Decrease of phosphofructokinase activity in relation to the pathogenesis of triorthocresyl-phosphate-induced delayed neuropathy.

A F Hernández; A Pla; E Villanueva

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PubMed · 1301629

Decrease of phosphofructokinase activity in relation to the pathogenesis of triorthocresyl-phosphate-induced delayed neuropathy.

A F Hernández·A Pla·E Villanueva

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Abstract

The in vivo effect of a single dose of the neuropathic compound triorthocresyl-phosphate (TOCP) on phosphofructokinase (PFC, E.C. 2.7.1.11) and its relation with the initiation step (inhibition and aging of neuropathy target esterase, NTE) in the TOCP-induced delayed neuropathy have been studied. Hens were treated with a neurotoxic dose of TOCP (500 mg/kg, p.o.) and with a protective compound (Phenylmethanesulfonyl fluoride, PMSF, 30 mg/kg s.c.) in different combinations: TOCP, TOCP + PMSF, PMSF + TOCP and PMSF. PFK activity was determined in brain and sciatic nerve 1, 3, 7 and 15 days after treatment. PFK activity decreased in sciatic nerve 15 days after dosing with TOCP or TOCP + PMSF. When animals were dosed with the protective agent (PMSF) alone or before administering the neurotoxic compound, PFK activity was unaltered and clinical signs of neuropathy were absent. The data presented here suggest that phosphofructokinase is involved in the pathogenesis of the neuropathy induced by TOCP.

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Acetylcholinesterase Animals Brain Butyrylcholinesterase Carboxylic Ester Hydrolases Chickens Female Lymphocytes Nerve Tissue Proteins Nervous System Diseases Phenylmethylsulfonyl Fluoride Phosphofructokinase-1 Sciatic Nerve Time Factors Tritolyl Phosphates Comparative Study Journal Article Research Support, Non-U.S. Gov't

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A F Hernández, A Pla, E Villanueva. 1992. Decrease of phosphofructokinase activity in relation to the pathogenesis of triorthocresyl-phosphate-induced delayed neuropathy.. https://pubmed.ncbi.nlm.nih.gov/1301629/

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