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Target Organ

Target organ senyawa toksik yang masuk ke dalam

sirkulasi sistemik:
 Sistem saraf,
Efek toksik tumbuhan racun  hati,
 darah,
 ginjal dan
 jantung

Exposure Site (skin, Gastro

Intestinum, respiratory, placenta)

D
Absorption e
Presystemic Elimination
Distribution L Distribution Away from
Reabsorption I Target Excretion
V
Toxication E
Detoxication
R
y

Ultimate Target
Target molecule
(protein, lipid, DNA,
RNA)

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Sistem saraf

 Blocking agents
 Depolarising agents
 Stimulan
 Depresan
 Antagonis reseptor
 Penghambat Asetilkolinesterase
 Anoksia
 Zat demyelinasi
(Tugas: tanaman dgn efek pada saraf)

Darah Hati

Pengaruh terhadap:  Nekrosis

 Eritrosit  Kolestatik
 Protrombin (Platelet)  Sirosis
 Leukosit

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Jantung
Aktivitas elektrik dikontrol oleh
 konsentrasi ion Na+, K+, dan Ca2+
 Pompa membran
 Gate
 Permeabilitas ion tersebut
Perubahan hal-hal tsb akan menyebabkan aritmia.
PerUbahan konduksi & aksi potensial, dll.
Toxicity may also be caused by
botanical drug interactions
 Pembentukan metabolit elektrofilik, reaksi alergi,
botanical-induced autoimmune reactions.
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Ginjal
Beberapa logam dapat menyebabkan gangguan
 Cd2+: mengganggu reabsorbsi protein dari tubulus
proksimal : proteinuria
 Mg2+ : mempengaruhi tubulus proksimal : awalnya
menimbulkan poliuria, proteinuria, anuria, edema &
kematian
 Pb2+ : mempengaruhi tubulus proksimal :
menimbulkan glukosuria, aminoasiduria, dan
hiperproteinuria
 CCl4, kloroform, mempengaruhi fungsi tubulus &
menyebabkan nekrosis
 Zat yang terkonsentrasi di cairan tubulus melampaui
kelarutannya sehingga terbentuk kristal. Kalsium
oksalat kemungkinan menyebabkan nefrotoksik
Bagaimana bahan herbal dapat
menimbulkan interaksi obat?
 Mempercepat atau menghambat biotransformasi
melalui efeknya pada enzim metabolisme
 Efek di atas bergantung pada terjadinya aktivasi
atau deaktivasi oleh enzim
 Mempengaruhi absorbsi dari GI
 Mengganggu ekskresinya dari ginjal
 Berkompetisi menduduki reseptor sehingga
mempengaruhi aksi farmakologi
 Penggunaan luar pada luka yang terbuka luas
dapat menimbulkan efek sistemik
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Interaksi
 Mekanisme: Pharmacokinetic &
pharmacodynamic
 Interaksi farmakokinetik meliputi: perubahan
ADME (absorpsi, distribusi, metabolisme, &
ekskresi) akibat obat atau tanaman.
 Interaksi Farmakodinamik, mengubah hubungan
antara konsentrasi obat dan respon farmakologi
obat atau tanaman.
Drug Metabolism
Inhibisi
 Lebih dari setengah obat yang telah digunakan
akan dieliminasi primer melalui metabolisme, dan
yang paling sering menyebabkan drug–drug
interaction yang nyata secara klinis adalah akibat
inhibisi atau induksi drug-metabolizing enzyme.
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Drug Absorption
1. Meningkatkan intestinal transit time,
2. Penggunaan tanaman yang mengandung
anthranoid laxatives (mis, aloe; Aloe spp.)
3. Pembentukan kompleks antara senyawa-
senyawa yang terdapat di dalam tanaman (mis,
polyphenols dalam green tea).
Inhibisi
 Jalur metabolisme obat yang paling umum
adalah oksidasi melalui cytochrome P-450 (CYP)
super family yang merupakan enzim yang berada
dalam endoplasmic reticulum sel-sel
hepatocytes.
 CYP superfamily yang bertanggungjawab
terhadap oksidasi obat pada manusia, adalah
CYP1, CYP2, dan CYP3.
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Inhibisi
 Inhibisi CYP terjadi setelah paparan
bergamottin (dalam grapefruit juice),
capsaicin (dalam chili peppers), glabridin
(dalam licorice root), isothiocyanat (dari
cruciferous vegetables), oleuropein (dari
olive oil), diallyl sulfone (dari garlic), dan
resveratrol, kandungan red wine
 of this irreversible inhibition is that
interactions take one to two weeks to
resolve on termination of the drug
because this is how long the CYP3A takes
to resume its predrug steady state.
Induksi
 Umumnya, induksi terjadi akibat peningkatan
kecepatan transkripsi, peningkatan kestabilan
mRNA atau efisiensi translasi, & stabilisasi protein
yang diinduksi oleh binding atau posttranslational
modifications.
 Tetapi mekanisme yang paling umum terjadi
adaLah binding & aktivasi nuclear factor yang
berbeda yang berperan dalam bentuk protein-
heteromer untuk meningkatkan kecepatan
transkripsi gen.
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Induksi
 Istilah ‘‘induksi’’ meliputi seluruh mekanisme
yang menyebabkan peningkatan konsentrasi
protein katalitik aktif – yg terlibat pada
metabolisme obat.
 Peningkatan aktivitas enzim akibat systemic-
clearance yang lebih tinggi & bioavailabilitas
yang lebih rendah dari obat-obat yang
termetabolisme secara ekstensif.
 Konsentrasi obat yang lebih rendah seringkali
diakibatkan oleh kesaalahan terapeutik.
 Misalnya, pil kontrasepsi oral menjadi tidak
effektif jika diresepkan bersama rifampin.
Induksi
 Contoh: tanaman St. John’s wort, adalah
penginduksi CYP3A4 yang poten dan
menyebabkan peningkatan metabolisme
cyclosporine & indinavir.
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Inhibisi Contoh Penghambatan

