Black Nightshade(8)
NightShade Alkaloid Toxins
Atropine, Scopolamine and Solanine

  Nightshade is just not one plant, but the term representsa family of toxic plants, Solancae . The plants are present throughoutthe world,with different species prevalent in different areas. These plantsproduceseveral toxins, such as atropine,scopolamine, and solanine. Thesetoxinsare most concentrated in the berries,even though all of the partsoftheplant are considered toxic. These alkaloidtoxins affect the neurotransmitteracetylcholine. Atropine and scopolamineare cholingeric antagonists, whilesolanine is an cholinesterase inhibitor.The antagonists cause excessive sympatheticstimulation, while cholinesteraseinhibtors will cause parasympatheticeffects.Since they are so toxic, thankgoodness, the nightshade plants are bitter tasting.

Soluble in alchol, benzene, glycerol, and dilute acids
LD50 in rats: 750mg/kg orally(5)
Scopolamine(13)C17 H21NO4Soluble in water, alcohol. insoluble in ether
LD50: 3800 mg/kg subcutanous(5)

Scopolamine and Atropine

Scopolamine and Atropine are found naturally in the plants of the Solancaefamily. Jimson weed (Daturastramonium), belladonna (Atropa Belladonna),and henbane (Hyocyamus niger)are found in all corners of the UnitedStatesand throughout the world. Animalpoisoning with these plants israre, sincethe alkaloids present in the plantmake it bitter tasting andmost animalsavoid them.

Poisoning with any of theseplants can be deadly, even with small doses.Atropine and Scopolamine arecholingeric antagonists, which means they interactwith acetylcholine bindingsites of neurons. Acetylcholine is the neurotransmitterfound at the terminalsof all preganglionic neurons and at the ending of allpostganglionic fibersof the parasympathetic nervoussystem and mediates theimpulses for skeletalmuscle control (2). The autonomic nervous system isthe "fight or flight"response, consisting of parasympatheticand sympathetic branches. The parasympathetic branch commands the day todayactions of the body, while the sympathetic branch is involved in the immediatesurvival response. The sympathetic system will increase heart rate, respirationrate, dilate the pupils, decrease digestion, decrease salivation, increasebody temperature, shunt blood to the limbs,and increase alertness.The parasympatheticsystem has just the opposite effect; it calms the body back into a state ofnormal rhythms and digestion. These two systems work against each other andare both active at all times. Theeffects of one are seen when that system isstimulated or the other systemis inhibited.

Since atropine and scopolamine bind to the receptors for acetylcholine,there is a lack of parasympathetic stimulation. Symptoms would be like thatofexcessive sympathetic stimulation. Mydriasis, or dilation of the pupils, impairedvision, muscle spasms, flushed skin, increased body temperature with a lackof sweating and increased heart rate and respiration are seen in patients poisonedby atropine. Differentanimals have different tolerance levels for possible digestion ofthese plants.Horses have a very high death rate after consumption of Jimson weed.In oneequine study, eleven out of 15 horses showing symptoms died.Pigs cantolerate2.2mg of Jimson weed seeds, but  at 2.7mg,pigs begin to showsigns ofpoisoning. Poultry on the other hand, can eat up to 15g of seed a dayandhave no ill effects (3).

Jimson Weed Plants and seeds(8)

Once poisoned with atropineor scopolamine, seek emergency medical attention!Treatment at the emergencyroom will include stomach lavage and/or irrigationof the colon to removethe plant material and toxin as quickly as possible.These poisons have ashort half life and are quickly biotransformed and excreted from the body.Morphinecan be titrated intravenously to counteract or amyl nitrate can beinhaled(10). Physostigmine, a cholinesterase inhibtor, can be cautoiuslyused ifthe situation is dire(8). If no medical facilities are available,vinegar canbe given to the victim orally. Vinegar is acidic and since thesemolecules can be protonated,rendering them lipophobic and unable to be absorbedby the body and thus quicklyexcreted in the urine (1)

These poisons also have therapeutic uses. Atropine is used as a "antidote"for organophosphate poisoning, Organophosphates are cholinesterase inhibitors,preventing the breakdown of acetylcholine and causing prolonged stimulation.Atropine is used to block the sites for acetylcholine and reduce the stimulation.This buys time to treat the organophosphate poisoning effectively. Atropinecan also be used to dilate the eyes for wide angle glaucoma. Atropine canalso be used for treating tremor disorders, since it effectsthe acetylcholineat the neuromuscular junctions also. Scopolamine is widelyused as an antinausea drug and as a precursor togeneral anesthesia.

