Group ProjectAmanita Mushrooms

Toxins

Ahmed AlghrouzAli Ahmed

James OlguinTristan Malin

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Amanita Mushrooms

History & Background

Species: A. muscaria (Fly Agaric) A. phalloides (Death Cap) A. virosa (Destroying Angel)

References

History & Background Introduction: A history of interaction.

Timeline

Psychoactive Compounds

Neuropharmacology of Psychoactive Amanita Compounds

References

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A History of InteractionA. muscaria has been proposed as the true

entity behind Soma, the apple in the Garden of Eden, the apples of Hesperides, the Golden Fleece, the fire of Prometheus, Kakulja kurakan ‘Lightning bolt One-leg’ of the Mayans, the Huitzilapochtli aspect of Tezcatlipoca of the Aztecs, Jesus Christ, and Santa Claus. (Hajicek-Dobberstein 1995)

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In today’s modern culture: A. muscaria makes appearances in gnome and fairy folklore/ornaments, in Alice in Wonderland, the Smurfs, Disney’s Fantasia, and the Super Mario Bros franchise.

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TimelineThe use of A. muscaria began sometime after

the last Ice Age in the northern Eurasian forest belt and spread north following the retreating polar ice cap, approximately 9,000 BCE. (Wasson 1968)

5,000-3,000 BCE: Earliest linguistic evidence of known intoxication from ingestion of A. muscaria.~4000 BCE: The Uralic language split into two

branches, containing similar root words for inebriation. The root "pang" signifies both 'intoxicated' and the A. muscaria. (Wasson 1968)

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1000-2000 BCE: Petroglyphs along the Pegtymel River in north eastern Siberia.The Chukchi culture, the areas current inhabitants, are known to have used A. muscaria. (Ott 1996)

1200 BCE: Rg Veda hymns mention a magical intoxicant called Soma.In 1968, R. Gordon Wasson published Soma: Divine Mushroom

of Immortality, arguing that Soma refers to A. muscaria.

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100 CE: 7.5 cm tall miniature statue of an A. muscaria, found in Nayarit, Mexico.

1250 CE: Albertus Magnus describes the insecticidal properties of A. muscaria, in De vegetabilibus. (Letcher 2007)These properties

led to the common name "fly agaric".Next

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1291 CE: Art

historians argue that this is a conventionalized tree type, prevalent in Romanesque and early Gothic art, referred to as a "mushroom tree". (Wasson 1968) Next

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1658 CE: Polish prisoner of war writing about a culture from western Siberia (Ob-Ugrian Ostyak of the Irtysh region): "They eat certain fungi in the shape of fly-agarics, and thus they become drunk worse than on vodka, and for them that's the very best banquet." (Wasson 1968) Originally published in Kamiensky Dluzyk.

Diary of Muscovite Captivity (1874) pg 382.1730 CE: Swedish Colonel Filip Johann von

Strahlenberg gives detailed descriptions of Siberians consuming tea made from A. muscaria and drinking the urine of those who previously ingested the mushroom, recycling the intoxicating ingredients. (Wasson 1968)Next

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1753 CE: Linnaeus describes the fly agaric mushroom in Species Plantarum: Tomus II. Holmiae (1753), naming it Agaricus muscarius.

1783 CE: Fly agaric placed in Amanita genus by Jean-Baptiste Lamarck. New name Amanita muscaria.  

1968 CE: R. Gordon Wasson publishes Soma: Divine Mushroom of Immortality. (Argument for sacramental use of A. muscaria by Indians in time of Vedas.) Next

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1972 CE: Robert Graves, in Difficult Questions, Easy Answers, proposes that the character of Santa Claus may be based on A. muscaria shamanism.Jonathan Ott later develops this in his book

Hallucinogenic Plants of North America (1976).2002 CE: Clark Heinrich, in Magic

Mushrooms in Religion and Alchemy (2002), argues that A. muscaria has played a large role in the worlds largest religions including: Hinduism, Judaism, and Christianity.

