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Ventilatory effects of low-dose paraoxon result from central muscarinic effects

Pascal Houze1, Laetita Pronzola, Maya Kayouka

  • 1Toxicology Laboratory, Faculty of Pharmacy, 75006 Paris, France.

Toxicology and Applied Pharmacology
|September 9, 2008
PubMed

Insights

Low-dose paraoxon causes respiratory toxicity by affecting the central nervous system. Atropine, which crosses the blood-brain barrier, reversed these effects, indicating a central origin for paraoxon

Area of Science:

  • Toxicology
  • Neuroscience
  • Respiratory Physiology

Background:

  • Paraoxon is an organophosphate pesticide known to induce respiratory toxicity.
  • Atropine effectively reverses parathion and paraoxon-induced respiratory toxicity.
  • The precise origin (peripheral or central) of paraoxon's ventilatory effects requires further investigation.

Purpose of the Study:

  • To determine whether the ventilatory effects of low-dose paraoxon originate in the peripheral or central nervous system.
  • To investigate the role of muscarinic signaling in paraoxon-induced respiratory toxicity.

Main Methods:

  • Male Sprague-Dawley rats were administered low-dose paraoxon (0.215 mg/kg).
  • Animals were treated with atropine (10 mg/kg) or escalating doses of methylatropine (5.42 to 542 mg/kg).
  • Ventilation was assessed using whole-body plethysmography, and body temperature was monitored via infra-red telemetry.

Main Results:

  • Paraoxon induced hypothermia, partially reversed by atropine but not methylatropine.
  • Paraoxon decreased respiratory rate by increasing expiratory time and tidal volume.
  • Atropine completely reversed paraoxon's ventilatory effects, while methylatropine showed no significant effect even at high doses.

Conclusions:

  • The ventilatory effects of low-dose paraoxon are primarily mediated by the central nervous system.
  • Disrupted muscarinic signaling within the central nervous system is the likely mechanism of paraoxon-induced respiratory toxicity.
  • Atropine's ability to reverse these effects highlights its efficacy in counteracting central neurotoxic effects of organophosphates.

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