Poisonous plants of India

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Presentation Description

giving list and introduction to poisonous plants of india mechanism of action of the poisonous constituents.


Presentation Transcript

Poisonous plants of India :

Poisonous plants of India Sachin B. Narkhede sachinnarkhede@yahoo.com

Paracelcus 1493-1541:

Paracelcus 1493-1541 “All substances are poisons; there is none which is not a poison. The right dose differentiates a poison from a remedy.”

Thevetia neriifolia:

Thevetia neriifolia Family: Apocyanaceae Sinhala name/s: kaner English/common name/s: yellow oleander, lucky nut Plant habitat: Native of Central and South America but now grown throughout tropical and subtropical regions Toxic part of the plant: seed (although all parts toxic) Lethal dose: Kernel of one fruit (or 2 leaves for a child) Main toxic constituent/s: Thevetin A, Thevetin B Constituent type: cardiac glycosides Mode of action: inhibit sodium-potassium ATPase increased intracellular sodium and serum potassium negative chronotropic, positive inotropic effects

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Na + /K + ATPase 3 Na + 2 K + Representative Cardiac Cell Na + channel Voltage dependent L-type Ca 2+ channel Na + /K + ATPase Na + /Ca 2+ exchanger SR (Mitochondria) Heart muscle K + channel(s) Na + /Ca 2+ Antiporter Ryanodine receptor 3 Na + Ca 2+ β -adrenergic receptor

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3 Na + 2 K + Cell Electrophysiology SR (Mitochondria) Ca 2+ Phase 2 Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ 3 Na + Ca 2+

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3 [Na + ] 2 [K + ] Therapeutic & Toxic MoA SR (Mitochondria) Ca 2+ Phase 2 Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ = Digoxin Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Digoxin Na + K+

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Clinical features of poisoning: “digoxin-like” Early on: burning sensation in mouth, tingling of tongue, dry throat, giddiness, nausea vomiting, diarrhoea Cardiovascular: sinus bradycardia, first and second degree heart block, junctional rhythms, atrial and ventricular extrasystoles, ventricular fibrillation Other: yellow vision, anxiety, convulsions, coma Diagnosis: cardiac glycoside blood levels seed remnants, vomitus, gastric aspirate may help identify monitor serum potassium and electrolytes Treatment of poisoning: induce emesis at home (ipecac) gastric lavage within 1 hour or activated charcoal atropine 0.5mg IV for bradycardia, repeated cardiac pacing for third degree heart block anti-digoxin Fab antibodies in severe cases

Datura metel :

Datura metel


Scientific name: Datura metel Synonyms: Datura fastuosa (L.) Datura alba (Nees.) Family: Solanaceae Common names: Devil's trumpet, downy thorn-apple, black datura, angel's trumpet

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Plant habitat: Native to China, India and South East Asia. It is a common weed in waste and cultivated land in Sri-lanka and now it is used in landscaping and gardening . Plant description: Shrub-like annual herb with large flowers, typically white or yellow with deep purple accents. Leaves are alternate and simple. Traditional use: Leaves/dried flowers are used to relieve asthma or wheezing like symptoms in many cultures eg Chinese herbal medicine ( yáng jīn huā). Leaf poultices are applied to engorged breasts to relief excess milk production, rheumatic swelling of joints and lumbago. Powdered root is rubbed into gums or stuffed into cavities for toothache. Toxic part of the plant : all parts. Main toxic constituents : tropane alkaloids

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Leaves/flowers - mainly atropine Seeds/roots - mainly hyoscyamine Fruits – scopolamine Dose: Accidentally (or intentionally) ingesting even a single leaf could lead to severe side effects Symptoms: anticholinergic Thirst, dry mouth, blurred vision, photophobia, urinary retention occur soon after ingestion. Skin is hot, dry and flushed. Pupils are dilated and fixed. Cardiovascular effects are sinus tachycarida, hypertension, supra/ventricular arrhythmias, orthostatic hypertension.Severe poisoning causes disorientation, agitation, violent behaviour, convulsions, delirium, visual and auditory hallucinations, ataxia, respiratory depression, coma.