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Psychoactive CompoundsThe primary active chemicals known in

Amanita muscaria and A. pantherina are: Muscimol, Ibotenic Acid, and Muscarine.

There are other chemicals present in trace amounts, below active levels in humans.

The pharmacology of A. muscaria is not fully understood.

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MuscimolMuscimol is considered the principle

psychoactive, with oral dosages of pure muscimol around 10-15 milligrams. (Spinella 2001, Ott 1996)

Muscimol is a potent, selective agonist of the GABA receptor.

Muscimol is the product of the decarboxylation of ibotenic acid.

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Ibotenic Acid Ibotenic acid, another psychoactive

compound, is also active orally, but at doses 5-8 times higher than those of muscimol. (Ott 1996, Schultes 1980)

Shown to be highly neurotoxic by injection directly into mice and rat brains, it is a powerful brain-lesioning agent. (Spinella 2001)

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MuscarineMuscarine was the first

parasympathomimetic substance ever studied.

By mimicking acetylcholine, it causes profound activation of the peripheral parasympathetic nervous system resulting in convulsions and possible death.

Muscarine is present only in trace amounts in A. muscaria.

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Neuropharmacology of Psychoactive Amanita compounds

Muscimol and Ibotenic Acid are both psychoactive.

First let us examine GABA, the primary pathway affected by ingestion of these compounds.

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GABAGABA (gamma-aminobutyric acid) was first

described as a plant and microbe metabolic product, and later identified as integral to the mammalian central nervous system.

In the hippocampus and neocortex, GABA is primarily excitatory in early development, regulating growth, migration, and elongation of neural progenitor cells and the formation of synapses.

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In adult mammals, GABA is the main inhibitory

neurotransmitter, playing an important role in regulating the nervous system.

Agonizing GABA receptors in mammals typically results in calming, anti-anxiety, and anti-convulsive effects.

GABA works by binding to specific receptors in the plasma membranes of pre- and post-synaptic neurons, and causes hyperpolarization.

Three types of receptors: GABAA and GABAC are ionotropic receptors (are ion channels) and GABAB metabotropic, which are G-protein coupled.

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MuscimolMuscimol is a potent agonist of the GABAa,

altering and inhibiting neural activity in the cerebral cortex, hippocampus, and cerebellum.

In vivo, muscimol will pass through the human body and excreted in the urine as muscimol.

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Ibotenic acidWhen ingested, a small portion is

decarboxylated into muscimol, which is the psychoactive effective portion.

Ibotenic acid is used clinically as a brain lesioning agent.Described by Olpe et al. 1978.

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Intoxicating EffectsThe effects of the ingestion of muscimol are

often described as unstructured hallucinations, likened to a lucid dream state.

Effects felt include: visual distortion, hallucination, loss of equilibrium, muscle twitching, and altered sensory perception.

Effects last 6-8 hours, peaking 2-3 hours after ingestion. However, this is dose sensitive, and potency varies between mushrooms.

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Taxonomy / Taxonomic Confusion

DescriptionDistribution / HabitatToxinsSymptoms / Treatment

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Amanita Virosa(The Destroying Angel)

TaxonomyKingdom: Fungi

Phylum: Basidiomycota Class: Agaricomycetes

Order: Agaricales Family: Amanitaceae

Genus: Amanita

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Taxonomic ConfusionDepending on the source, one or more species

of Amanita mushroom are considered to be death angels. However, the general consensus is that there are three types of mushrooms that fit the category. They are: A. bisporiga, A. ocreata, and A. virosa.

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Taxonomic ConfusionOne method used to define the destroying

angel is the potassium hydroxide test (KOH test). When a destroying angel comes into contact with KOH, its flesh turns yellow. One source of taxonomic confusion is that mushrooms, incorrectly labeled as one of the destroying angels, have tested negative on the KOH test, therefore casting doubt on their classification.

