The mechanism of delayed neuropathy caused by some organophosphorus esters: using the understanding to improve safety.
The mechanism of delayed neurotoxicity of some OP (organophosphorus) esters such as DFP (di-isopropyl phosphorofluoridate) and TOCP (tri-o-cresyl phosphate) involves an initial two-step process affecting an esterase called NTE (neurotoxic esterase). This understanding permits the assessment of delayed neuropathic potential in terms of a quantitative measurement of inhibition of NTE in tissue taken from dosed hens. Structure/activity relationships have been rationalized and the neurotoxic potential of those OP esters which are direct inhibitors of esterases may now be assessed in vitro. The response of human NTE can usefully be compared with that of hen NTE. Nil delayed neurotoxic potential is associated with carbamate or phosphinate anticholinesterases which may be designed as insecticides.
D000818:Animals; D001259:Ataxia / Q000139:chemically induced; D002265:Carboxylic Ester Hydrolases / Q000037:antagonists & inhibitors*; D002645:Chickens; D005260:Female; D006801:Humans; D009422:Nervous System Diseases / Q000139:chemically induced*; D062025:Organophosphate Poisoning; D013329:Structure-Activity Relationship; D013997:Time Factors
D002265:Carboxylic Ester Hydrolases; C021859:neurotoxic esterase