Enzim
 Efek bahan yang mengandung garlic (Allium  Sianida menghambat enzim sitokrom oksidase
sativum): yang berpengaruh pada transpor oksigen di
mitokondria menyebabkan hipoksia

Pada human liver microsome pada uji in vitro drug

metabolism model, Foster et al. menunjukkan bahwa
garlic menghambat CYP3A4-mediated drug
metabolism

Effect of Grapefruit Juice on

Felodipine Plasma Concentration

5mg tablet
with juice

without

Cl
Cl

Cl
H Cl
CH 3 O 2 C CO 2 CH 3 3A4
CH 3 O 2 C CO 2 CH 3

CH 3 N CH 3
CH 3 N CH 3
H

Review- D.G. Bailey, et al.; Br J Clin Pharmacol 1998, 46:101-110

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Manihot utilissima
Scientific name: Manihot utilissima
Synonyms: Jatropha manihot (Kunth),
Manihot manihot (Cockerell),
Manihot melanobasis (Muell)
Family: Euphhorbiaceae
English /common name:
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.
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
cassava, manioc, tapioca 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.

Plant description: shrub with a big tuberous root

Lethal dose :
One dose of pure cassava cyanogenic glucoside (40mg) is sufficient to kill even a cow.
Planthabitat: Hence about 300 grams of fresh root is enough to kill an adult human and about 125 grams
The sweet and bitter cassava plants are indigenous to Southern and of fresh root would be enough to kill a child
Central America but have been introduced to almost all tropical countries
Mode of action :
Traditional use : 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
Used as a food source. American Indians use the brown juice for burns 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.

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 (Na2S2O3), 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.