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KOH Test

An image of the yellow flesh, that is the result of application of Potassium Hydroxide Next

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Taxonomic ConfusionA. verna has at times also been included in the

category of destroying angel, however, this is not generally considered to be the case. For the purposes of this slide show, the category of destroying angel will include A. bisporiga, A. virosa, and A. ocreata only.

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DescriptionAll destroying angels form ectomycorrhizal

relationships with tree roots.

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DescriptionYoung destroying angels are often spherical or

conical in shape, until they emerge through the universal veil.

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A. virosa at three different stages of life.

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DescriptionOther identifying

characteristics of destroying angels are the partial veil, which forms a ring on the upper stalk, free gills (unattached to stalk), and the volva, or the remnants of the universal veil, found near the base of the mushroom.

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Distribution

A map of the distribution of A. ocreata, a geographically limited species.

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A. virosa occurs all over North America, Europe

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HabitatLike most fungi,

destroying angels tend to grow in moist, low light conditions. They grow near and around trees, and forests, and their mycelium (a structure resembling roots) interact with the tree roots.

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HabitatThe destroying angel’s mycorrhizal relationship

with tree roots is a symbiotic one. The fungus supplies the tree with phosphorous, while the tree nourishes the fungus with sugars.

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Glucose molecules

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ToxinsDestroying angels produce and maintain two

types of toxins: amatoxins and phallotoxins. Amatoxins are considered to be the more dangerous of the two, because phallotoxins are not absorbed through the gastrointestinal tract. In fact, many commonly eaten mushrooms contain phallotoxins.

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Toxins: AmatoxinsAmatoxins consist of several cyclic octapeptidal

compounds, the most toxic of which are α-amanitin and β-amanitin. α-amanitin has a suspected LD50

of .1mg/kg in humans.Name R1 R2 R3 R4 R5

α-Amanitin NH2 OH OH OH OH

β-Amanitin OH OH OH OH OH

γ-Amanitin NH2 OH H OH OH

ε-Amanitin OH OH H OH OH

Amanullin NH2 H H OH OH

Amanullinic acid

OH H H OH OH

Amaninamide

NH2 OH OH H OH

Amanin OH OH OH H OH

Proamanullin

NH2 H H OH HNext

Toxins: AmatoxinsAmatoxins function to

inhibit RNA polymerase II, which is essential to the creation of mRNA and snRNA (small nuclear). With RNA polymerase inhibited, it is impossible to synthesize proteins, and the afflicted cell undergoes apoptosis.

RNA polymerase II unraveling dsDNA

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SymptomsThe symptoms of Amatoxin poisoning occur in

two stages. First, vomiting, diarrhea and other GI symptoms occur. These initial symptoms may last around 2 – 3 days, but are not generally life threatening.

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SymptomsAfter initial symptoms are resolved, the second

set of symptoms begins. Sometimes as many as 1 – 2 weeks pass before the liver begins to fail. The afflicted individual would experience jaundice, and in many cases, hepatic encephalopathy, or the impairment of brain cells due to the buildup of toxic substances usually removed from the body by a healthy liver.

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TreatmentThe only certain way to prevent death from

ingestion of a destroying angel is a liver transplant, which itself carries no small risk. In patients that did recover from destroying angel poisoning, as many as half suffered from irreversible liver damage.

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TreatmentIn addition to a liver transplant, there are

several other treatments that are to some degree effective. Silibinin (from the blessed milk thistle plant) prevents the uptake of amatoxins in hepatocytes that are not yet damaged. One other effect of amatoxins is the depletion of glutathione in the liver. By administering N-acetylcysteine, a precursor to glutathione, this exhaustion of glutathione stores can be averted.

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Amanita Muscaria(Fly Agaric)

• General Facts• Description• Habitat• What people think of A.

muscaria• Toxicity• Symptoms• Treatment• References

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Facts Also known as fly agaric or fly Amanita.

