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Postscript to the symposium on organophosphorus compound induced delayed neuropathy
1University of Surrey, Robens Institute of Health and Safety, Guildford, UK.
Abstract:
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.
Insights
The organophosphorus compound hypothesis for delayed neuropathy requires modification. New findings suggest aging of neuropathy target esterase (NTE) may involve linked esterases, not just NTE alone.
Area of Science:
- Toxicology
- Neuroscience
- Biochemistry
Background:
- Organophosphorus compounds can cause delayed neuropathy.
- The neuropathy target esterase (NTE) hypothesis explains this mechanism.
- The NTE hypothesis involves the reaction of organophosphorus compounds with NTE.
Purpose of the Study:
- To review the development of the hypothesis for organophosphorus-induced delayed neuropathy.
- To assess the general applicability of the original NTE hypothesis.
- To propose modifications to the NTE hypothesis based on recent findings.
Main Methods:
- Review of experimental data on protection and promotion in organophosphorus compound toxicity.
- Analysis of phosphorothioamidates that induce delayed neuropathy without aging.
- Evaluation of the role of neuropathy target esterase (NTE) in the aging process.
Main Results:
- The original NTE hypothesis is not universally applicable.
- Some compounds cause delayed neuropathy without the characteristic 'aging' of NTE.
- Phosphorothioamidates highlight limitations in the current hypothesis.
Conclusions:
- The hypothesis for organophosphorus-induced delayed neuropathy needs revision.
- The aging process of phosphorylated NTE may be facilitated by additional esterases.
- A modified hypothesis suggests a more complex enzymatic interaction in NTE aging.