Immunotherapeutic Protection From a Soman Nerve Agent Model Compound

Chemical warfare agents include potent nerve agents (NAs). NAs covalently inhibit cholinesterases (ChEs) in the blood and in the central nervous system of animals administered NAs. An example of a very toxic NA is soman. After administration to animals, NA-ChE inhibition results and causes acetylcholine (ACh) to build up in the synapse where ordinarily only small amounts of ACh are present. This stimulates autonomic receptors and blocks neuromuscular junction receptors, causes severe neurological side effects including seizures and neuropathology and can result in death by respiratory failure. Even with standard of care (SOC) intervention, NA exposure can be life-threatening, and improvements to the SOC are needed. However, even with intervention, NA exposures produce high morbidity and mortality, in part, because the SOC and overall treatment paradigm lack a therapeutic to decrease in vivo levels of NA. Currently, a countermeasure for soman does not exist. Thus, the aim of the present study was to investigate the prophylactic effect exerted by ip administration of a vaccine in Swiss Webster mice to protect against a soman nerve agent model compound. This approach is directed as a model to pretreat the warfighter before potential NA exposure. Results of the vaccine treatment showed that, compared to controls, prophylactic protection against a soman nerve agent model compound can be achieved.

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Publication Details

Journal
Journal of Biochemical and Molecular Toxicology
Published
2025-11-01
DOI
https://doi.org/10.1002/jbt.70600
Primary Topic
Pesticide Exposure and Toxicity
Type
article
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article

Immunotherapeutic Protection From a Soman Nerve Agent Model Compound

John Richard Cashman
Journal of Biochemical and Molecular Toxicology
Pesticide Exposure and Toxicity
article

Immunotherapeutic Protection From a Soman Nerve Agent Model Compound

John Richard Cashman
article en

Abstract

Chemical warfare agents include potent nerve agents (NAs). NAs covalently inhibit cholinesterases (ChEs) in the blood and in the central nervous system of animals administered NAs. An example of a very toxic NA is soman. After administration to animals, NA-ChE inhibition results and causes acetylcholine (ACh) to build up in the synapse where ordinarily only small amounts of ACh are present. This stimulates autonomic receptors and blocks neuromuscular junction receptors, causes severe neurological side effects including seizures and neuropathology and can result in death by respiratory failure. Even with standard of care (SOC) intervention, NA exposure can be life-threatening, and improvements to the SOC are needed. However, even with intervention, NA exposures produce high morbidity and mortality, in part, because the SOC and overall treatment paradigm lack a therapeutic to decrease in vivo levels of NA. Currently, a countermeasure for soman does not exist. Thus, the aim of the present study was to investigate the prophylactic effect exerted by ip administration of a vaccine in Swiss Webster mice to protect against a soman nerve agent model compound. This approach is directed as a model to pretreat the warfighter before potential NA exposure. Results of the vaccine treatment showed that, compared to controls, prophylactic protection against a soman nerve agent model compound can be achieved.

Journal of Biochemical and Molecular ToxicologyVol. 39(11)
Human BioMolecular Research Institute (US)
Openalex Percentile: Top 75%
Pesticide Exposure and Toxicity
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