Street names: Magic mushrooms, Liberties, magics, mushies, liberty cap, shrooms, Amani, agaric.

Kingdom: Fungi, Phylum: Basidiomycota, Class: Basidiomycetes, Order: Agaricales, Family: Amanitaceae, Genus: Agaricus.

It’s a psychoactive fungus; affects central nervous system.

It grows in symbiosis with arboreal trees such as Birch, Pine or Fir.

Native throughout the temperate and boreal regions of the Northern Hemisphere.

It’s not very toxic but it can be depending on the amount, season,

It was used as an intoxicant and entheogen by the peoples of Siberia, India and others throughout history and it has a religious significance in these cultures.

Amanita muscaria

DescriptionPileus:

Cap 6-39 cm broad, rounded at first, then plane in age, surface viscid when moist; margin striate often with adhering partial veil fragments when young; cap red, usually with white warts but in some variety, yellow warts.

Lamellae:Gills adnexed to free, white to cream, edges roughened.

Stipe:Stipe white, 7-16 cm long, 2-3 cm thick, tapering to a bulbous base; partial veil membranous, breaking to form a superior skirt-like veil. Volva consisting of two to three concentric rings at the stipe base.

Spores:Spores 9-13 x 6.5-9.5 µm elliptical, smooth, nonamyloid. Spore print white.

Amanita muscaria

Range & HabitatA. muscaria is native to conifer and deciduous woodlands

throughout the temperate and boreal regions of the Northern Hemisphere, including high elevations of warmer latitudes in regions like the Hindu Kush and the Mediterranean.

A recent molecular study proposes an ancestral origin in the Siberian–Beringian region in the Tertiary period before radiating outwards across Asia, Europe and North America.

This type of mushroom was introduced to Australia, Africa and New Zealand with pine trees imported from Europe.

It’s generally grows throughout the summer and early fall but in some regions of the pacific coast it can be found in late fall and even early winter.

Amanita muscaria

What do people think of A. muscaria?

The effects of the mushrooms can take between 30 minutes to two hours to happen. The strongest part of the trip takes 4-10 hours and the after-effects usually last a further 2-6 hours. The more you take, the longer your trip could last.

Magic mushrooms can make you feel confident, relaxed and in good spirits. They can distort color, sound and objects. One effect can be that your

senses get mixed up so that, for example, you think you can hear colors and you can see sounds.

They can also speed up and slow down your sense of time and movement. You may feel like you're dreaming when you're awake.

You can feel more emotionally sensitive. Some people become creative and feel enlightened.

Fly agaric (Amanita Muscaria) is risky to take. ‘Bad trips’ are seriously frightening and unsettling. And you can't tell

whether you're going to have a bad trip or a good trip. Also you can get flashbacks some time afterwards.

You may be at risk when you’re not in complete control of what you're doing. Your perception of your body and the world around you can be distorted.

Eating the wrong kind of mushroom can make you seriously ill, and even kill you.

Magic mushrooms can complicate any mental health issues you may have. Amanita muscaria

ToxicityMuscimol: A psychoactive compound; an

agonist of the GABA receptor in the brain.

Ibotenic acid: A powerful neurotoxin; an agonist of NMDA glutamate receptors in the brain.

Amanita muscaria and related species are known as effective bioaccumulators of vanadium; some species concentrate vanadium to levels of up to 400 times those typically found in plants. Vanadium is present in fruit-bodies as an organometallic compound called amavadine. However, the biological importance of the accumulation process is unknown.

Amanita muscaria

Muscimol

Chemical Name: 5-(Aminomethyl)-3(2H)-isoxazolone Molecular weight: 114.10 Muscimol is the product of the decarboxylation or drying of

Ibotenic acid and it is thought that Muscimol is as much as ten times more potent than ibotenic acid.