References Affran DK. Cassava and its economic importance. Ghana Farmer 1968; 12(4): 172-178; Bellotti AC et al. Recent advances in cassava
pest management. Ann Rev Entomol 1999; 44: 343-370;

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Datura metel Scientific name:

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

Plant habitat: Leaves/flowers - mainly atropine

Native to China, India and South East Asia. Seeds/roots - mainly hyoscyamine
Fruits – scopolamine
Plant description:
Shrub-like annual herb with large flowers, typically white or yellow with
deep purple accents. Leaves are alternate and simple. Dose: Accidentally (or intentionally)
ingesting even a single leaf could
Traditional use: lead to severe side effects
Leaves/dried flowers are used to relieve asthma or wheezing like
symptoms in many cultures eg Chinese herbal medicine (yáng jīn
huā). Symptoms:
Leaf poultices are applied to engorged breasts to relief excess milk
production, rheumatic swelling of joints and lumbago. Anticholinergic Thirst, dry mouth, blurred vision,
Powdered root is rubbed into gums or stuffed into cavities for toothache. photophobia, urinary retention occur soon after
ingestion. Skin is hot, dry and flushed. Pupils are
dilated and fixed.
Toxic part of the plant : all parts. Cardiovascular effects are sinus tachycarida,
hypertension, supra/ventricular arrhythmias,
Main toxic constituents : tropane alkaloids 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.
References:
 www.wikipedia.org/wiki/Datura_metel
 www.ces.ncsu.edu/depts/hort/consumer/
poison/Daturme.htm
 www.people.vcu.edu/~asneden/tropane%20alkaloids.
pdf
 waynesword.palomar.edu/ww0703.htm

Scientific name: Abrus precatorius L. Toxicity:

Synonyms: A.minor, A.pauciflorus One seed well masticated can cause fatal poisoning (adults and
children)
Family: Leguminosae
Main toxins: Abrin - concentrated in seeds
Common names:
 Abrus seed, crabs eye, Indian bead, Indian liquorice, wild liquorice, lucky
bean, prayer or rosary beads, precatory bean, weather plant, jumble
Mode of action:
beads, jequirity bean
 Abrin exerts its toxic action by attaching itself to the cell membranes
Plant description: slender perennial twiner  It has a direct action on parenchymal cells (eg liver and kidney cells)
and red blood cells
Traditional use:
 To cure itch, sores and wounds due to bites of dogs, cats and rats Clinical effects:
 Leaves: conjunctivitis, painful swellings; ground with lime for acne, boils,
abscesses and tetanus  Early features of toxicity - burning of the mouth and oesophagus, and
 Seeds: diabetes, Bright’s disease severe gastroenteritis with vomiting, diarrhoea and abdominal pain.
Haematemesis and melaena are less common
Toxic part of the plant: seed
 Later - drowsiness, disorientation, weakness, stupor, convulsions,
 The most poisonous parts of the plant involved in poisoning are the small, shock, hepatotoxicity, cyanosis, retinal haemorrhages, haematuria,
scarlet seeds, that have a black eye at the hilum
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
Myristica
fragrans
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.

References:

http://www.inchem.org/documents/pims/plant/abruspre.htm

Mode of action:
Scientific name: Myristica fragrans
 Elemicin undergoes oxidation of its oleficin side chain to produce TMA (3,4,5-
trimethoxyamphetamine), a psychotropic drug agent
Family: M yristicaceae  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
English/common names: Nutmeg, Mace tree
Clinical features of poisoning:
Plant habitat:  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
 A native of E.Moluccas and other Indian Islands
 intoxication resembles anti-cholinergic intoxication ie profuse sweating, flushed
 Now cultivated in Sri Lanka, Malaya, Philippines, W.Indies & South America face, dry mouth, burning epigastric pain, tachycardia, restlessness, giddiness,
hallucinations
Traditional use:  unlike anti-cholinergic symptoms pupils constrict
 As a spice in foods
 As a traditional medicine for diarrhoea
Diagnosis:
 Blood monitoring (electrolytes, liver enzymes, renal function) and urinalysis
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
Treatment of poisoning: symptomatic and supportive
Animals: oral dose of 24mg nutmeg oil per kg body weight  Induce emesis (with ipecac) or gastric lavage
Main toxins: myristicin & elemicin  Activated charcoal
 Diazepam for restlessness or hallucinations

myristicin References: http://www.rain tree nutmeg.com/plant images/myristica pic.htm

http://www.inchem.org/documents/pims/plants/pim335.htm

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Nicotiana Scientific name Nicotiana tabacum