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Mode of action: It stimulates the central nervous system and simultaneously depresses peripheral nerves and dilates the pupils by peripheral action. The most probable action in this case is paralysis of the occulomotor nerve ending or its myoneural junction. Treatment of poisoning: Ipecac to induce emesis or gastric lavage. Activated charcoal to reduce absorption of toxic substances. Catheterization to empty bladder if necessary Diazepam for hallucinations and delirium.

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Abrus precatorius

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Scientific name: Abrus precatorius L. Synonyms: A.minor , A.pauciflorus Family: Leguminosae Common names: Abrus seed, crabs eye, Indian bead, Indian liquorice, wild liquorice, lucky bean, prayer or rosary beads, precatory bean, weather plant, jumble beads, jequirity bean Plant description: slender perennial twiner Habitat: grows wild in dry regions of India at low elevations Traditional use: To cure itch, sores and wounds due to bites of dogs, cats and rats Leaves: conjunctivitis, painful swellings; ground with lime for acne, boils, abscesses and tetanus Seeds: diabetes, Bright’s disease

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Toxic part of the plant: seed The most poisonous parts of the plant involved in poisoning are the small, scarlet seeds, that have a black eye at the hilum Toxicity: One seed well masticated can cause fatal poisoning (adults and children) Main toxins: Abrin - concentrated in seeds Mode of action: Abrin exerts its toxic action by attaching itself to the cell membranes It has a direct action on parenchymal cells (eg liver and kidney cells) and red blood cells Clinical effects: Early features of toxicity - burning of the mouth and oesophagus, and severe gastroenteritis with vomiting, diarrhoea and abdominal pain. Haematemesis and melaena are less common Later - drowsiness, disorientation, weakness, stupor, convulsions, shock, hepatotoxicity, cyanosis, retinal haemorrhages, haematuria, and acute renal failure (oliguria) can occur (Contact with the eyes can cause conjunctivitis and even blindness)

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Diagnosis: Diagnosis is made by the presence of the typical manifestations following ingestion: gastroenteritis with risk of dehydration, haematemesis and melaena. Drowsiness and convulsions may occur. Toxicological analysis of body fluids for the poison is not helpful. Plant material, seeds or remnants of seeds, vomitus and gastric aspirate should be collected in clean bottles for identification. Main risks and target organs: The main risk is the severe gastroenteritis leading to dehydration and shock. Ingested seeds can affect the gastrointestinal tract, the liver, spleen, kidney, and the lymphatic system. Treatment: Administration of fluids and electrolytes will alleviate dehydration.

Myristica fragrans:

Myristica fragrans

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Scientific name: Myristica fragrans Family : Myristicaceae English/common names: Nutmeg, Mace tree Plant habitat: A native of E.Moluccas and other Indian Islands Now cultivated in Sri Lanka, Malaya, Philippines, W.Indies & South America Traditional use: As a spice in foods As a traditional medicine for diarrhoea Toxic part of the plant: seeds (nutmeg) and, to a lesser extent, the aril (mace) Lethal dose: Humans: 1-3 nutmegs (5-15g) for adults, 2 nutmegs for children Animals: oral dose of 24mg nutmeg oil per kg body weight Main toxins: myristicin & elemicin myristicin

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Mode of action : Elemicin undergoes oxidation of its oleficin side chain to produce TMA (3,4,5-trimethoxyamphetamine), a psychotropic drug agent Myristicin produces MMDA which is metabolised to form TMA. MMDA has a higher potency than TMA Nutmeg has monoamineoxidase inhibition properties and anti-prostaglandin synthesis effects Clinical features of poisoning: symptoms are usually seen within 3-6 hours after ingestion and vary according to the dose taken and the variability between different samples of nutmegs intoxication resembles anti-cholinergic intoxication ie profuse sweating, flushed face, dry mouth, burning epigastric pain, tachycardia, restlessness, giddiness, hallucinations unlike anti-cholinergic symptoms pupils constrict Diagnosis: Blood monitoring (electrolytes, liver enzymes, renal function) and urinalysis Treatment of poisoning: symptomatic and supportive Induce emesis (with ipecac) or gastric lavage Activated charcoal Diazepam for restlessness or hallucinations

