Crotylsarin

From WikiMD's Food, Medicine & Wellness Encyclopedia

Crotylsarin (also known as O-Isobutyl S-2-(N,N-diethylaminoethyl) methylphosphonothioate) is a lethal organophosphorus compound that is structurally related to the nerve gas sarin. It is a potent acetylcholinesterase inhibitor, which means it prevents the breakdown of acetylcholine in the body, leading to a build-up of this neurotransmitter and causing overstimulation of the muscles and glands.

History[edit | edit source]

Crotylsarin was first synthesized in the mid-20th century as part of a series of organophosphorus compounds with potential for use as chemical warfare agents. Its lethal effects were quickly recognized, and it was classified as a nerve gas due to its mechanism of action.

Structure and Properties[edit | edit source]

Crotylsarin is a liquid at room temperature and has a slightly fruity odor. It is highly volatile, which means it can easily evaporate and be inhaled. Its chemical formula is C9H20NO2PS, and it has a molecular weight of 247.31 g/mol.

Mechanism of Action[edit | edit source]

Crotylsarin inhibits the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine in the body. When acetylcholinesterase is inhibited, acetylcholine accumulates in the body, leading to overstimulation of the muscles and glands. This can cause a range of symptoms, from mild discomfort to severe respiratory distress and death.

Symptoms of Exposure[edit | edit source]

Exposure to crotylsarin can cause a range of symptoms, depending on the dose and route of exposure. These can include difficulty breathing, blurred vision, drooling, excessive sweating, nausea, vomiting, diarrhea, and seizures. In severe cases, exposure can lead to respiratory failure and death.

Treatment[edit | edit source]

Treatment for crotylsarin exposure involves removing the victim from the source of exposure, decontaminating their skin and clothing, and administering antidotes such as atropine and pralidoxime. These drugs work by blocking the effects of acetylcholine and reactivating acetylcholinesterase, respectively.

See Also[edit | edit source]

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Contributors: Prab R. Tumpati, MD