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)

Mode of action
 Nicotine binds stereo specifically to acetylcholine receptors at autonomic
ganglia, the adrenal medulla, the neuromuscular junction and the brain
Strychnos nux-vomica
 This evokes the release of catecholamine
 nicotine produces ganglionic blockade, vagal afferent nerve stimulation,
or direct depressor effects mediated by action on the brain

Scientific name : Strychnos nux-vomica

Clinical features of poisoning
 Mild: salivation, nausea, dizziness, drowsiness, headache, vomiting, Synonyms : S.lucida, S.colbrina, S.aromatica
diarrhoea, hand tremor
Family : Loganiaceae
 Serious: mental confusion, circulatory collapse (shallow rapid pulse, ‘cold
sweating’), convulsions, loss of consciousness, cardiac arrest, respiratory English/common name : Poison nut, Nux vomica, Quaker buttons
paralysis
Plant habitat :
Diagnosis
 dry forests of Ceylon, flowers in August
 Blood monitoring (blood gases) and urinanalysis
 A moderate sized or large tree with an erect trunk,
Treatment of poisoning Traditional use : Root - cures fever and bites of venomous snakes
 induced emesis (ipecac) or gastric lavage and activated charcoal Used for preparation of homeopathic medicine
 supportive therapy directed towards maintaining respiration and blood
pressure (IV fluids) and controlling convulsions Toxic part of the plant : seed (although all parts toxics)

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Main toxic constituents : strychnine, (brucine) Diagnosis :

Constituent type : alkaloids  Based on history of ingestion and development of muscular
stiffness
Lethal dose : plant poisoning is rare possibly due to bitter taste
 Strychnine (and brucine) can be measured chemically but there is
 The quantity of strychnine in one seed could be fatal no time to perform this procedure before treatment
 If seeds are swallowed uncrushed they are not poisonous
 Measure acidosis, serum potassium, SGOT, LDH, CPK etc
Mode of action :
 Strychnine is a potent convulsant. It causes increased reflex Treatment of poisonings :
excitability in the spinal cord  Activated charcoal
 Support respiratory and cardiovascular functions
 Brucine – resembles strychnine activity but it is less potent
 If convulsions cannot be controlled with diazepam (IV or rectal), or
if they recur, administer phenobarbitone or phenytoin.
Clinical features of poisonings :
 Intubation with suxamethonium chloride may be necessary
 Symptoms appear within 15 - 30 min of ingestion
 When convulsions and hyperactivity are completely controlled,
- Initial symptoms – bitter taste in mouth, feeling of suffocation
gastric lavage can be performed safely
- 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.
References : http://www.inchem.org/documents/pims/plant
- Complications - lactic acidosis, rhabdomyolysis, acute
renal failure
- Death is caused by asphyxia or muscular paralysis

Scientific name: Ricinus communis Linn.

Synonyms:
Ricinus africanus Willd., Ricinus communis L. var. viridis (Willd.) Müll. Arg., Ricinus

Ricinus communis
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:
 Probably of African origin but now grows in tropical, subtropical
and temperate areas
 Commercially cultivated mainly in Brazil, India, Italy, etc.
 Traditional use:
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)

Diagnosis:
Lethal dose: 1mg/kg pure ricin in man
Blood gases and electrolytes analysis
 Ingestion of a single well chewed bean has caused death Close monitoring of renal, hepatic hematological systems & blood clotting.
 1-3 seeds can be fatal to a child Botanical & pharmacognostical identification of a sample of the plant or v omitus