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Alocasia macrorrhiza

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Scientific name: Alocasia macrorrhiza Synonyms: A.odora , A.commutata , Colocasia macrorrhiza , Caladium glycyrrhizum , Philodendron peregrinum , Arum grandiflorum Family: Araceae (Magnoliophyta) English/common names: giant taro, elephant ear, ape flower Plant habitat: grows in all tropical countries including India, Sri Lanka, Malaya & Philippines Traditional use: Acrid juice of the leaf gives instant relief to stings of the giant nettle Chopped leaves & roots used as an application on painful joints Cut stem + lime/water applied to dogs bites Dried stems for haemorrhoids & chronic fevers Crystals destroyed on boiling or roasting so starch in stem can be used as a foodsource Flower of the Alocasia plant Taro corms

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Toxic part of the plant: all parts Main toxic constituent/s: all parts of the plant contain specialized cells containing bundles of needle-like calcium oxalate crystals and toxic proteins Mode of action: When the plant is chewed the sharp crystals injure the mucous membrane allowing toxic proteins to penetrate Lethal dose: The extreme oropharyngeal response generally limits the amount of plant ingested and oxalate absorbed through the oral mucosa is unlikely to cause systemic poisoning Symptoms: Eating parts of the plant causes a severe burning in mouth and throat. Other symptoms may include: Redness, swelling, pain, burning pain of the tongue and mucous membranes, profuse salivation, dysphagia Swelling can rarely cause obstruction and respiratory compromise Loss of speech may last several days and swelling more than a week Treatment of poisoning: wipe out the mouth with a cold, wet cloth and give milk to drink antihistamines, mouthwashes, antiseptics and steroids may be used

Nicotiana tabacum:

Nicotiana tabacum

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Scientific name Nicotiana tabacum Family Solanceae English name Tobacco Plant habitat native of tropical and subtropical America but it is now commercially cultivated worldwide Traditional use - as an insecticide - intestinal worms or constipation - dried tobacco leaves for chewing, snuffing or smoking Toxic part of the plant leaves, stems, roots and flowers Main toxic constituents nicotine Constituent type alkaloid Lethal dose 0.5-1 mg/kg body weight nicotine (~ 40 - 60 mg)

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Mode of action Nicotine binds stereo specifically to acetylcholine receptors at autonomic ganglia, the adrenal medulla, the neuromuscular junction and the brain This evokes the release of catecholamine nicotine produces ganglionic blockade, vagal afferent nerve stimulation, or direct depressor effects mediated by action on the brain Clinical features of poisoning Mild: salivation, nausea, dizziness, drowsiness, headache, vomiting, diarrhoea, hand tremor Serious: mental confusion, circulatory collapse (shallow rapid pulse, ‘cold sweating’), convulsions, loss of consciousness, cardiac arrest, respiratory paralysis Diagnosis Blood monitoring (blood gases) and urinanalysis Treatment of poisoning induced emesis (ipecac) or gastric lavage and activated charcoal supportive therapy directed towards maintaining respiration and blood pressure (IV fluids) and controlling convulsions

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Scientific name : Strychnos nux-vomica Synonyms : S.lucida , S.colbrina , S.aromatica Family : Loganiaceae English/common name : Poison nut, Nux vomica, Quaker buttons Plant habitat :  dry forests of Ceylon, flowers in August  A moderate sized or large tree with an erect trunk, Slide 5  Bark  Wood  Leaves  Flowers  Fruit Traditional use : Root - cures fever and bites of venomous snakes Used for preparation of homeopathic medicine Toxic part of the plant : seed (although all parts toxics) POISON NUT ! W a t h s a l a W i m a l a s e n a K a n i s h k a J a y a w e e r a

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Main toxic constituents : strychnine, (brucine) Constituent type : alkaloids . Lethal dose : plant poisoning is rare possibly due to bitter taste  T he quantity of strychnine in one seed could be fatal  If seeds are swallowed uncrushed they are not poisonous Mode of action :  Strychnine is a potent convulsant. It causes increased reflex excitability in the spinal cord  Brucine – resembles strychnine activity but it is less potent Clinical features of poisonings :  Symptoms appear within 15 - 30 min of ingestion - Initial symptoms – bitter taste in mouth, feeling of suffocation - Twitching of the muscles in neck, body and limbs - Extreme contractions affecting all muscles in the body - The patient is conscious and has intense pain. - Complications - lactic acidosis, rhabdomyolysis, acute renal failure - Death is caused by asphyxia or muscular paralysis

