In vivo and in vitro regional differential sensitivity of neuropathy target esterase to Di-n-butyl-2,2-dichlorovinyl phosphate

  title={In vivo and in vitro regional differential sensitivity of neuropathy target esterase to Di-n-butyl-2,2-dichlorovinyl phosphate},
  author={Angelo Moretto and Marcello Lotti and Peter S. Spencer},
  journal={Archives of Toxicology},
Organophosphate-induced delayed polyneuropathy (OPIDP) is initiated by inhibition/aging of more than 70–75% of neuropathy target esterase (NTE). Di-n-butyl-2,2-dichlorovinyl phosphate (DBDCVP) (1 mg/kg s.c.) inhibited 96%, 86% and 83% of NTE in brain, spinal cord and peripheral nerve, respectively, and induced a typical central peripheral distal axonopathy in hens. A lower dose (0.45 mg/kg s.c.) caused 90%, 83% and 54% NTE inhibition in the same organs; by contrast, hens developed a spastic… 
Age-related differences in the inhibition of neuropathy target esterase and susceptibility to triphenyl phosphite-induced delayed neurotoxicity in chickens.
  • K. Katoh
  • Biology, Medicine
    Nihon eiseigaku zasshi. Japanese journal of hygiene
  • 1992
Results confirmed age-specific susceptibility to TPP, not only clinically but also histopathologically, and suggested that the differences in both TPP metabolism and NTE recovery are related to and/or contribute to this age specificity.
Organophosphate polyneuropathy and neuropathy target esterase: Studies with methamidophos and its resolved optical isomers
It is concluded that when racemic methamidophos is given to hens, initiation and protection from OPIDP is due to the interaction of d-(+) methamodophos with NTE, and both isomers are likely to be due to interactions with another unknown target.
Interaction of methamidophos with hen and human acetylcholinesterase and neuropathy target esterase
The larger and faster reactivation of human AChE inhibited in vitro byl-(−) methamidophos suggests that a corresponding effect might be possible in vivo and therefore explain, in part, the relatively higher susceptibility of man to delayed polyneuropathy induced by racemic methamodophos.
Phenylmethanesulfonyl fluoride elicits and intensifies the clinical expression of neuropathic insults
It was observed in hens that promotion affects a site other than NTE and that it acts at a point downstream from initiation, and it is concluded that promotion might be a common feature in neuropathies of different origin.
Acetylcholinesterase and neuropathy target esterase inhibitions in neuroblastoma cells to distinguish organophosphorus compounds causing acute and delayed neurotoxicity.
It is demonstrated that neuroblastoma cell lines can be used to differentiate between neuropathic OPs and acutely neurotoxic OPs, and esterase inhibition occurred at lower concentrations than those needed for cytoxicity.
The relationship between isofenphos cholinergic toxicity and the development of polyneuropathy in hens and humans
Results showed that phoxim was not a promoter of OPIDP in hens and that the ratio AChE inhibition:NTE inhibition by microsome-activated isofenphos was similar for both hen and human enzymes.
Triphenylphosphite neuropathy in hens
TPP neuropathy in the hen is likely to be the same as typical OPIDP, and the unusual effects of combined treatment to hens with TPP and PMSF are explained by the prolonged pharmacokinetics of TPP and by the dual effect of PMSF i.e. protection from and promotion of OPIDs.


Progressive Deficit of Retrograde Axonal Transport Is Associated with the Pathogenesis of Di‐n‐Butyl Dichlorvos Axonopathy
It is demonstrated that induced deficits in retrograde transport are associated with the pathogenesis of OP‐induced nerve‐fiber degeneration and the threshold‐initiating mechanism thereof.
Hen Sciatic Nerve Contains a Soluble and a Particulate Form of Neuropathy Target Esterase
The distribution of a glucose-6-Pase, ATPase and LDH as marker enzymes suggests a soluble nature of the NTE in the sciatic nerve supernatant, and a partial solubilization of particulated brain NTE suggests that thesolubilized protein has to be separated from a membrane factor.
Repeated small doses of a neurotoxic organophosphate
“NTE-like” activity in spleen was consistently inhibited but to a lesser extent than that in the brain or spinal cord, while Brain AChE and BuChE were not affected and there was no correlation between inhibition of NTE in the nervous tissue and the “N TE-like" activity in lymphocytes.
Reactivation and aging of neurotoxic esterase inhibited by a variety of organophosphorus esters.
Ageing has now been demonstrated with a number of neurotoxic compounds and effects seem incompatible with an SN1 (dealkylation) mechanism.
Neurotoxic esterase
The excellent sensitivity and high specificity of the NTE differential test is demonstrated and an excellent correlation to NTE activity is found simultaneously tested with a differential NTE assay.