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Cyclooxygenase-2 contributes to VX-induced cell death in cultured cortical neurons

Catherine C Tenn1, M Tracy Weiss, Claire Beaup

  • 1DRDC Suffield, Station Main, Medicine Hat, Alberta, Canada. catherine.tenn@drdc-rddc.gc.ca

Toxicology Letters
|February 7, 2012
PubMed

Insights

Organophosphorus nerve agent VX increases cyclooxygenase-2 (COX-2) activity, contributing to neurotoxicity in rat neurons. Inhibiting COX-2 reduces cell death, suggesting a key role for this enzyme in nerve agent poisoning.

Area of Science:

  • Neuroscience
  • Toxicology
  • Biochemistry

Background:

  • The precise mechanisms linking cell death and cyclooxygenase-2 (COX-2) activity remain unclear.
  • Organophosphorus nerve agents, like VX, pose significant neurotoxic threats.

Purpose of the Study:

  • To investigate if COX-2 activation mediates neurotoxicity induced by the organophosphorus nerve agent VX.
  • To explore the role of COX-2 in VX-induced neuronal cell death.

Main Methods:

  • Cultured rat cortical neurons were exposed to VX.
  • COX enzyme activity, COX-2 mRNA and protein levels, and prostaglandin release were measured.
  • The effect of the selective COX-2 inhibitor NS 398 on VX-induced neurotoxicity was assessed.

Main Results:

  • VX exposure significantly increased COX enzyme activity, specifically COX-2, in a concentration-dependent manner.
  • VX exposure led to increased COX-2 mRNA and protein levels and prostaglandin release.
  • Pre-treatment with NS 398 reduced COX-2 activity, prostaglandin release, and neuronal cell death.

Conclusions:

  • Increased COX-2 activity is implicated in the neurotoxic mechanism of VX.
  • Targeting COX-2 may offer a therapeutic strategy against organophosphorus nerve agent toxicity.

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