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Diagnosis :  Based on history of ingestion and development of muscular stiffness  Strychnine (and brucine) can be measured chemically but there is no time to perform this procedure before treatment  Measure acidosis, serum potassium, SGOT, LDH, CPK etc Treatment of poisonings :  Activated charcoal  Support respiratory and cardiovascular functions  If convulsions cannot be controlled with diazepam (IV or rectal), or if they recur, administer phenobarbitone or phenytoin.  Intubation with suxamethonium chloride may be necessary  When convulsions and hyperactivity are completely controlled, gastric lavage can be performed safely

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Leaf Flower Fruit Bark Seed

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Glorisa superba as a Poisonus Plant in India

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Scientific name: Gloriosa superba Synonyms: G.simplex , Methonica doniana, Eugonia superba Family: Colchicaceae, Liliaceae English/common names: flame lily, glory lily, tiger claw Plant habitat: native of tropical Africa, India, Malaya, etc found in low country Sri Lanka Traditional use: tuber – bruises and sprains Poisonous parts of the plant: The entire plant, especially the tubers, are extremely poisonous

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Main toxic constituents: colchicine (+ ‘gloriosine’ in tubers) Constituent type: alkaloid Mode of action: Colchicine has an antimitotic effect It stops cell division by disrupting the spindle apparatus during the metaphase Cells with rapid turnover are affected (bone marrow, intestinal epithelium, hair-producing cells -> hair loss) It can alter neuromuscular function (It can withstand drying, storage and boiling - tubers not a foodsource!) Clinical features of poisoning: Initial symptoms develop within 6-12 hours of ingestion burning pain, numbness, itching and tingling around the mouth and throat with thirst nausea, intense vomiting abdominal pain, severe diarrhoea with blood and mucus These lead to electrolyte imbalance, dehydration, hypovolaemic shock manifested hypotension and tachycardia

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After 24 hours patients develop Muscle weakness, myoglobinuria, bronchial constriction, leucopenia, thrombocytopenia, clotting defects with bleeding, polyneuropathy cardiac arrhythmias, hepatic insufficiency, acute renal failure In severe cases there may be Respiratory depression, confusion, delirium, convulsions, coma Death occurs due to shock or respiratory failure Diagnosis: Toxicological, biomedical, blood gas, haematological analyses Treatment of poisoning: hospitalize the patient immediately induce vomiting (ipecac) / gastric lavage give repeated activated charcoal supportive care eg IV fluid, assisted ventilation may be needed

Poisonus plants of Sri lanka Ricinus communis:

Poisonus plants of Sri lanka Ricinus communis

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Scientific name: Ricinus communis Linn. Synonyms : Ricinus africanus Willd., Ricinus communis L. var. viridis (Willd.) Müll. Arg., Ricinus inermis Jacq., Ricinus lividus Jacq., Ricinus macrocarpus G. Popova, Ricinus microcarpus G. Popova, Ricinus persicus G. Popova, Ricinus speciosus Burm., Ricinus viridis Willd., Ricinus vulgaris Mill., Ricinus zanzibaricus G. Popova, Croton spinosus Family: Euphorbiaceae (spurge family) English/common name/s: castor bean, castor-oil plant, Palma Christii Plant habitat: Cultivated as a decorative plant in village gardens in India Probably of African origin but now grows in tropical, subtropical and temperate areas Commercially cultivated mainly in Brazil, India, Italy, etc. Traditional use: In India the root of the plant is used in pleurodynia (muscular rheumatism) and rheumatic pains while seeds are used for lumbago and sciatica Africans use the bark for stitching up wounds & as a dressing for sores Local application of fresh leaves to the lactating breast is said to produce a powerful galactogogic action. They are also used headaches The root is a remedy for abdominal pains and diarrhoea while root bark (and seed oil) is a purgative also used for skin diseases and sores

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Toxic part of the plant: seeds are the most toxic part (leaves are also poisonous) Lethal dose: 1mg/kg pure ricin in man Ingestion of a single well chewed bean has caused death 1-3 seeds can be fatal to a child 2-4 seeds cause severe poisoning in an adult poisoning is unlikely if seeds are swallowed without chewing Main toxic constituent/s: Ricin Constituent type: Glycoprotein or a toxalbumin member of a class of plant toxins known as type 2 ribosome inactivating proteins Mode of action: Ricin impairs chain elongation in protein synthesis, causing cell death and tissue damage Clinical features of poisoning: Early on - burning sensation of the mouth and throat occurs After 3-6 hrs - nausea, vomiting, severe abdominal pain and diarrhoea resulting in dehydration electrolyte imbalance and shock Cardiovascular - hypotention, tachycardia, ECG changes and circulatory failure Other - prostration, blurring of vision, loss of consciousness, convulsions, haemolysis, uraemia and liver necrosis