Interesting Facts about Atropine and Scopolamine

In William Shakespeare's Hamlet, Hamlet's father, the king of Denmarkwaspoisoned with "henbone" dripped into his ear while he slept.  Shakespeare's henbone was quite possibly the plant today known as henbane. The membranes of the ear would have been permeable to scopolamine(toxic principle of henbane) and the quick absoption into the bloodstream would resulted in a fast onset of symptoms and death. Such aquick death resulted, that the King of Denmark was unable to confess hissins and was condemned to wander through purgatory forever(6).
henbane Henbane(8)

Henbane was widely used as a way of making beer more potent. In one of stories of ancient Egypt, Hathor was created by her father Re as the Sekmet, or the destroyer of men, who were disobedient to him. Later Re changed his mind, but even he could not stop her from killing men. He then disguised beer as blood, laced the beer with henbane and when Sekemt became drunk,she could no longer kill and was known thereafter as Hathor, a goddess oflove(6). The Egyptians must have believed that not only was beer fun, butthat it saved the world and could change a killer into a lover.

Atropine was used in witches ointment, which was thought to allow thewitchto have sex with the devil.The ointment was applied all over thebody andin orifices (vaginally, anally). This created feelings of flying,dancing,love, and hallucinations. Ointment users couldn't discern realityform theirdrug-induced state. It was even thought that the plant from which the ointmentwas made were only found under thegallows where a evilperson was hanged.Their urine or semen were the seedfor these plants.

blue nightshade
Blue Nightshade(8)


Solanine is found in blue nightshade (Solanum dulcamara), black nightshade(Solanum nigrum), potatoes (Solanumtuberosum), tomatos (Lycoperiscon esculentum),green peppers, and ornamentalJerusalem cherries (Solanum pseudocapsicum).The most poisonous componentis the unripe berries, but all of parts oftheplant contain solanine. Thealkaloids are very bitter tasting and arefoundin disturbed soil, such asin gardens, fence posts, and along highways.Poisoningis very rare, sincemost animals have no interest in this plant.Only curiousyoung animals orbored confined animals, will sample the plant.Animals willalso eat this plantif no other nutrition in available. Human poisoning isusually accidental.The huckleberry looks very similar toblack nightshade;it is even thoughtto be a domesticated form of the deadly nightshade plant.Children who eathuckleberries may mistake the purple-blackberries of theblack nightshadefor the delicious huckleberry and become poisoned (4). Unripepotatoes andtomatoes peelings also have high levelsof the toxin and poisoningshave beenreported.

Solanidine(15)                                                                                                    Solanine(15)

This glycoalkaloid is has asugar component attached to a steriod-likepart, solanidine. Solandine aloneis much less toxic. The sugar is necessary for the extreme toxicity. Solanineis very poisonous even in very small quantities.The LD50 in mice is 42 mg/kgwhen injected peritoneally(5). A fatal human dose can be as little as 420mg.It is much more toxic when injected since solanine is poorly absorbed through the gut wall. If not absorbed, the body will begin biotransformation and cleave the glycoalkaloid into the sugar and solanidine. These are excreted from the body via the feces.

Solanine acts to cause destruction in two different ways. It is a gastrointestinal irritant. It directly irritates the mucous membranes of the gastrointestinaltract and if absorped into the bloodstream, will cause the hemolysis of erthrocytes(3). In addition to directly causing cellular damage, it causes neurologic effects. Unlike atropine and scopolamine, solanine affects the enzyme that breaks down acetylcholine. Likethe organophosphates, it inhibts the breakdown of the parasympathetic neurotransmitter, acetylcholine.Solanine neural effects are characterized by excessive stimulation of the parasympatheticnervous system. Signs of solanine poisoning are apathy,excessive salivation,diarrhea,and a decreasein heartrate and respirationwhich can lead to cardiacarrest.

Treatment for solanine poisoning is mostly supportive. In animals, fluid levelsmust be monitored and maintained. Vasopressors and cardiac monitoring are alsoa key treatment for seriously ill animals (4). If diarrhea is present, surivialis good; the body is actively flushing the toxin out. In humans, emesis orvomiting will be induced at the hospital and supportive treatmentwill be given(7).Without medical advicefrom a physican or the Poison Control Center, vomitingshould not be induced.This poisoning is very serious and should only be treated by a medical professional.

