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Group Project Amanita Mushrooms Toxins Ahmed Alghrouz Ali Ahmed James Olguin Tristan Malin Start.

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Presentation on theme: "Group Project Amanita Mushrooms Toxins Ahmed Alghrouz Ali Ahmed James Olguin Tristan Malin Start."— Presentation transcript:

1 Group Project Amanita Mushrooms Toxins Ahmed Alghrouz Ali Ahmed James Olguin Tristan Malin Start

2 Amanita Mushrooms History & Background Species: A. muscaria (Fly Agaric) A. phalloides (Death Cap) A. virosa (Destroying Angel) References

3 History & Background Introduction: A history of interaction. Timeline Psychoactive Compounds Neuropharmacology of Psychoactive Amanita Compounds References Back to Amanita Homepage

4 A History of Interaction A. 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) Next Back to History & Background

5 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. Back to History & Background

6 Timeline The 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) Next Back to History & Background

7 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. Next Back to History & Background

8 100 CE: 7.5 cm tall miniature statue of an A. muscaria, found in Nayarit, Mexico 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 Back to History & Background

9 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 Back to History & Background

10 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 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 Back to History & Background

11 1753 CE: Linnaeus describes the fly agaric mushroom in Species Plantarum: Tomus II. Holmiae (1753), naming it Agaricus muscarius CE: Fly agaric placed in Amanita genus by Jean- Baptiste Lamarck. New name Amanita muscaria CE: R. Gordon Wasson publishes Soma: Divine Mushroom of Immortality. (Argument for sacramental use of A. muscaria by Indians in time of Vedas.) Next Back to History & Background

12 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) 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. Back to History & Background

13 Psychoactive Compounds The 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. Next Back to History & Background

14 Muscimol Muscimol is considered the principle psychoactive, with oral dosages of pure muscimol around 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. Next Back to History & Background

15 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) Next Back to History & Background

16 Muscarine Muscarine 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. Back to History & Background

17 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. Next Back to History & Background

18 GABA GABA (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. Next Back to History & Background

19 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: GABA A and GABA C are ionotropic receptors (are ion channels) and GABA B metabotropic, which are G-protein coupled. Next Back to History & Background

20 Muscimol Muscimol 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. Next Back to History & Background

21 Ibotenic acid When 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 Next Back to History & Background

22 Intoxicating Effects The 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. Back to History & Background

23 Taxonomy / Taxonomic Confusion Description Distribution / Habitat Toxins Symptoms / Treatment Back to Amanita Homepage Amanita Virosa (The Destroying Angel)

24 Taxonomy Kingdom: Fungi Phylum: Basidiomycota Class: Agaricomycetes Order: Agaricales Family: Amanitaceae Genus: Amanita Next Back to A. virosa

25 Taxonomic Confusion Depending 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. Next Back to A. virosa

26 Taxonomic Confusion One 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. Next Back to A. virosa

27 KOH Test An image of the yellow flesh, that is the result of application of Potassium Hydroxide Next Back to A. virosa

28 Taxonomic Confusion A. 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. Back to Destroying Angel Back to A. virosa

29 Description All destroying angels form ectomycorrhizal relationships with tree roots. Next Back to A. virosa

30 Description Young destroying angels are often spherical or conical in shape, until they emerge through the universal veil. Next A. virosa at three different stages of life. Back to A. virosa

31 Description Other 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. Back to Destroying Angel Back to A. virosa

32 Distribution A map of the distribution of A. ocreata, a geographically limited species. Next A. virosa occurs all over North America, Europe Back to A. virosa

33 Habitat Like 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. Next Back to A. virosa

34 Habitat The 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. Back to Destroying Angel Glucose molecules Back to A. virosa

35 Toxins Destroying 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. Next Back to A. virosa

36 Toxins: Amatoxins Amatoxins 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. NameR1R1 R2R2 R3R3 R4R4 R5R5 α-AmanitinNH 2 OH β-AmanitinOH γ-AmanitinNH 2 OHH ε-AmanitinOH H AmanullinNH 2 HHOH Amanullinic acid OHHH Amaninamid e NH 2 OH H AmaninOH H Proamanulli n NH 2 HHOHH Next

37 Toxins: Amatoxins Amatoxins 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 Back to A. virosa

38 Symptoms The 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. Next Back to A. virosa

39 Symptoms After 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. Next

40 Treatment The 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. Next

41 Treatment In 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. Back to Destroying Angel

42 Amanita Muscaria (Fly Agaric) General Facts Description Habitat What people think of A. muscaria What people think of A. muscaria Toxicity Symptoms Treatment References Back to Amanita Homepage