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Diagnosis: Blood gases and electrolytes analysis Close monitoring of renal, hepatic hematological systems & blood clotting. Botanical & pharmacognostical identification of a sample of the plant or vomitus Radioimmunoassay with antiricin antibodies labeled with iodine 125 for ricin in plasma or urine Treatment of poisoning: Induce emesis at home (ipecac) Immediate gastric lavage or activated charcoal Correct fluid & electrolyte imbalance immediately In case of bronchial asthma, oxygen, B2-agonist eg salbutamol and corticosteroids may be necessary (if acute poisoning occurred by inhalation) Antihistamines or corticosteroids may be beneficial in treating skin lesions (if acute poisoning occurred by skin exposure)

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Scientific name : Manihot utilissima Synonyms : Jatropha manihot (Kunth), Manihot manihot (Cockerell), Manihot melanobasis (Muell) Family : Euphhorbiaceae English /common name : cassava, manioc, tapioca Plant description : shrub with a big tuberous root Plant habitat : The sweet and bitter cassava plants are indigenous to Southern and Central America but have been introduced to almost all tropical countries Traditional use : Used as a food source. American Indians use the brown juice for burns Manihot utilissima

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Toxicity of the plant : The leaves and roots contain free and bound forms of the cyanogenic glycoside linamarin, which is converted to cyanide in the presence of linamarinase, a naturally occurring enzyme in cassava or via exposure to the atmosphere. ( Slide 5 ) Two varieties Sweet - contains as little as 20 milligrams of cyanide (CN) per kilogram of fresh roots Bitter - may produce more than 50 times as much (1 g/kg) The paralytic neurological disease caused by long-term consumption of cassava is called mantakassa. Yam that is cut, washed and boiled in an open container at 72°C for long enough will destroy the enzyme and any hydrocyanic acid formed will evaporate. Lethal dose : One dose of pure cassava cyanogenic glucoside (40mg) is sufficient to kill even a cow. Hence about 300 grams of fresh root is enough to kill an adult human and about 125 grams of fresh root would be enough to kill a child Mode of action : A "large" sudden dose (HCN) is highly poisonous to all humans and animals because it rapidly inactivates cellular respiration thereby causing death. This means that it stops cells from being able to use oxygen. The heart, respiratory system and central nervous system are most susceptible to cyanide poisoning and cease to function as a result of lack of oxygen.

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Clinical features of poisoning : Acute: Within 3-6 hours of ingestion burning epigastric pain, vomiting, flushing of skin, dry mouth, tachycardia, pupil constriction, restlessness, giddiness and hallucinations occur. Chronic: initial symptoms are described as tremor, cramps, a heavy feeling and/or weakness in the legs, a tendency to fall down and difficulty remaining upright There is a visible hypertonic gait when walking or running Occasionally there will be lower back pain, blurred vision, speech difficulties and/or paresthesia of the legs, but they disappear within a month, later some people will develop dysarthria, abnormalities of eye movement, hypertonicity of the arms Diagnosis Acute poisoning: signs of extreme metabolic acidosis Chronic poisoning: a visible hypertonic gait when walking or running, bilateral brisk knee and Achilles tendon reflexes without signs of vertebral lesions The onset of the disease takes less than one week and then remains stable Urinary concentrations of ( thiocyanate and linamarin are elevated) (Cyanide (CN - ) is normally converted thiocyanate (SCN - ) by the enzyme rhodanase) Treatment of poisoning There is no known treatment for cyanide poisoning . Treatment with sodium thiosulphate (Na 2 S 2 O 3 ), a cyanide antidote, gave disappointing results. A good and varied diet, high dose multivitamins (specially B12 ,it detoxifies the HCN) and physical rehabilitation are advised.

