Central-peripheral delayed neuropathy caused by diisopropyl phosphorofluoridate (DFP): Segregation of peripheral nerve and spinal cord effects using biochemical, clinical, and morphological criteria

Lotti, Marcello; Caroldi, Stefano; Moretto, Angelo; Johnson, Martin K.; Fish, C. J.; Gopinath, C.; Roberts, Naomi L.

doi:10.1016/0041-008x(87)90272-9

Cited by 45 publications

(10 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PMSF has been used in mechanistic studies of organophosphate-induced delayed polyneuropathy (OPIDP) because it protects hens from this toxicity (Johnson 1982). When neuropathy target esterase (NTE), the putative target for the initiation of OPIDP, is sulfonylated in vivo byPMSF prior to neuropathic doses of organophosphates (OPs), no OPIDP develops (Johnson 1974;Lotti et al 1987). PMSF shares this effect with other NTE inhibitors, e. g., some phosphinates and carbamates.…”

Section: Introductionmentioning

confidence: 99%

Phenylmethanesulfonyl fluoride elicits and intensifies the clinical expression of neuropathic insults

et al. 1992

Self Cite

View full text Add to dashboard Cite

It has been recently reported that phenylmethanesulfonyl fluoride (PMSF) when given to hens after a neuropathic organophosphate (OP) promotes organophosphate-induced delayed polyneuropathy (OPIDP). Chicks are resistant to OPIDP despite high inhibition/aging of neuropathy target esterase (NTE), the putative target of OPIDP initiation. However, when PMSF (300 mg/kg s.c.) is given to chicks after di-butyl 2,2-dichlorovinyl phosphate (DBDCVP, 1 or 5 mg/kg s.c.), OPIDP is promoted. Inhibition/aging of at least 30% of NTE was thought to be an essential prerequisite for promotion to be elicited in adult hens. However, we observed in hens that when NTE is maximally affected (greater than 90%) by phenyl N-methyl N-benzyl carbamate (40 mg/kg i.v.), a non-ageable inhibitor of NTE, and then PMSF is given (120 mg/kg/day s.c. x 3 days) clinical signs of neuropathy become evident. Methamidophos (50 mg/kg p.o. to hens), which produces in vivo a reactivatable form of inhibited NTE, was shown either to protect from or promote OPIDP caused by DBDCVP (0.45 mg/kg s.c.), depending on the sequence of dosing. Because very high doses of methamidophos cause OPIDP, we considered this effect to be a "self-promoted" OPIDP. We concluded that NTE inhibitors might have different intrinsic activities for producing OPIDP once NTE is affected. Aging might differentiate highly neuropathic OPs, like DBDCVP, from less neuropathic OPs, like methamidophos, or from the least neuropathic carbamates, which require promotion in order for neuropathy to be expressed.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

Section: Introductionmentioning

confidence: 99%

Phenylmethanesulfonyl fluoride elicits and intensifies the clinical expression of neuropathic insults

et al. 1992

Self Cite

View full text Add to dashboard Cite

show abstract

“…Studies of NTE in the sciatic nerve have centered on the development of appropriate methods for NTE assay (Caroldi and Lotti, 1982;Baml et al, 1988) and on the study of NTE proximodistal distribution (Car-rington and Abou-Donia, 1984; Baml et al, 1988). In turn, sciatic nerve NTE activity has been determined in some toxicological studies (Lotti et al, 1987; Pellin et al, 1988; Johnson et al, 1989). However, peripheral NTE has not been biochemically characterized, and it is not certain whether the protein is the same as that isolated in the brain.…”

mentioning

confidence: 99%

Soluble and Participate Forms of the Organophosphorus Neuropathy Target Esterase in Hen Sciatic Nerve

Vilanova

Barril

Carrera

et al. 1990

Journal of Neurochemistry

View full text Add to dashboard Cite

Neuropathy target esterase (NTE) is the suggested "target" molecule involved in the initiation of organophosphorus-induced delayed polyneuropathy. Sciatic nerve NTE was separated into particulate (P-NTE) and soluble (S-NTE) fractions by ultracentrifugation at 100,000 g for 1 h in 0.32 M sucrose and compared with the corresponding brain extract. Total sciatic NTE activity was 80-100 nmol/min/g tissue from which 50-60% was recovered in the soluble supernatant fraction and the remaining 40-50% in the pellet fraction. About 90% of brain tissue activity (approximately 1,800 nmol/min/g tissue) was recovered as P-NTE. A similar distribution was obtained when more drastic centrifugation without sucrose was performed. P-NTE and S-NTE were distributed with the membrane and cytosolic markers assayed, respectively, glucose-6-phosphatase, Na+,K(+)-ATPase, 5'-nucleotidase, phospholipids, and lactate dehydrogenase. When the pH during the centrifugation was increased from 6.4 to 11, recovered P-NTE activity decreased from 1,750 to 118 nmol/min/g tissue for brain and from 31 to 12 nmol/min/g for sciatic nerve. However, S-NTE activity and total nonfractionated control activity were only slightly affected by the same pH treatment. The distribution pattern encountered may be better understood as representing two different proteins than an equilibrium between soluble and membrane-bound portions of a single protein, with P-NTE activity depending on a membrane factor from which it is separated through fractionation at high pH.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