43 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

44 Description Pileus: 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 µm elliptical, smooth, nonamyloid. Spore print white. Amanita muscaria

45 Range & Habitat A. 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

46 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

47 Toxicity Muscimol : A psychoactive compound; an agonist of the GABA receptor in the brain. Muscimol Ibotenic acid : A powerful neurotoxin; an agonist of NMDA glutamate receptors in the brain. Ibotenic acid 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

48 Muscimol Chemical Name: 5-(Aminomethyl)-3(2H)-isoxazolone Molecular weight: 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). Mechanism  Mechanism  ToxicityAmanita muscaria

49 Muscimol Mechanism 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

50 Ibotenic acid Chemical name: alpha-Amino-2,3-dihydro-3-oxo-5-iso- xazoleacetic acid. Molecular weight: 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) ToxicityAmanita muscaria

51 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: Nausea Twitching Drowsiness, Cholinergic crisis-like effects (low blood pressure and sweating) Auditory and visual distortions Mood changes Euphoria and relaxation Ataxia Loss 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

52 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

53 Habitat Description Symptoms Treatment Death Cap Toxins Mechanism of Action Toxicity Interesting Facts References Back to Amanita Homepage

54 Habitat Primarily 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

55 Description The cap is 2¼--6" (6--16 cm) wide The fully open caps are commonly centimeters in diameter The color of the cap can be pale, yellowish, or olive-green The cap is usually sticky or slippery but sometimes dry The gills are white, crowded together, and very finely attached to the upper stalk membranous partial veil tissue extends from the edge of the cap to the upper stalk The stem is white and from 5 to 15 centimeters long and 1 to 2 centimeters in diameter Volva(cup-like structure) encasing the base, frequently underground or broken up. Amanita phalloides

56 Symptoms First 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 death Death usually occurs one to two weeks after ingestion of mushroom Amanita phalloides

57 Treatment There is no “antidote” for A. Phalloides poisonings Treatments 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

58 Death Cap Toxins Consist of Amatoxins and Phallotoxins Amatoxins are multicyclic (ring-shaped) peptides Consist of at least eight compounds with a similar structure, that of eight amino-acid rings Amatoxins include α-amanitin, which is the chief component and along with β-amanitin Lead to inhibition of RNA-polymerase 2 (which is essential for the synthesis of mRNA Cell metabolism stops and the cells die Organs most affected include liver and kidneys. GI tract also affected by toxins Phallotoxins 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

59 Mechanism of Action The 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

60 Toxicity 0.1 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 medications Toxicity varies from patients due to factors of weight, age, and overall health Amanita phalloides

61 Interesting Facts A. phalloides is one of the most poisonous of all known toadstools Could 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

62 References Kuo, M. (2001, September). Amanita phalloides. Retrieved from the MushroomExpert.Com Web site: Fischer, David. W. “The Death Cap Amanita phalloides The World's Most Dangerous Mushroom.” American Mushrooms Cornell University. 25 April, 2009 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 Trakia University. 20 April, ^ Köppel C (1993). "Clinical symptomatology and management of mushroom poisoning". Toxicon 31 (12): 1513–40. doi: / (93)90337-I. PMID ^ doi / (93)90337-IPMID Wasson RG. Soma: Divine Mushroom of Immortality. Harcourt Brace Jovanovich, Ott. J. Pharmacotheon. Natural Products Co, Letcher A. Shroom: A Cultural History of the Magic Mushroom. HarperCollins Linnaeus C. Species Plantarum: Tomus II. Holmiae Ott J. Hallucinogenic Plants of North America. Wingbow Press Heinrich C. Magic Mushrooms in Religion and Alchemy. Park Street Press Hajicek-Dobberstein S. Soma siddhas and alchemical enlightenment: psychedelic mushrooms in Buddhist tradition. Journal of Ethnopharmacology. 1995; 48(2): O’Nell, M., et al. The Merck Index: An Encyclopedia of Chemicals, Drugs, and Biologicals: 14th Ed. Merck & Co Spinella, Marcello. Psychopharmacology of Herbal Medicine. MIT Press, pp Schultes & Hofmann. Botany & Chemistry of Hallucinogens. Charles C Thomas, pp Olpe HR, Koella WP. The action of muscimol on neurones of the substantia nigra of the rat Experientia 34: 235. Michelot D, Melendez-Howell LM. Amanita muscaria: chemistry, biology, toxicology, and ethnomycology. Mycological Research (2): More References 

63 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: Carter, C.A., Wojciechowski N.H., and Skoutakis V.A. (1983). Management of mushroom poisoning. Clinical Toxicology Consultant 5: 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. 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.Identification of structural features involved in binding of α-amanitin to a monoclonal antibody 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. Back to Amanita Homepage


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