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Peganum harmala Botanical Name: Peganum harmala FamilyName: Zygophyllaceae Local Name: Ispandur Urdu Name: Harmal English name: Wild Rue Part used: Whole plant Flowering: May - June

Plant habitat:

Plant habitat US states of Arizona,California Montana, Texas - grows in salt deserts and shrub lands. Grows in India, Persia, Mediterranean region, Central Asia, Arabia, North Africa

Multibranched, leafy, perennial, bright green, succulent herb. Leaves divided, seed angled, Flowers white, single.:

Multibranched, leafy, perennial, bright green, succulent herb. Leaves divided, seed angled, Flowers white, single. Constituent type: alkaloids Harmaline Harmine Harmalol Tetrahydroharmine Vasicine Mode of action: Harmaline is a reversible monoamine oxidase inhibitor found especially in higher quatities in ripe seeds The plant also has antibacterial, antioxidant, anti-inflammatory and antitumour activity

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CLINICAL FEATURES Overdose is potentially comprised of hallucinations and neurosensorial syndromes, bradycardia, low blood pressure, raised body temperature and gastrointestinal disturbances such as nausea and vomiting DIAGNOSIS ON Physical examination TREATMENTS Supportive therapy IV fluids Antacids (or H2 antagonists) References : IPCS Inchem.Peganum harmala [Accessed at http://www.inchem.org/documents/pims/plant 04 July 2008 ] Massoud M et al. Toxicity of Peganum harmala: Review and a Case Report. Iranian Journal of Pharmacology & Therapeutics 2002: 1(1); 1-4

Adenia palmata:

Synonyms: Adenia hondala, Granadilla hondala, Modecca palmata Family: Passifloraceae English/common name/s: ? Plant habitat: large aerial plant climbing by tendrils attached to large trees growing in the wet and dry zones along forest edges Traditional use: ? Toxic part of the plant: fruit (which closely resembles passion fruit -> accidental ingestion by children) Lethal dose: ? Main toxic constituent/s: a cyanogenic glycoside, a toxalbumin and emulsin (an enzyme) Constituent type: cyanogenic glycoside Adenia palmata

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Mode of action: 1 st phase – hydrocyanic acid 2 nd phase – local toxalbumin effects 3 rd phase - hypersensitivity reaction Clinical features of poisoning: 1 st phase – vomiting, fever, restlessness, dizziness, disorientation, abdominal pain and diarrhoea within one hour 2 nd phase – necrotising enteritis -> diarrhoea with blood and mucus, abdominal colic and right iliac fossa tenderness after a variable period of time 3 rd phase – myocarditis with ECG changes, tender hepatomegaly, retinopathy with papilloedema, exudates and haemorrhages may be seen 2-3 weeks after ingestion – all transient Diagnosis : cardiac glycoside blood levels seed remnants, vomitus, gastric aspirate may help identify monitor serum potassium and electrolytes Treatment of poisoning : if no vomiting occurs induce emesis with ipecac syrup or perform gastric lavage activated charcoal will help with the absorption of toxic substances IV fluid therapy may be needed antidotes for cyanide poisoning not usually necessary blood transfusion may be necessary in the 2 nd phase

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Datura metel atropine, hyoscine, hyoscyamine alkaloids seed (all) Gloriosa superba colchicine tuber Nicotiana tabacum nicotine leaf (all) Pagiantha dichotoma ? narcotic, datura-like seed (Peganum harmala) harmaline seed Strychnos nux vomica strychnine seed Alocasia macrorrhiza calcium oxalate crystals (needle-like), toxic proteins leaf/stem (all) Anthurium sp. Dieffenbachia sp. Scindapsus aureus Zantedeschia aethiopica Cerbera manghas cerberine, odollum,thevetin cardiac glycosides fruit kernel Thevetia neriifolia thevetin A, theventin B fruit Adenia palmata cyanogenic glycoside, toxalbumin, emulsin enzyme cyanogenic glycosides fruit Manihot utilissima linamarin, (linase enzyme) tuber Abrus precatorius abrin toxalbumins seed Jatropha curcas curcin seed (all) Jatropha multifida Jatrophin Ricinus communis ricin Eucalyptus robusta oil of eucalyptus (eugenol) volatile oils all Myristica fragrans myristicin seed (aril) Amanita phalloides phalloidin, phalloin, phallolysin alpha, beta, gamma amanitin phlallatoxins amatoxins aerial parts (mushroom)

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