Tabun (nerve agent)
Overview of the nerve agent Tabun
Overview[edit | edit source]
Tabun, also known by its military designation GA, is a nerve agent that was developed in Germany in the late 1930s. It is one of the first of the G-series nerve agents, which also includes Sarin (GB) and Soman (GD). Tabun is a highly toxic organophosphorus compound that disrupts the normal functioning of the nervous system by inhibiting the enzyme acetylcholinesterase.
Chemical Properties[edit | edit source]
Tabun is chemically classified as an organophosphate. Its chemical formula is C_H__N_O_P, and it is a clear, colorless, and tasteless liquid at room temperature. Tabun is soluble in most organic solvents but only slightly soluble in water. It has a faint fruity odor, which is not a reliable indicator of its presence.
Mechanism of Action[edit | edit source]
Tabun exerts its toxic effects by inhibiting the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine in the synaptic cleft. When acetylcholinesterase is inhibited, acetylcholine accumulates, leading to continuous stimulation of muscles, glands, and central nervous system structures. This results in a range of symptoms, including muscle twitching, respiratory failure, and convulsions.
Symptoms of Exposure[edit | edit source]
Exposure to Tabun can occur through inhalation, skin contact, or ingestion. Symptoms of exposure include:
- Miosis (constricted pupils)
- Rhinorrhea (runny nose)
- Bronchospasm
- Dyspnea (difficulty breathing)
- Nausea and vomiting
- Muscle weakness
- Seizures
- Loss of consciousness
Treatment[edit | edit source]
The primary treatment for Tabun poisoning involves the administration of atropine and pralidoxime. Atropine acts as an antagonist to acetylcholine at muscarinic receptors, while pralidoxime reactivates acetylcholinesterase if administered soon after exposure. Supportive care, including ventilation and oxygen therapy, is also critical.
History[edit | edit source]
Tabun was first synthesized by German chemist Gerhard Schrader in 1936 while he was working for the chemical company IG Farben. It was initially developed as a pesticide, but its potential as a chemical weapon was quickly recognized. During World War II, Tabun was produced in large quantities by Nazi Germany, although it was never used in combat.
Synthesis[edit | edit source]
The synthesis of Tabun involves the reaction of dimethylamine with phosphoryl chloride to form dimethylamidophosphoryl dichloride, which is then reacted with sodium cyanide to produce Tabun. The process is depicted in the adjacent image.
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Contributors: Prab R. Tumpati, MD