“…Of the controls, two hens were also chosen at random. These hens were deeply anesthetized with pentobarbitone, the thoraxes were opened and the tissues fixative (buffered glutaraldehyde, pH 7.4) inserted via a needle into the left ventricle of the heart 7) . Perfusion by means of a gravityfeed system with a pressure head of 1 m was continued for a period of 5-10 min until all muscles became rigid (volume of 200-300 ml fixative).…”

Section: Histopathologymentioning

confidence: 99%

“…The clinical signs of OPIDN are characterized by a delay period followed by ataxia which may progress to paralysis 1) . Histopathologic changes consist of Wallerian-type degeneration of the longest and largest diameter axon and myelin of the central and peripheral nervous systems [6][7][8][9] . Clinical, electrophysiological and nerve biopsy data revealed a were examined.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Effects of Prednisolone and Complex of Vitamin B₁, B₂, B₆ and B₁₂ on Organophosphorus Compound‐Induced Delayed Neurotoxicity

Piao

Yamamoto

et al. 2004

Journal of Occupational Health

View full text Add to dashboard Cite

Protective effects of prednisolone as a synthetic adrenal cortical hormone and complex of vitamin B(1), B(2), B(6) and B (12) on organophosphorus compound-induced delayed neurotoxicity (OPIDN) caused by leptophos and tri-o-cresyl phosphate (TOCP) as organophosphates (OPs) were examined. Nine groups of hens (six for each) were used. Eight groups received intravenous injection of 30 mg/kg of leptophos or 40 mg/kg of TOCP (four groups in each). Among them, three groups which received leptophos were given (p.o.) predonisolone (2 mg/body), vitamin B complex (25 mg/body) or both 3 h after OPs injection and then every day for 15 d (one group for each); the same treatment was performed on three groups which received TOCP. The remaining one group served as controls. It was observed that delayed neuropathy induced by OPs could not be resisted completely by the treatment with prednisolone or vitamin B complex, but clinical signs of OPIDN and pathological changes in hens that received these two protective agents after OPs were less severe than those in hens that received only OPs. Of these groups, the improvement in clinical signs was best shown in hens that received the both two protective agents. In addition, improvement in clinical signs among the hens that did not deteriorate to paralysis was observed. In particular, those which developed mild ataxia recovered well. It is indicated that combining administration of prednisolone and vitamin B complex early before clinical signs are manifest is effective in alleviating neuropathy. It is also suggested that recovery or good prognosis will be expected, as long as progression of the clinical signs is prevented before paralysis develops in delayed neuropathy.

show abstract

Central-peripheral delayed neuropathy caused by diisopropyl phosphorofluoridate (DFP): Segregation of peripheral nerve and spinal cord effects using biochemical, clinical, and morphological criteria

Cited by 45 publications

References 24 publications

Phenylmethanesulfonyl fluoride elicits and intensifies the clinical expression of neuropathic insults

Phenylmethanesulfonyl fluoride elicits and intensifies the clinical expression of neuropathic insults

Soluble and Participate Forms of the Organophosphorus Neuropathy Target Esterase in Hen Sciatic Nerve

Effects of Prednisolone and Complex of Vitamin B₁, B₂, B₆ and B₁₂ on Organophosphorus Compound‐Induced Delayed Neurotoxicity

Contact Info

Product

Resources

About

Central-peripheral delayed neuropathy caused by diisopropyl phosphorofluoridate (DFP): Segregation of peripheral nerve and spinal cord effects using biochemical, clinical, and morphological criteria

Cited by 45 publications

References 24 publications

Phenylmethanesulfonyl fluoride elicits and intensifies the clinical expression of neuropathic insults

Phenylmethanesulfonyl fluoride elicits and intensifies the clinical expression of neuropathic insults

Soluble and Participate Forms of the Organophosphorus Neuropathy Target Esterase in Hen Sciatic Nerve

Effects of Prednisolone and Complex of Vitamin B1, B2, B6 and B12 on Organophosphorus Compound‐Induced Delayed Neurotoxicity

Contact Info

Product

Resources

About

Effects of Prednisolone and Complex of Vitamin B₁, B₂, B₆ and B₁₂ on Organophosphorus Compound‐Induced Delayed Neurotoxicity