24

Season 5; Episode 13; 7:00-8:00 p.m.


"Attention all CTU personnel, this facility has been contaminated with Sentox VX-1 nerve gas!"

U.K. CERTIFICATE: 15

RUNTIME: 44 mins

VIDEO CLIP: CLIP 1, CLIP 2

SOUND CLIP: AUDIO

SYNOPSIS: Russian separatists utilize a fictional variant of VX called "Sentox VX-1" from a weaponized canister on American soil.


VX (Nerve Agent)

History: Developed in the Porton Down Chemical Weapons Research Centre, Wiltshire, England in 1952. Britain traded this deadly VX technology with America for information on thermonuclear weapons.

Properties: With its high viscosity and low volatility, it is normally in its liquid state despite its name, and has the texture and feel of high-grade motor oil. This makes it especially dangerous, as it has a high persistence in the environment. It is odourless, tasteless and is an excellent adhesive, which can be distributed as a liquid or, through evaporation, into small amounts of vapour. 


 

Click on the picture above to interact
with the 3D model of the
VX Gas structure

Chemical Formula: CH3CH2O-P(O)(CH3)-SCH2CH2N(C3H7)2

Chemical Name: O-ethyl S-(2-diisopropylaminoethyl) methylphosphonothioate
Molecular Formula: C11H26NO2PS


Mode of Action
 

Mason: What exactly does this stuff do?
Goodspeed: It's a cholinesterase inhibitor. Stops the brain from sending nerve messages down the spinal cord within thirty seconds. Any epidermal exposure or inhalation and you'll know. A twinge at the small of your back as the poison seizes your nervous system. Your muscles freeze, you can't breathe, and you spasm so hard you break your own back and spit your guts out. But this is after your skin melts off. (The Rock)

 

VX works as a nerve agent by inhibiting the function of the enzyme acetylcholinesterase. Normally, an electric nerve impulse would result in the release of acetylcholine over a synapse, stimulating a muscle contraction. The enzyme subsequently hydrolyses (breaks down) acetylcholine into acetic acid and choline (non-reactive substances). If more muscle tension is required then the nerve must release more acetylcholine.


Acetylcholine

Once absorbed through the eyes, skin, or via inhalation, the phosphorous atom of VX covalently binds to a serine hydroxyl group in the active site of acetylcholinesterase, inactivating the enzyme and thus preventing acetylcholine hydrolysis. This results in sustained contractions of all muscles in the body. Ultimately constant stimulated contraction of the diaphragm muscle causes death by asphyxiation.

 

 

Click on the image to view the the protein structure (-helices and -strands) of the acetylcholine receptor.

The mechanism of action of acetylcholinesterase 

 


Death: Nerve gases generally cause death by asphyxiation. The symptoms preceding this include:

  • Blurred vision
  • Runny nose
  • Slurred speech
  • Tightness in the chest and constriction of the pupils
  • Breathing difficulties, along with vomiting, drooling, urinating, defecating
  • Areflexia (loss of reflexes)
  • Ataxia (lack of muscle control) - twitching and jerking

After the victim has lost control of their bodily functions, they will lapse into a coma and suffocate to death as a result of convulsive spasms.

Antidote: Atropine, although a toxin itself this anti-nerve agent counteracts the deadly effects of VX by removing it from the enzyme. It is normally administered by injecting intravenously into the arm or thigh, however for gaseous attacks atropine must go immediately into the heart.

 


Atropine

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