Curare is a general name for a number of plant-derived poisons known to be used by South and Central American tribes. Curare is an alkaline poison, meaning that the poison is basic in pH, or exists above a pH of 7.
There are many plants from which curare can be derived, as many plant poisons have evolved to defend the plants from attack from mammalian herbivores. Hunters from South American tribes often used this to their advantage by tipping their arrows in curare.
The poison causes paralysis of the muscles and can eventually lead to death if the diaphragm becomes paralyzed.
Structure of Curare
Curare is made up of organic compounds that are known as isoquinoline or indole alkaloids. Tubocurarine is the main active ingredient in the South American dart poison tubocurarine.
Tubocurarine is an alkaloid, a naturally occurring compound made up of nitrogenous bases, though the chemical composition of alkaloids varies greatly.
Curare binds to Acetylcholine receptors because the three compounds have similar functional groups.
Tubocurarine and C toxiferine, like most alkaloids, are made up of a cyclic framework with a nitrogen atom in an amine group. Acetylcholine, on the other hand, does not have a cyclic system but does have an amine group.
Properties of Curare
- Curare is a non-depolarizing muscle relaxant that works at the neuromuscular junction by blocking the nicotinic acetylcholine receptor (nAChR), one of two forms of acetylcholine (ACh) receptors.
- Curare’s key toxin, d-tubocurarine, binds to the same receptor as ACh with equal or greater affinity and produces no response, rendering it a competitive antagonist.
- Curare compounds are too large and highly charged to move through the lining of the digestive tract and be absorbed into the bloodstream if taken orally. As a result, people can easily consume curare-poisoned prey, and the taste is unaffected.
- The onset time of curare ranges between one minute (for tubocurarine in intravenous administration, entering a larger vein) and 15 to 25 minutes (for tubocurarine in intravenous administration, penetrating a smaller vein) (for intramuscular administration, where the substance is applied in muscle tissue).
Preparation of Curare
Alexander von Humboldt published the first first-hand account of curare preparation in 1807. For two days, a mixture of young Strychnos plant bark scrapings, other washed plant bits, and sometimes snake venom is boiled in water.
This liquid is then strained and evaporated, yielding a dark, thick, viscid paste that will be checked later for potency. The flavor of this curare paste has been characterized as bitter.
Richard Gill and his expedition collected samples of processed curare and identified its traditional preparation method in 1938; Chondrodendron tomentosum was one of the plant species used at the time.
The preparation includes a variety of irritating plants, stinging insects, poisonous worms, and assorted amphibian and reptile pieces. Some of these hasten the onset of action or increase toxicity, while others obstruct wound healing or blood coagulation.
What is curare and what was it originally used for?
Curare is the name given to various highly toxic substances used by certain indigenous tribes in South America to poison their hunting arrows.
Curare is also the name given to the plants that produce toxic substances.
Curare paste was applied to arrowheads and used to kill prey when hunting. Animals struck by the poisoned arrowheads are unable to run away and die within minutes.
Where does Curare come from?
The various highly toxic substances referred to as ‘curare’ are extracted from plants. Curare can be extracted from plants such as those from the genus Strychnos, including S. toxifera and S. castelnaea, and plants from the Menispermaceae family, including chondrodendron tomentosum.
How does Curare work?
Curare works in different ways depending on the plant it is extracted from and exactly what toxin it is. In general, however, curare is known for being a neurotoxin that can cause muscle paralysis when it enters the bloodstream.
Curare is specifically a non-depolarising neuromuscular blocking agent (NMBA). It blocks neuromuscular transmission – a process that allows the central nervous system (CNS) to control the movement of muscles – at the neuromuscular junction, which is the junction between a nerve cell and a muscle cell.
Curare causes muscle paralysis by acting as a competitive acetylcholine (ACh) antagonist. ACh is a neurotransmitter that is released into the neuromuscular junction to enable the transmission of information between nerve and muscle cells.
Curare binds directly to nicotinic receptors on the postsynaptic membrane of the neuromuscular junction, which prevents the binding of ACh and depolarization of the motor endplate, leading to muscle paralysis. Curare repeatedly binds and dissociates from the receptor, so it can be displaced by ACh and its effects reversed.
When curare is taken by mouth it has no effect on people.
What medical uses did curare have?
During the late 19th and early 20th centuries, curare began to be used for the treatment of various diseases, including hydrophobia (an irrational fear of water and symptom of rabies), chorea (jerky involuntary movements), epilepsy, and conditions causing muscle spasms.
In psychiatric patients, it was used during shock treatment to help modify convulsions and was also used from time to time for the treatment of tetanus over a period of 80 years.
A purified version of curare called intocostrin was first used as a muscle relaxant during surgery on January 23, 1942, in a 20-year-old man having his appendix removed. Curare was subsequently replaced by more modern neuromuscular blockers such as pancuronium.