Organophosphate polyneuropathy in chicks.

  title={Organophosphate polyneuropathy in chicks.},
  author={Maja Peraica and E Capodicasa and Angelo Moretto and Marcello Lotti},
  journal={Biochemical pharmacology},
  volume={45 1},
Neuropathology of organophosphate-induced delayed neuropathy (OPIDN) in young chicks
It is demonstrated that after neuropathic DFP exposure, 2-week-old chicks develop pathological lesions in the spinal cord without neurological deficits, and the claim of apparent age resistance of chicks to OPIDN needs to be re-evaluated.
Organophosphate-Induced Delayed Polyneuropathy
This article mainly discusses OP pesticide poisoning, particularly when caused by chlorpyrifos, dichlorvos, isofenphos, methamidophos, mipafox, trichlorfon,trichlornat, phosphamidon/mevinphos and by certain carbamates.
Potentiation of organophosphorus-induced delayed neurotoxicity following phenyl saligenin phosphate exposures in 2-, 5-, and 8-week-old chickens.
  • P. Harp, D. Tanaka, C. Pope
  • Biology, Psychology
    Fundamental and applied toxicology : official journal of the Society of Toxicology
  • 1997
It is concluded that posttreatment with neuropathic or nonneuropathic NTE inhibitors, following virtually complete NTE inhibition by either single or repeated doses of a neuropathic agent in sensitive age groups, can modify both the clinical and morphological indices of delayed neurotoxicity.
Effects of various post-treatment by phenylmethylsulfonyl fluoride on delayed neurotoxicity induced by leptophos.
It is indicated that post-treatment with PMSF promotes leptophos-induced OPIDN and reduces the period to OPIDn onset and variations in both the dose and the time intervals of PMSF post- Treatment suggest that PMSF should not be used for either the treatment or the prevention ofOPIDN.


The pathogenesis of organophosphate polyneuropathy.
  • M. Lotti
  • Biology
    Critical reviews in toxicology
  • 1991
This review discusses the facts regarding organophosphate-induced delayed polyneuropathy (OPIDP) as they are related to its pathogenesis rather than being a comprehensive review of all available
Potentiation of organophosphorus-induced delayed neurotoxicity by phenylmethylsulfonyl fluoride.
  • C. Pope, S. Padilla
  • Biology, Chemistry
    Journal of toxicology and environmental health
  • 1990
The data indicate that PMSF only protects against OPIDN if given prior to exposure to the neurotoxicant; treatment with PMSF after OP exposure critically exacerbates the delayed neurotoxicity from exposure to organophosphorus compounds.
Protection by some Carbamates against the Delayed Neurotoxic Effects of Di-isopropyl Phosphorofluoridate
The effect produced by di-isopropyl phosphorofluoridate (DFP) is studied because it is a potent neurotoxic compound and does not need to be metabolized to produce the active agent.
Acute Tricresylphosphate Intoxication in Childhood
A case of severe intoxication in a 4½-year-old child following ingestion of a lubricant containing TCP is reported, typical of previously reported acute ingestions in adults.
Jamaica ginger paralysis. Forty-seven-year follow-up.
In 1930, thousands of Americans were poisoned by an illicit extract of Jamaica ginger ("jake") used to circumvent the Prohibition laws. A neurotoxic organophosphate compound, triorthocresyl phosphate
Purification of Neuropathy Target Esterase from Avian Brain After Prelabelling with [3H]Diisopropyl Phosphorofluoridate
Neuropathy target esterase from hen brains was radiolabelled at the active site with [3H]diisopropyl phosphorofluoridate and the 150‐kDa subunit polypeptide appears as a single band on analytical SDS‐PAGE.