Figure 1
Representatives of the G-series (tabun, sarin, soman, cyclosarin), V-series (VX, VR), IVA agents (GV), and Novichok series (16) of nerve agents (A-230, A-232, A234, A242, A-262)
Figure 2
Hydrolysis of acetylcholine (A), phosphylation and aging (B), and reactivation of nerve agent-inhibited acetylcholinesterase (C)
Table 1
Symptoms of nerve agent poisoning arising from acetylcholine build-up at muscarinic and nicotinic membrane receptors (8, 23, 40, 41)
| System | Symptoms |
|---|---|
| Brain | Restlessness, headache, dizziness, convulsions, inhibition of central respiratory centres, loss of consciousness, coma |
| Eyes | Blurred vision, conjunctivitis, myosis |
| Respiratory | Rhinorrhoea, bronchoconstriction, bronchorrhea, pulmonary oedema |
| Cardiovascular | Either tachycardia or bradycardia, and either hypotension or hypertension |
| Gastro-intestinal | Cramping, abdominal pain, nausea, salivation, vomiting, defecation, urinary incontinence |
| Muscle | Twitching, fasciculation, tremors, muscle cramps, paralysis |
| Skin | Increased sweating |
Figure 3
Standard pyridinium aldoxime reactivators of phosphylated acetylcholinesterase, antimuscarinic atropine, and anticonvulsant diazepam, currently approved for nerve agent poisoning therapy
Figure 4
Non-oxime compounds investigated as potential treatment in case of nerve agent poisoning (120, 123)
Figure 5
Bioscavenging of native acetylcholinesterase from inhibition with nerve agents. A) stoichiometric bioscavenging; mole-to-mole reaction between exogenous enzyme scavenger and nerve agent, B) oxime-assisted catalytic scavenging; exogenous enzyme turned into catalytic bioscavenger in the presence of an oxime enabling nerve agent degradation by cycles of inhibition and reactivation of exogenous enzyme scavenger, C) catalytic bioscavenging; low amount of exogenous enzyme scavenger rapidly hydrolyses nerve agent with a turnover