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NEUROPATHY TARGET ESTERASE INHIBITION BY ORGANOPHOSPHORUS ESTERS IN HUMAN NEUROBLASTOMA CELLS
Citation:
Ehrich, M., L. Correl, AND B. Veronesi. NEUROPATHY TARGET ESTERASE INHIBITION BY ORGANOPHOSPHORUS ESTERS IN HUMAN NEUROBLASTOMA CELLS. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-94/521 (NTIS PB95148839), 1994.
Description:
Certain organophosphorus compounds (OPs) produce a delayed neuropathy (OPIDN) in man and some animal species. apability 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. ells were exposed for 1 hr to equimolar (1 X 10-5 M) concentrations of 6 OPs associated with OPIDN in vivo, and 8 OPs that do not produce delayed neuropathy in animal models. he -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. hese results indicate that human neuroblastoma cells have potential use in the initial screening of bioactive OPs with capability for causing OPIDN.