It is also a potent partial agonist at the GABAc receptor which is distributed in different parts of the brain and highly expressed in the retina.

Muscimol gets secreted unchanged in the urine. Muscimol lacks cholinergic effects at the neuromuscular junction LD50 mice: 3.8 mg/kg s.c, 2.5 mg/kg (I.P.) LD50 rats: 4.5 mg/kg (I.V.), 45 mg/kg (orally).

MechanismToxicity

Amanita muscaria

MuscimolMechanism

• Muscimol activates the receptor for the brain's major inhibitory neurotransmitter, GABA.

• It binds to the same binding site on the GABAa receptor complex as GABA itself.

• It alters neural activity in multiple regions including the cerebral cortex, hippocampus, and cerebellum. These regions of the brain have many functions including thinking and balance, so administering Muscimol could have an impact on any of these higher brain functions.

Toxicity

Amanita muscaria

Ibotenic acid

Chemical name: alpha-Amino-2,3-dihydro-3-oxo-5-iso-xazoleacetic acid.

Molecular weight: 158.11 It is a powerful neurotoxin that is used as a brain-

lesioning agent.Ibotenic acid is an agonist of NMDA glutamate

receptors and certain metabotropic glutamate receptors[73] which are involved in the control of neuronal activity

Peak intoxication is reached approximately 2-3 hours after oral ingestion.

LD5015 mg/kg (I.V.), 38 mg/kg (oral)-(mice)LD5042 mg/kg (I.V.), 129 mg/kg (oral)-(rats)

Toxicity

Amanita muscaria

Symptoms Symptoms typically appear after around 30 to 90 minutes and peak

within three hours, but certain effects can last for a number of days

Depending on habitat and the amount ingested per body weight, effects can range including:

NauseaTwitching Drowsiness, Cholinergic crisis-like effects (low blood pressure and

sweating)Auditory and visual distortions Mood changes Euphoria and relaxation AtaxiaLoss of equilibrium

In cases of serious poisoning it causes a delirium characterized by bouts of marked agitation with confusion, hallucinations, and irritability followed by periods of central nervous system depression.

Seizures and coma may also occur in severe poisonings. Amanita muscaria

Treatment

Medical attention should be sought in cases of suspected poisoning.

Initial treatment consists of gastric decontamination. If the delay between ingestion and treatment is less than

four hours, activated charcoal is given. Gastric lavage can be considered if the patient presents

within 1 hour of ingestion. There is no antidote, and supportive care is the mainstay of

further treatment for intoxication. If a patient is delirious or agitated, this can usually be

treated by reassurance and, if necessary, physical restraints.

Additionally, benzodiazepine such as diazepam or lorazepam can be used to control combativeness, agitation, muscular overactivity, and seizures.

Serious cases may develop loss of consciousness or coma, and may necessitate intubation and artificial ventilation.

Amanita muscaria

Amanita phalloides (Death Cap)

•Habitat•Description•Symptoms•Treatment•Death Cap Toxins•Mechanism of Action•Toxicity•Interesting Facts•References

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HabitatPrimarily a European species, there is no

evidence that the Death Cap is native to North America

Usually found from late September through late October

Has been found in Oregon, New Jersey, New York, California, Canada, Australia, north Africa, and New Zealand

The Death Cap appears most commonly under oaks but also under beeches, chestnuts, horse-chestnuts, birches, filberts, hornbeams, pines, and spruces

Amanita phalloides

DescriptionThe cap is 2¼--6" (6--16 cm) wideThe fully open caps are commonly 10-15 centimeters in

diameterThe color of the cap can be pale, yellowish, or olive-greenThe cap is usually sticky or slippery but sometimes dryThe gills are white, crowded together, and very finely

attached to the upper stalkmembranous partial veil tissue extends from the edge of

the cap to the upper stalkThe stem is white and from 5 to 15 centimeters long and

1 to 2 centimeters in diameterVolva(cup-like structure) encasing the base, frequently

underground or broken up.

