tumor cells ;
In vitro analysis ;
In vivo analysis ;
Animal disease models ;
Reprints ;
|
Holdings |
Library |
Call Number |
Additional Info |
Location |
Last Modified |
Checkout Status |
NTIS |
PB95-148839 |
Some EPA libraries have a fiche copy filed under the call number shown. |
|
07/26/2022 |
|
Collation |
6p |
Abstract |
Certain organophosphorus compounds (OPs) produce a delayed neuropathy (OPIDN) in man and some animal species. Capability to cause OPIDN is generally predicted in animal models by early and irreversible inhibition of neuropathy target esterase (NTE, neurotoxic esterase). In this study, NTE inhibition in response to OP exposure was examined in cell culture, using the human SH-SY5Y neuroblastoma cell line. Cells were exposed for 1 hr to equimolar (1 x 10 to the minus fifth power M) concentrations of 6 OPs associated with OPIDN in vivo (including 2 protoxicants and 4 active (-P = O) toxicants) and 8 OPs that do not produce delayed neuropathy in animal models (including 5 protoxicants and 3-P = O compounds). The -P = O compounds that cause OPIDN in animal models inhibited NTE > 60% at the test concentration; -P = O compounds that do not cause OPIDN in animal models inhibited NTE < 30%. Protoxicants did not inhibit NTE at the test concentration, reflecting their limited metabolism in the human cell line. These results indicate that human neuroblastoma cells have potential use in the initial screening of bioactive OPs with capability for causing OPIDN. (Copyright (c) 1994 Intox Press, Inc.) |