The Molecular Toxicology of Chemical Warfare Nerve Agents

Abstract

Chemical warfare nerve agents continue to be a threat to both military personnel and civilian populations. Organophosphorus nerve agents irreversibly inhibit the enzyme acetylcholinesterase, resulting in accumulation of high levels of the neurotransmitter acetylcholine (ACh) at muscarinic and nicotinic receptors. This accumulation of ACh induces clinical symptoms including myosis, difficulty in breathing, convulsions, seizures, and can result n death. Current medical countermeasures for treating nerve agent intoxication increase survival if administered rapidly after exposure but may not fully prevent brain injury. The downstream neurological damage induced by nerve agent exposure is not well characterized. Researchers are now utilizing molecular approaches to understand the molecular pathways involved in nerve agent-induced brain injury, with the goal of developing treatment strategies that are effective when administered after the onset of seizures and secondary responses that lead to nerve agent-induced brain injury.

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Document Details

Document Type
Technical Report
Publication Date
Jan 01, 2011
Accession Number
ADA559311

Entities

People

  • J. F. Dillman Iii
  • K. D. Spradling

Organizations

  • United States Army Medical Research Institute of Chemical Defense

Tags

DTIC Thesaurus Topics

  • Acetylcholinesterases
  • Brain Injuries
  • Chemical Warfare
  • Civilian Population
  • Diseases And Disorders
  • Infectious Diseases
  • Intoxication
  • Medical Countermeasures
  • Medical Personnel
  • Military Personnel
  • Nerve Agents
  • Seizures
  • Toxicology
  • Warfare

Fields of Study

  • Medicine

Readers

  • Molecular and Cellular Biology
  • Neurotoxicology
  • Neurotrauma and Rehabilitation Medicine.