Amanita phalloides

SymptomsFirst symptoms usually occur 6 to 12 hours after ingestion of

mushroom Initial symptoms include: stomach pains, vomiting, diarrhea

and dehydration. More severe symptoms include hypotension, tachycardia, and hypoglycemia(initial symptoms usually last 2 to 3 days)

Clinical improvement occurs with supportive care. Despite the resolution of symptoms, hepatic and renal damage is ongoing

After 2 to 3 more days, patients usually have GI disturbances once again, accompanied by jaundice.

Other symptoms include delirium, seizures, and coma.Patient s eventually have Liver failure along with renal failure

which lead to deathDeath usually occurs one to two weeks after ingestion of

mushroom

Amanita phalloides

TreatmentThere is no “antidote” for A. Phalloides poisoningsTreatments include: a High-dose continuous intravenous

injection of Penicillin G (Benzylpenicillin), There is some evidence that intravenous silibinin, an extract from the blessed milk thistle(Silybum marianum) decreases affects of ingestion, as well as N-acetylcysteine and Thioctic acid.

Silibinin prevents the uptake of amatoxins by hepatocytes, thereby protecting undamaged hepatic tissue

N-acetylcysteine helps to reduce liver damage.In the most severe cases, liver transplantation is the last

option.Treatments are most effective if poisoning is immediately

diagnosed

Amanita phalloides

Death Cap ToxinsConsist of Amatoxins and PhallotoxinsAmatoxins are multicyclic (ring-shaped) peptidesConsist of at least eight compounds with a similar

structure, that of eight amino-acid ringsAmatoxins include α-amanitin, which is the chief

component and along with β-amanitinLead to inhibition of RNA-polymerase 2 (which is

essential for the synthesis of mRNACell metabolism stops and the cells dieOrgans most affected include liver and kidneys. GI

tract also affected by toxinsPhallotoxins consist of at least seven compounds, all

of which have seven similar peptide rings.Phallotoxins have little input in the toxicity of the

Death Cap. Amanita phalloides

Mechanism of ActionThe main element of the amatoxins is

alpha-amanitin.When filtered through the kidneys, it

attacks the convoluted tubules and instead of entering the urine,

it is reabsorbed into the bloodstream and recirculated, causing repeated liver and kidney damage

This eventually leads to liver and kidney failure.

Amanita phalloides

Toxicity0.1 mg/kg is the minimal lethal dose of

amatoxin for adults-about 8mg for an 80kg person.

30 grams (1 oz), or half a cap, of this mushroom is enough to kill a human

Overall mortality estimated from 5% to 40% -This percentage is dropping due to

advances in general care and medicationsToxicity varies from patients due to factors

of weight, age, and overall health

Amanita phalloides

Interesting FactsA. phalloides is one of the most poisonous

of all known toadstoolsCould have possibly lead to the deaths of

Roman Emperor Claudius and Holy Roman Emperor Charles VI

New studies show that ethanol diminishes effect of toxins in mice

Amanita phalloides

References Kuo, M. (2001, September). Amanita phalloides . Retrieved from the MushroomExpert.Com Web site:

http://www.mushroomexpert.com/amanita_phalloides.html Fischer , David. W. “The Death Cap Amanita phalloides The World's Most Dangerous Mushroom.”

American Mushrooms. 1997. Cornell University. 25 April, 2009 <http://americanmushrooms.com/deathcap.htm>

A. Zheleva, A. Tolekova, M. Zhelev, Z. Dobreva, K. Halacheva, S.Popova. “IN VIVO ANTIOXIDANT AND PROOXIDANT PROPERTIES OF AMANITA PHALLOIDES MUSHROOM TOXINS.” Trakia Journal of Sciences, Vol. 3, No. 3, 2005, pp 34-38. Trakia University. 20 April, 2009. < http://www.uni-sz.bg/tsj/Vol3No3/Zheleva%20A%20et%20al%5B1%5D%20_1_.pdf>

^ Köppel C (1993). "Clinical symptomatology and management of mushroom poisoning". Toxicon 31 (12): 1513–40. doi:10.1016/0041-0101(93)90337-I. PMID 8146866.

