VG (nerve agent): Difference between revisions

Latest revision as of 12:09, 15 February 2025

Overview[edit]

VG, also known as nerve agent VG, is a chemical compound that belongs to the class of organophosphates. It is a potent acetylcholinesterase inhibitor, which disrupts the normal function of the nervous system by preventing the breakdown of the neurotransmitter acetylcholine. This leads to an accumulation of acetylcholine in the synaptic cleft, causing continuous stimulation of muscles, glands, and central nervous system functions.

Chemical Properties[edit]

VG is structurally similar to other nerve agents such as VX and Sarin. It is characterized by its phosphorus-sulfur bond and the presence of a thioether group. The chemical formula for VG is C7H16NO2PS, and it is typically a colorless to yellowish liquid at room temperature.

Mechanism of Action[edit]

VG acts by irreversibly binding to the active site of the enzyme acetylcholinesterase. This enzyme is responsible for the hydrolysis of acetylcholine into choline and acetic acid, a process that is crucial for terminating synaptic transmission. Inhibition of acetylcholinesterase by VG results in the accumulation of acetylcholine, leading to overstimulation of cholinergic receptors throughout the body.

Symptoms of Exposure[edit]

Exposure to VG can result in a range of symptoms due to its effects on the autonomic nervous system and somatic nervous system. These symptoms include:

Miosis (constriction of the pupils)
Bronchoconstriction and respiratory distress
Muscle twitching and fasciculations
Seizures
Bradycardia (slow heart rate)
Hypotension (low blood pressure)

Treatment[edit]

The primary treatment for VG exposure involves the administration of atropine and pralidoxime. Atropine acts as a muscarinic antagonist, blocking the effects of excess acetylcholine at muscarinic receptors. Pralidoxime reactivates acetylcholinesterase by cleaving the bond between the enzyme and the nerve agent, if administered promptly.

Related Pages[edit]

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-{{Short description|Organophosphorus chemical compound}}
+{{DISPLAYTITLE:VG (nerve agent)}}
-{{Use dmy dates|date=October 2023}}
-'''VG''' is a [[nerve agent]] of the [[organophosphorus]] class, similar in structure and function to other agents such as [[VX (nerve agent)|VX]]. It is a potent inhibitor of the enzyme [[acetylcholinesterase]], leading to the accumulation of [[acetylcholine]] in the synaptic cleft and resulting in continuous stimulation of [[muscle]]s, [[gland]]s, and [[central nervous system|central nervous system structures]].
+== Overview ==
+[[File:VG-2D-skeletal.png|thumb|right|200px|Skeletal structure of VG nerve agent]]
+VG, also known as [[nerve agent]] VG, is a chemical compound that belongs to the class of [[organophosphates]]. It is a potent [[acetylcholinesterase inhibitor]], which disrupts the normal function of the [[nervous system]] by preventing the breakdown of the neurotransmitter [[acetylcholine]]. This leads to an accumulation of acetylcholine in the synaptic cleft, causing continuous stimulation of [[muscles]], [[glands]], and [[central nervous system]] functions.
-==Chemical structure and properties==
+== Chemical Properties ==
-VG is an organophosphorus compound with the chemical formula C<sub>11</sub>H<sub>26</sub>NO<sub>2</sub>P. It is a [[chiral]] molecule, meaning it has non-superimposable mirror images, or [[enantiomer]]s. The compound is typically a colorless liquid at room temperature and is known for its high toxicity and persistence in the environment.
+VG is structurally similar to other nerve agents such as [[VX (nerve agent)|VX]] and [[Sarin]]. It is characterized by its phosphorus-sulfur bond and the presence of a [[thioether]] group. The chemical formula for VG is C7H16NO2PS, and it is typically a colorless to yellowish liquid at room temperature.
-[[File:VG-2D-skeletal.png|thumb|right|Skeletal formula of VG]]
+== Mechanism of Action ==
+VG acts by irreversibly binding to the active site of the enzyme [[acetylcholinesterase]]. This enzyme is responsible for the hydrolysis of acetylcholine into [[choline]] and [[acetic acid]], a process that is crucial for terminating synaptic transmission. Inhibition of acetylcholinesterase by VG results in the accumulation of acetylcholine, leading to overstimulation of [[cholinergic receptors]] throughout the body.
-==Mechanism of action==
+== Symptoms of Exposure ==
-VG acts by inhibiting the enzyme acetylcholinesterase, which is responsible for breaking down acetylcholine in the synaptic cleft. The inhibition of this enzyme leads to an accumulation of acetylcholine, causing continuous stimulation of [[muscle]]s and [[nerve]]s. This results in symptoms such as [[muscle twitching]], [[paralysis]], [[respiratory failure]], and potentially death if not treated promptly.
+Exposure to VG can result in a range of symptoms due to its effects on the [[autonomic nervous system]] and [[somatic nervous system]]. These symptoms include:
+* [[Miosis]] (constriction of the pupils)
+* [[Bronchoconstriction]] and respiratory distress
+* [[Muscle twitching]] and [[fasciculations]]
+* [[Seizures]]
+* [[Bradycardia]] (slow heart rate)
+* [[Hypotension]] (low blood pressure)
-==Symptoms of exposure==
+== Treatment ==
-Exposure to VG can result in a range of symptoms, depending on the dose and route of exposure. Initial symptoms may include [[miosis]] (constriction of the pupils), [[rhinorrhea]] (runny nose), and [[dyspnea]] (difficulty breathing). As exposure increases, symptoms can progress to [[convulsions]], [[coma]], and [[respiratory arrest]].
+The primary treatment for VG exposure involves the administration of [[atropine]] and [[pralidoxime]]. Atropine acts as a [[muscarinic antagonist]], blocking the effects of excess acetylcholine at muscarinic receptors. Pralidoxime reactivates acetylcholinesterase by cleaving the bond between the enzyme and the nerve agent, if administered promptly.
-==Treatment==
+== Related Pages ==
-The primary treatment for VG poisoning involves the administration of [[atropine]], which acts as an [[antagonist]] to acetylcholine at muscarinic receptors, and [[pralidoxime]], which can reactivate acetylcholinesterase if administered soon after exposure. Supportive care, including [[ventilation]] and [[oxygen therapy]], may also be necessary.
+* [[Nerve agent]]
+* [[Acetylcholinesterase]]
-==History and development==
-VG was developed as part of a series of nerve agents in the mid-20th century. It was one of several compounds investigated for potential military use due to its high potency and persistence. However, like other nerve agents, its use is restricted under the [[Chemical Weapons Convention]].
-==Related pages==
 * [[VX (nerve agent)]]
 * [[Sarin]]
-* [[Tabun (nerve agent)]]
+* [[Organophosphate poisoning]]
-* [[Chemical Weapons Convention]]
-==References==
-* {{cite book |last=Sidell |first=Frederick R. |title=Medical Aspects of Chemical and Biological Warfare |publisher=Office of The Surgeon General, Department of the Army, United States of America |year=1997 |isbn=978-0-16-045135-3}}
-* {{cite journal |last=Eddleston |first=Michael |title=Organophosphorus poisoning |journal=BMJ |year=2008 |volume=334 |issue=7594 |pages=629–634 |doi=10.1136/bmj.39134.566979.BE}}
 [[Category:Nerve agents]]
 [[Category:Organophosphates]]