Abstract:

As an organophosphorus nerve agent， soman exerts its neurotoxic effects by irreversibly inhibiting acetylcholinesterase activity. This inhibition leads to the accumulation of acetylcholine at neural synapses and neuromuscular junctions， triggering persistent epileptic states and potentially fatal symptoms such as respiratory failure. Despite the existence of standard treatment protocols， their efficacy heavily relies on early intervention， as delayed treatment often fails to prevent neurological damage and death. Even with timely administration of medication， uncontrolled epileptic activity within 20 min can cause widespread neuropathological damage across multiple brain regions， significantly increasing the mortality rate. Further exploration of novel combination therapy strategies， expansion of the therapeutic time window， and improvement of outcomes for delayed treatment are crucial for emergency response to soman poisoning. This article provides a comprehensive review of the neurotoxic mechanisms of soman and recent advancements in therapeutic drugs， aiming to offer a reference for the further development of new treatment strategies for soman poisoning.

Key words: Soman, Nerve agent, Acetylcholinesterase, Epilepsy