 2-4 seeds cause severe poisoning in an adult Radioimmunoassay w ith antiricin antibodies labeled w ith iodine 125 for ricin in plasma or urine

 poisoning is unlikely if seeds are swallowed without

chewing Treatment of poisoning:
Main toxic constituent/s: Ricin I nduce emesis at home (ipecac)
I mmediate gastric lav age or activ ated charcoal
Correct fluid & electrolyte imbalance immediately
Constituent type: Glycoprotein or a toxalbumin
I n case of bronchial asthma, oxygen, B2-agonist eg salbutamol and corticosteroids may be necessary (if
 member of a class of plant toxins known as type 2 acute poisoning occurred by inhalation)
ribosome inactivating proteins Antihistamines or corticosteroids may be beneficial in treating skin lesions (if acute poisoning occurred by
skin exposure)

Mode of action: Ricin impairs chain elongation in protein synthesis,

causing cell death and tissue damage

Clinical features of poisoning:

References:
Early on - burning sensation of the mouth and throat http://www.inchem.org/documents/pims/plant.htm
occurs
www.wikipedia.org
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

Main toxic constituents:

Scientific name: Gloriosa superba  colchicine (+ ‘gloriosine’ in tubers)

Synonyms: G.simplex, Methonica doniana, Constituent type: alkaloid

Eugonia superba
Mode of action:
Family: Colchicaceae, Liliaceae
 Colchicine has an antimitotic effect
 It stops cell division by disrupting the spindle apparatus during the
metaphase
English/common names:
 Cells with rapid turnover are affected (bone marrow, intestinal epithelium,
 flame lily, glory lily, tiger claw hair-producing cells -> hair loss)
 It can alter neuromuscular function
Plant habitat:  (It can withstand drying, storage and boiling - tubers not a foodsource!)
 native of tropical Africa, India, Malaya, etc
 found in low country Sri Lanka Clinical features of poisoning:
 Initial symptoms develop within 6-12 hours of ingestion
Traditional use:  burning pain, numbness, itching and tingling around the mouth and throat
 tuber – bruises and sprains with thirst
 nausea, intense vomiting
Poisonous parts of the plant:  abdominal pain, severe diarrhoea with blood and mucus
 The entire plant, especially the tubers, are extremely poisonous  These lead to
 electrolyte imbalance, dehydration, hypovolaemic shock manifested
hypotension and tachycardia

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 After 24 hours patients develop

Datura metel atropine, hyoscine, hyoscyamine alkaloids seed (all)
 Muscle weakness, myoglobinuria, bronchial constriction, Gloriosa superba Colchicine tuber
leucopenia, thrombocytopenia, clotting defects with bleeding,
polyneuropathy cardiac arrhythmias, hepatic insufficiency, acute Nicotiana tabacum Nicotine leaf (all)
renal failure Pagiantha dichotoma ? narcotic, datura-like seed

 In severe cases there may be (Peganum harmala) Harmaline seed

Strychnos nux vomica Strychnine seed

 Respiratory depression, confusion, delirium, convulsions, coma
Alocasia macrorrhiza calcium oxalate crystals leaf/stem (all)
 Death occurs due to shock or respiratory failure Anthurium sp.
(needle-like), toxic proteins

Dieffenbachia sp.

Diagnosis: Scindapsus aureus

Zantedeschia aethiopica
 Toxicological, biomedical, blood gas, haematological analyses Cerbera manghas cerberine, odollum,thevetin cardiac glycosides fruit kernel

Thevetia peruviana thevetin A, theventin B fruit

Treatment of poisoning: Adenia palmata cyanogenic glycoside, toxalbumin,

emulsin enzyme
cyanogenic glycosides fruit

 hospitalize the patient immediately Manihot utilissima linamarin, (linase enzyme) tuber

 induce vomiting (ipecac) / gastric lavage Abrus precatorius abrin toxalbumins seed

Jatropha curcas curcin seed (all)

 give repeated activated charcoal
Jatropha multifida Jatrophin
 supportive care eg IV fluid, assisted ventilation Ricinus communis ricin
may be needed Eucalyptus robusta oil of eucalyptus (eugenol) volatile oils all

Myristica fragrans myristicin seed (aril)

Amanita phalloides phalloidin, phalloin, phallolysin phlallatoxins aerial parts

alpha, beta, gamma amanitin amatoxins (mushroom)

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