A review of experimental evidence linking neurotoxic organophosphorus compounds and inflammation

Neurotoxicology. 2012 Jun;33(3):575-84. doi: 10.1016/j.neuro.2012.02.002. Epub 2012 Feb 10.


Organophosphorus (OP) nerve agents and pesticides inhibit acetylcholinesterase (AChE), and this is thought to be a primary mechanism mediating the neurotoxicity of these compounds. However, a number of observations suggest that mechanisms other than or in addition to AChE inhibition contribute to OP neurotoxicity. There is significant experimental evidence that acute OP intoxication elicits a robust inflammatory response, and emerging evidence suggests that chronic repeated low-level OP exposure also upregulates inflammatory mediators. A critical question that is just beginning to be addressed experimentally is the pathophysiologic relevance of inflammation in either acute or chronic OP intoxication. The goal of this article is to provide a brief review of the current status of our knowledge linking inflammation to OP intoxication, and to discuss the implications of these findings in the context of therapeutic and diagnostic approaches to OP neurotoxicity.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Humans
  • Inflammation / chemically induced*
  • Inflammation / immunology
  • Inflammation / pathology
  • Inflammation Mediators / metabolism
  • Neurons / drug effects*
  • Neurons / immunology
  • Neurons / pathology
  • Neurotoxicity Syndromes / etiology*
  • Neurotoxicity Syndromes / immunology
  • Neurotoxicity Syndromes / pathology
  • Organophosphorus Compounds / toxicity*
  • Risk Assessment
  • Risk Factors


  • Inflammation Mediators
  • Organophosphorus Compounds