Postscript to the symposium on organophosphorus compound induced delayed neuropathy.
A short review is presented on the key points in the development of the hypothesis for the initiation of delayed neuropathy by reaction of organophosphorus compounds with neuropathy target esterase (NTE). It is now clear from information derived from experiments showing protection and promotion and from the action of some phosphorothioamidates (which cause delayed neuropathy without aging) that the original NTE hypothesis is not generally applicable and requires modification. A suggestion is made that aging of phosphorylated and phosphonylated NTE is facilitated perhaps by two linked esterases, one being NTE.
Aldridge
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University of Surrey, Robens Institute of Health and Safety, Guildford, UK.
D000818:Animals; D002265:Carboxylic Ester Hydrolases / Q000037:antagonists & inhibitors; D006801:Humans; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000201:enzymology; D009943:Organophosphorus Compounds / Q000633:toxicity*
D009943:Organophosphorus Compounds; D002265:Carboxylic Ester Hydrolases; C021859:neurotoxic esterase