The use of chemical warfare agents is an ongoing, significant threat to both civilians and military personnel worldwide. Nerve agents are by far the most formidable toxicants in terms of their lethality and toxicity. Nerve agents initiate neurotoxicity by the irreversible inhibition of acetylcholinesterase and resultant accumulation of acetylcholine in excitable tissues. The cholinergic toxidrome presents as miosis, lacrimation, diarrhea, fasciculations, seizures, respiratory arrest and coma. Current medical countermeasures can attenuate acute mortality and confer limited protection against secondary neuronal injury when given rapidly after exposure. However, there is an urgent need for the development of novel, add-on neuroprotective therapies to prevent mortality and long-term toxicity of nerve agents. Increasing evidence suggests that pathways other than direct acetylcholinesterase inhibition contribute to neurotoxicity and secondary neuronal injury. Among these, oxidative stress is emerging as a key therapeutic target for nerve agent toxicity. In this review, we discuss the rationale for targeting oxidative stress in nerve agent toxicity and highlight research investigating antioxidant therapy as a neuroprotective medical countermeasure to attenuate oxidative stress, neuroinflammation and neurodegeneration.

化学战剂的使用对全世界的平民和军事人员都是一个持续的、重大的威胁。就其致死性和毒性而言，神经毒剂是迄今为止最强大的毒物。神经毒剂通过对乙酰胆碱酯酶的不可逆抑制和乙酰胆碱在可兴奋组织中的积累而引发神经毒性。胆碱能中毒症状表现为瞳孔缩小、流泪、腹泻、震颤、癫痫、呼吸停止和昏迷。当前的医疗对策可以降低急性死亡率，并在暴露后迅速给予时对继发性神经元损伤提供有限的保护。然而，迫切需要开发新型的附加神经保护疗法，以防止神经毒剂的死亡和长期毒性。越来越多的证据表明，除了直接的乙酰胆碱酯酶抑制之外，其他途径也会导致神经毒性和继发性神经元损伤。其中，氧化应激正在成为神经毒剂毒性的关键治疗靶点。在这篇综述中，我们讨论了在神经毒剂毒性中靶向氧化应激的基本原理，并重点研究了抗氧化疗法作为减轻氧化应激的神经保护医学对策的研究，