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Poisons and fever

C J Gordon1, P J Rowsey

  • 1Neurotoxicology Division, National Health Effects and Environmental Research Laboratory, US Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA. GORDON@HERL45.HERL.EPA.GOV

Clinical and Experimental Pharmacology & Physiology
|March 11, 1998
PubMed
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Organophosphate pesticides can cause a regulated fever by activating the cyclo-oxygenase (COX) and prostaglandin E2 (PGE2) pathway in the central nervous system. This poison-induced fever mechanism may mimic infection-related fevers.

Area of Science:

  • Toxicology
  • Neuroscience
  • Physiology

Background:

  • Thermoregulatory system dysfunction is a known pathology from toxic chemical exposure.
  • Mechanisms behind poison-induced fevers are not fully understood.
  • Organophosphate (OP) pesticides and metal fumes can cause prolonged, regulated body temperature elevations.

Purpose of the Study:

  • To investigate the mechanism of poison-induced fever.
  • To establish an experimental animal model for studying poison-induced fever.

Main Methods:

  • Radiotelemetric monitoring of core body temperature in rodents.
  • Administration of OP agents (chlorpyrifos, diisopropyl fluorophosphate).
  • Assessment of fever blockade using sodium salicylate.

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Main Results:

  • OP exposure induced an initial hypothermia followed by a delayed hyperthermia (24-72 hours).
  • The hyperthermia was blocked by sodium salicylate, indicating involvement of the cyclo-oxygenase (COX) and prostaglandin E2 (PGE2) pathway.
  • This suggests activation of central nervous system thermoregulatory pathways.

Conclusions:

  • Poison-induced fever, specifically from OP exposure, involves the COX-PGE2 pathway in the central nervous system.
  • The mechanism shares similarities with infection-mediated fever pathways.
  • This provides a model for understanding toxic chemical effects on thermoregulation.