
Poisonous plants have a seed, root, leaf, stalk, fruit or juice where even a relatively small amount, taken either internally or eternally, can lead to injury to the human body. In some species the poisonous constituents occur throughout the whole plant. In others they are concentrated in one or more parts. The degree of toxicity also depends on the location (including height above sea level), climatic factors including the local microclimate (light, warmth, humidity), the growing season, type of soil, fertilisation, plant variety and age. Some plants are harmless unless they have been contaminated with fungi or live in symbiosis with these. One example which is well-known to farmers is tall fescue grass, Festuca arundinacea, infected with the endophytic fungus Neotyphodium coenophialum (previously known as Acremonium coenophialum). The endophyte gives the plant several advantages such as resistance to some insects and soil nematodes, better tolerance of drought, but cattle eating infected grass will exhibit signs of poisoning.
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The condition of the poisonous plant material is equally important (dried, chewed, cooked, as tea). The dose of course is the most important factor. Small children form the most important risk group. Babies and toddlers always stick things in their mouths, including poisonous berries and leaves. What is more, children react much more quickly to poisonous substances than adults, because their body weight is much lower. The poisonous substances therefore reach considerably higher concentrations. Data from the Antipoison Centre in Brussels show that children under the age of 4 in Belgium are at as much risk as all other age categories put together. Those who seek healing or nutrition by wild plants are also at a higher risk of poisoning. Herbal medicine also involves similar dangers. The difference between the terms ‘medicinal’ and ‘poisonous’ is sometimes smaller than one might think.

Some plants contain substances which induce toxic effects when the plant is eaten or the juice is drunk. We do not of course mean the insecticides or fungicides which remain on edible vegetables after harvest. Sometimes individual sensitivity plays a role, as in favism (some people with severe G6PD-deficiency exhibit haemolysis after eating fava beans). However, there is generally good correlation between the amount of poison ingested and the severity of the clinical symptoms. The best known example in history is the forced suicide of Socrates. He drank a poison cup with the juice of hemlock (Conium maculatum) and in the following hours related his progressive symptoms to his friend, who recorded them. In the Far East opium was the poison used for murder and suicide for many years. Aconitum sp. (monkshood with the deadly aconitine), Strophantus species, Strychnos nuxvomica (vomit nut, with strychnine), Strychnos toxifera, Datura stramonium (thornapple), Urechites suberecta (in the Caribbean) and Cerbera odollam are further examples of very poisonous plants. In the Caribbean huratoxin, obtained from Hura crepitans was (and is) a powerful local indigenous plant arrow poison. Buckthorn poisoning is seen in Mexico and Central America and often mistaken for Guillain-Barré or poliomyelitis. In South America various plants were used to prepare curare.
Do not mistake curare for blow dart poison (batrachotoxins) obtained from wild "poison arrow frogs" such as Phyllobates terribilis (fam. Dendrobatidae). Sometimes the effect of poison is only noticeable after long-term exposure, e.g. the neurotoxic effect of the laxative Senna on the myenteric plexus of the colon. Repeated and long-term use reduces the peristalsis and make constipation worse, so that the patient again turns to the laxative agent. Sometimes the poison is active when administered parenterally, but is destroyed in the stomach or intestine. Thus a prey killed by a dart or an arrow tipped with curare, can be safely eaten afterwards.*
Some plants contain psychoactive substances. Among these are the peyotl cactus which contains mescaline and plays a part in traditional Indian society. It is sometimes confused with mescal beans, which contain LSD. Less well-known is the ayahuasca liana (Banisteriopsis caapi, fam. Malpighiaceae) from the Amazon basin. The plant contains 1 to 2% beta-carbolines such as harmine, tetrahydroharmine and harmaline. The name is taken from Peganum harmala (Zygophyllaceae), an Indian weed that contains the same constituents and is toxic for cattle. These substances are indole alkaloids, derived from the amino acid tryptophan and structurally related to serotonin. They are monoamine-oxidase inhibitors. Extract of B. caapi is often mixed with Psychotria viridis, another hallucinogenic plant which contains N,N,dimethyltryptamine. Extracts of Brunfelsia (which contains scopoletin) and Brugmansia (which contains atropine and scopolamine) are also used. In South America it has been known that inquisitive tourists, having heard an intriguing story, have drunk tea or the juice of Banisteriopsis caapi, after which they became confused, hallucinated and exhibited psychotic reactions. Not all acute confused states in tourists can be attributed to mefloquine! Ibogaine is an alkaloid compound that comes from the roots of a shrub, Tabarnathe iboga, which grows in Gabon, Africa. In the country, followers of the Bwiti religion use it in ceremonies for its vision-giving properties. The hallucinogenic compound is being investigated for its impressive ability to stop morphine, heroin and cocaine craving for prolonged periods. This might help drug addicts to overcome their addiction. Less toxic derivatives, such as 18-methoxycoronaridine and noribogaine, are also being evaluated.
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An indirect effect of poison is illustrated by the following story. In 1860-61 Robert O’Hara Burke, William John Wills, John King and Charles Gray were the first Europeans to cross the Australian continent from Melbourne in the south to the Gulf of Carpentaria in the north. However, all except King died on the return journey. King was left with permanent disturbance of gait. Extreme fatigue, disturbed gait, painful joints and weak pulse preceded death. Why did they die? Because of various difficulties the explorers had to live off the land, including from fresh water mussels (Velesunio ambiguus) and nardoo flour. This flour was obtained from the nardoo fern (Marsilea drummondii). The shellfish and in particular the nardoo flour contained a large amount of heat resistant thiaminase, so that the members of the expedition developed acute beriberi. (The thiaminase can be leached out by washing the plant in water. This permits its use by the aborigines. The explorers did not know this). In veterinary medicine beriberi in horses has long been known (staggers), due to eating Pteridium aquilinum, a related plant.

Organic compounds containing nitrogen, most of which exhibit strong physiological activity. e.g. colchicine, nicotine, aconitine, taxine, cocaine and many others.
Examples
These substances are constructed from an aglycon to which one or more sugar chains are bound.
