Tabun (nerve agent): Difference between revisions
CSV import Tags: mobile edit mobile web edit |
CSV import |
||
| Line 1: | Line 1: | ||
{{Short description|Overview of the nerve agent Tabun}} | |||
{{Use dmy dates|date=October 2023}} | |||
== | ==Overview== | ||
Tabun was | [[File:TabunSynthesis.png|thumb|right|Synthesis of Tabun]] | ||
'''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]]. | |||
== Properties | ==Chemical Properties== | ||
Tabun is a liquid at room temperature | 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== | |||
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 [[muscle]]s, [[gland]]s, and [[central nervous system]] structures. This results in a range of symptoms, including [[muscle twitching]], [[respiratory failure]], and [[convulsions]]. | |||
Symptoms of | ==Symptoms of Exposure== | ||
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 | ==Treatment== | ||
The | 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== | ||
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== | |||
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. | |||
==Related pages== | |||
* [[Nerve agent]] | * [[Nerve agent]] | ||
* [[ | * [[Sarin]] | ||
* [[ | * [[Soman]] | ||
* [[Acetylcholinesterase]] | * [[Acetylcholinesterase]] | ||
* [[ | * [[Organophosphate]] | ||
[[Category:Nerve agents]] | [[Category:Nerve agents]] | ||
[[Category: | [[Category:Organophosphates]] | ||
[[Category:Chemical weapons]] | |||
Latest revision as of 11:15, 15 February 2025
Overview of the nerve agent Tabun
Overview[edit]
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]
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]
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]
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]
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]
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]
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.
