saligenin/atrophy

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Catecholamine concentrations and contractile responses of isolated vessels from hens treated with cyclic phenyl saligenin phosphate or paraoxon in the presence or absence of verapamil.

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Blood samples and vascular segments from the ischiadic artery of hens treated with either cyclic phenyl saligenin phosphate (PSP; 2.5 micrograms/kg, im) or paraoxon (PXN; 0.1 micrograms/kg, im) in the presence or absence of verapamil, a calcium channel antagonist (7 micrograms/kg, im, given 4

The biventer cervicis nerve-muscle preparation of adult hens: effects of phenyl saligenin phosphate administration.

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A biventer cervicis nerve-muscle preparation was used to assess in vitro neuromuscular function in adult white leghorn hens with clinical signs of delayed neuropathy induced by phenyl saligenin phosphate (PSP). Denervation of fast-twitch muscle fibers 13-15 days after PSP was indicated by higher

Altered expression of transcripts for alpha-tubulin and an unidentified gene in the spinal cord of phenyl saligenin phosphate treated hens (Gallus gallus).

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Phenyl saligenin phosphate (PSP) induces a central-peripheral distal axonopathy in domestic fowl that develops 7-21 days after a single exposure. Neurotoxic esterase (NTE) is the initial molecular target for this neurotoxicity. PSP has to covalently bind to NTE and chemically "age" for induction of

Potentiation of organophosphorus-induced delayed neurotoxicity following phenyl saligenin phosphate exposures in 2-, 5-, and 8-week-old chickens.

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Phenylmethylsulfonyl fluoride (PMSF), a nonneuropathic inhibitor of neurotoxic esterase (NTE), is a known potentiator of organophosphorus-induced delayed neurotoxicity (OPIDN). The ability of PMSF posttreatment (90 mg/kg, sc, 4 hr after the last PSP injection) to modify development of delayed

Neuropathological effects of phenyl saligenin phosphate in chickens.

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Cyclic phenyl saligenin phosphate (PSP) proved to be a potent delayed neurotoxin, eliciting clinical disease and lesions, and depressing neuropathy target esterase and plasma cholinesterase at much lower doses than the protoxicant tri-ortho-tolyl phosphate (TOTP). Using adult White Leghorn chickens,

Antibodies to neural proteins in organophosphorus-induced delayed neuropathy (OPIDN) and its amelioration.

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The development of OPIDN and the efficacy of experimental intervention using the calcium-channel blocker verapamil were used as a model to test the serial time-measurements of serum autoantibodies against neuronal cytoskeletal proteins [e.g., neurofilament triplet (NF)] and glial proteins

Use of the biventer cervicis nerve-muscle preparation to detect early changes following exposure to organophosphates inducing delayed neuropathy.

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Indices of organophosphorus (OP)-induced delayed neuropathy (OPIDN) in the hen model have traditionally been restricted to the early inhibition of neuropathy target esterase (NTE) and ataxia with associated pathological changes in hind limb peripheral nerve which occur more than 7 days after OP

Murine susceptibility to organophosphorus-induced delayed neuropathy (OPIDN).

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This study reports that CD-1 strain mice are neuropathologically and biochemically responsive to acute doses of tri-ortho-cresyl phosphate (TOCP). Young (25-30 g) male and female animals were exposed (po) to a single dose of TOCP (580-3480 mg/kg) and sampled for neurotoxic esterase (NTE) activity at

Relationship of neuropathy target esterase inhibition to neuropathology and ataxia in hens given organophosphorus esters.

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Adult White Leghorn hens were acutely exposed to 3 dosages of the following organophosphorus compounds: mipafox, tri-ortho-tolyl phosphate (TOTP), phenyl saligenin phosphate, and diisopropylphosphorofluoridate (DFP). Neuropathy target esterase (NTE) activity was measured in brain and spinal cord 4

Neuropathologic effects of phenylmethylsulfonyl fluoride (PMSF)-induced promotion and protection in organophosphorus ester-induced delayed neuropathy (OPIDN) in hens.

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The serine/cysteine protease inhibitor phenylmethylsulfonyl fluoride (PMSF) has been used both to promote and to protect against neuropathic events of organophosphorus-induced delayed neuropathy (OPIDN) in hens (Veronesi and Padilla, 1985; Pope and Padilla, 1990; Lotti et al., 1991; Pope et al.,

Immunohistochemical study of phosphorylated neurofilaments during the evolution of organophosphorus ester-induced delayed neuropathy (OPIDN).

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Organophosphorus ester-induced delayed neuropathy (OPIDN) is manifest by delayed degeneration of distal levels of long myelinated fibers following an appropriate neurotoxic exposure. We investigated the dynamics of cytoskeletal changes during nerve fiber degeneration in this condition, focusing on

Possible involvement of a neurotrophic factor during the early stages of organophosphate-induced delayed neurotoxicity.

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Little is known regarding early biochemical events in organophosphate-induced delayed neurotoxicity (OPIDN) except for the essential inhibition of neurotoxic esterase (NTE). We hypothesized that a trophic factor may be produced in situ shortly after exposure to the OP which participates in the

Organophosphorus compound-induced delayed neurotoxicity in white leghorn hens assessed by Fluoro-Jade.

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Certain organophosphorus (OP) compounds can induce a delayed neuropathy, termed OPIDN, that involves central and peripheral nervous system axons, terminals, and perikarya. Historically, OPIDN has been characterized by staining neural sections with silver or hematoxylin and eosin (H and E). This

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