Wasson RG. Soma: Divine Mushroom of Immortality. Harcourt Brace Jovanovich, 1968. Ott. J. Pharmacotheon. Natural Products Co, 1996. Letcher A. Shroom: A Cultural History of the Magic Mushroom. HarperCollins. 2007. Linnaeus C. Species Plantarum: Tomus II. Holmiae. 1753. Ott J. Hallucinogenic Plants of North America. Wingbow Press. 1976. Heinrich C. Magic Mushrooms in Religion and Alchemy. Park Street Press. 2002. Hajicek-Dobberstein S. Soma siddhas and alchemical enlightenment: psychedelic mushrooms in Buddhist tradition. Journal of

Ethnopharmacology. 1995; 48(2):99-118 O’Nell, M., et al. The Merck Index: An Encyclopedia of Chemicals, Drugs, and Biologicals: 14th Ed. Merck & Co. 2006. Spinella, Marcello. Psychopharmacology of Herbal Medicine. MIT Press, 2001. pp 386-390. Schultes & Hofmann. Botany & Chemistry of Hallucinogens. Charles C Thomas, 1980. pp 45-55. Olpe HR, Koella WP. The action of muscimol on neurones of the substantia nigra of the rat. 1978. Experientia 34: 235. Michelot D, Melendez-Howell LM. Amanita muscaria: chemistry, biology, toxicology, and ethnomycology. Mycological Research.

2003. 107(2):131-146.

More References

References Michelot, D. and Melendez-Howell, L. M. (February 2003). "Amanita muscaria: chemistry, biology,

toxicology, and ethnomycology". Mycological Research 107 (Pt 2): 131–46. Page, L.B. (1984). Mushroom toxins and the nervous system: some facts and speculations. McIlvainea,

6:39-43. Carter, C.A., Wojciechowski N.H., and Skoutakis V.A. (1983). Management of mushroom poisoning.

Clinical Toxicology Consultant 5:103-108. Borthwick, P.W. and Steward E.G. (1976). Ibotenic acid: Further observations on its conformational

models. Journal of Molecular Structure, 33:141 Chilton, W.S. (1978). Chemistry and mode of action of mushroom toxins. In: Rumack, B.H. and Salzman,

E. Eds. Mushroom poisoning: Diagnosis and Treatment. West Palm Beach (Florida), CRC Press Inc. 87:124.

Jordan, P. and Wheeler, S. (2001). The Ultimate Mushroom Book. Hermes House. Garner, C. D.; Armstrong, E. M.; Berry, R. E. et al (May 2000). "Investigations of Amavadin". Journal of

Inorganic Biochemistry 80 (1–2): 17–20. http://botit.botany.wisc.edu/ http://www.ipm.iastate.edu/ipm/hortnews/2006/4-5/fungi.html K. Baumann, K. Muenter, and H. Faulstich (1993). "

Identification of structural features involved in binding of α-amanitin to a monoclonal antibody". Biochemistry 32 (15): 4043–4050.

http://dohs.ors.od.nih.gov/pdf/Amatoxins%20REVISED.pdf Benjamin, Denis R. (1995). Mushrooms: poisons and panaceas — a handbook for naturalists,

mycologists and physicians. New York: WH Freeman and Company. Hruby K, Csomos G, Fuhrmann M, Thaler H (1983). "Chemotherapy of Amanita phalloides poisoning

with intravenous silibinin". Human toxicology 2 (2): 183–95. Chyka P, Butler A, Holliman B, Herman M (2000). "Utility of acetylcysteine in treating poisonings and

adverse drug reactions". Drug safety 22 (2): 123–48.

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