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

A F Hernández1, A Pla, E Villanueva

  • 1Departamento de Medicina Legal, Facultad de Medicina, Universidad de Granada, Spain.

Revista Espanola De Fisiologia
|September 1, 1992
PubMed
Summary

Triorthocresyl-phosphate (TOCP) causes delayed neuropathy by affecting phosphofructokinase (PFK) activity in hens. This neurotoxic effect on PFK is linked to neuropathy initiation, suggesting PFK

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Toxicology

Background:

  • Triorthocresyl-phosphate (TOCP) is a known neurotoxicant that induces delayed neuropathy.
  • Neuropathy target esterase (NTE) inhibition and aging are key steps in TOCP-induced neuropathy.
  • The role of specific enzymes like phosphofructokinase (PFK) in this process requires further investigation.

Purpose of the Study:

  • To investigate the in vivo effect of TOCP on phosphofructokinase (PFK) activity.
  • To determine the relationship between PFK activity changes and the initiation of TOCP-induced delayed neuropathy.
  • To explore the potential involvement of PFK in the pathogenesis of TOCP neurotoxicity.

Main Methods:

  • Hens were administered TOCP, Phenylmethanesulfonyl fluoride (PMSF), or combinations thereof.

Related Experiment Videos

  • PFK activity was measured in brain and sciatic nerve tissues at multiple time points post-treatment (1, 3, 7, and 15 days).
  • Clinical signs of neuropathy were monitored throughout the study.

    • Main Results:

    • PFK activity significantly decreased in the sciatic nerve 15 days after treatment with TOCP or TOCP + PMSF.
    • Administration of PMSF alone or prior to TOCP prevented PFK activity reduction and clinical neuropathy.
    • These findings correlate PFK activity reduction with the development of TOCP-induced neuropathy.

    Conclusions:

    • Phosphofructokinase (PFK) activity is implicated in the pathogenesis of TOCP-induced delayed neuropathy.
    • The study suggests a link between PFK modulation and the neurotoxic effects of TOCP.
    • PFK may represent a potential therapeutic target for TOCP-induced neurotoxicity.