Interesting facts about Solanine

Tomatoes are prized by humans for their cancer-fightingantioxidants. People eat these to gain their benefits and may try to extendthis benefit to their pets. A cat can be fatally poisoned by just 100g of ripetomato(11)! that someone carelessly left out or if unknowing of the danger, tries to feed their animal. Even though catswill not normally eat tomatoes, bored animals or young young animals will. This cat was in the hospitalfor two weeks, excessively vomiting, continous diarrhea, dehydration, and the inability tomove. The cat barelyrecovered even after such a small dose.

Potato farmers harvest their crop before ripening to prevent the spreadof viruses. The green vines are often used as animal feed. Yet if cattle or pigs are fed the peeling of unripe or spoiled potatoes, the poisioning and death rates will incrase dramatically.This is because the toxinis more concentrated in the fruit (or the reproductiveportion of the plant, such as the eye of the potato).

In the 1960's, the search for a new potato was completed. The UnitedStateshas interested in producing a potato strictly for french fry production. Lenapewas an excellent candiate. This crossbred potato had all the qualitesofagreat french fry potato. After commerical production, it was found that Lenapehad very high levels of solanine. Fourteen mg/100g causes a bitter taste andabove twenty mg/100g causes a burning in the mouth and throat. Lenape was foundto have 30mg/100g. This createda new standard that all potatoes had to be testedfor levels of solanine prior to production (2).

Your mom was right; don't eat green potatoes or old potatoes! Exposure to light or stress (or evenaging) causes transformation of a potato's amyloplasts to chloroplasts, followedby thesynthesis of the green pigment, chlorophyll. Light, stress, and aging also causethe potato to produce chaconine and solanine. The appearance of chlorophyll is thus a warning that something is wrong with the potato. About 30% to 80%of the glycoalkaloid content of a potato is inits peel with the remainderin the flesh of the tuber(15). And don't think that just cooking the greenpotato will deactivate the toxin. Boiling, microwaving, or freezing as noeffect on the toxin. Deep-frying (my favorite) has been shown to reduce thelevels of toxin(15).

Points to Ponder
The Nightshade family members make two distinctly different catergories of toxins. No one plant hasd both kinds of toxins since the toxins have opposite effects. The Atropine side of the family makes cholingeric antagonists, causing depression of the parasympathetic system, while the Solanine producers make cholinesterase inhibtors, causing stimulation of the parasympatheic branch of the central nervous system. Nowhere in the literature mentioned that possibly one member of the family could be used (carefully!!!) to treat the poisoning from another type of nightshade. Nightshade can be the family that honestly has both the poison and the cure(depending on the circumstances)!

One question remains; why doesthe plant produce these toxins in the first place? These toxins could beserving as a defense mechanism. Since the alkaloids cause the plant to bebitter tasting and the effects of low dose consumption are uncomfortableto an animal, these poisons could prevent the plants from being grazed onand destroyed. They could also serve as a fungicide or an insecticide toprevent damage to the plant.


1.Bailey, Christina. Notes from Chem 377-Drugs and Poisons. Fall 2000

2.Cheeke, Peter and Skull, Lee. Natural Toxicants in Feeds and PoisonousPlants.AVI.1985. Pgs. 131-135

3.Clarke, EGC and Clarke Myra. Garner's Veterinary Toxicology3rd edition. Williams and Wilkins Co. 1967. Pgs. 395-397

4.Ellenhorn, Matthew. Ellenhorn's Medical Toxicology. WilliamsandWilkinsCo. 1997. Pgs. 1854-1855.

5.Merck Index 12th edition.Merck and Co INC. 1996 Pg 148-149, 1444,1485-1486

6.Muller, Jurgen. "Love Potions and The Ointment of Witches:Historical Aspects of the Nightshade Alkaloids". Clinical Toxicology.Vol. 36. 1998. Pgs. 617-627.

Web References

7."Blue Nightshade". WebMDHealth. 1999.

8.Guide to Poisonous Plants. Colorado State Veterinary Science Department.


10. "Poisons and Antidotes."

11."Poisoned by Tomato"