Poisons from plant origin

Group 3
1. Jemila Redwan ugr/9277/12
2. Kidist Alemnew ugr/4153/12
3. Lencho Tesfaye ugr/0981/12
4. Lidiya Tadege ugr/9464/12
5. Lucy Tewodros ugr/1766/12
6. Markos Hamiso ugr/3683/12
7. Melat Maedot ugr/5714/12
8. Melat Salle ugr/1574/12
9. Meron Asfaw ugr/0336/12
10. Melkamedil Yihun ugr/7219/12
11. Mezid Mohammed ugr/9636/12

Submitted to:- Mr. Abel

6/10/2022
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 1. Organic acids (oxalate)

2. Alcohol (cicutoxin, tremetol)

3. Resin and resinoid (tetrahydrocannabinol, urushiol)

4. Proteinaceous compound-
content 4.1-toxalbumins (abrin, ricin) and amines (Aminopropionitrile)

4.2- polypeptide (amatoxin, phallotoxin, phalloidin)

5. alkaloids-

5.1-tropines, pyrrolizidines, pyridine

5.2.-purine, isoquinoline, steroid, diterpines

6. Glycoside (steroids, coumarins)

7. Clinical studies

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1. Organic acids
oxalate
 It is colorless, water soluble, crystallized
organic acid
 spinach, rhubarb and sorrel are major

sources
 glycine, ascorbic acid, ethylene glycol and

other organic compounds metabolism also

produces it

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Route of intoxication
 inhalation, ingestion and contact with body

parts
Mechanism of intoxication
 Formation of calcium oxalate which is seen

like the figure below in urine.

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 Signs and symptoms
 asymptomatic for the first 12 hours
 hyperoxalurea, Dark colored urine Nausea,

Severe myalgia Abdominal discomfort

Treatment
• to decrease calcium oxalate formation
• Increase fluid intake
• Limit high oxalate foods and salt
• Lumasiran (Oxlumo) and thiazide diuretics
• If stone is formed it can be managed by dialysis
and kidney transplant

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2 Alcohols
Tremetol
 It is mixture of ketone and alcohol and is
found in white snakeroot and rayless
goldenrod.
 it induces trembling in animals and milk
sickness in humans when it’s consumed.

Route of poisoning
 If contaminated milk or meat is ingested
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Mechanism of intoxication
 Unclear but suggested mechanism is by

inhibition of TCA cycle  lactic acid build up

acidic pH
Possible organ damages
 muscular degeneration.
 Lactating animals are likely less susceptible

because of excretion via milk

 Due to conduction problems, cardiac myopathy

causes heart irregularity, which can lead to

death

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 Cicutoxin
 Is chemically instable plant component which
is found in Apiaceae family example :-
hemlock (Cicuta species) and water dropwort
(Oenanthe crocata).

Mechanism of intoxication
Non competitive antagonism at GABA receptor

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Sign and symptom
 CNS disruption
 Coma, cyanosis, amnesia
 Absence of muscle reflex….

Treatment for alcohol poisoning

 Immediate bowel evacuation
 Using benzodiazepines if cicutoxin poisoning
 Using naso gastric activated charcoal if

tremetol

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3. Resin and Resinoids
 Resins are mixtures of terpenoids and
resinoids are products of the resinous plants
or animals example :- oleo resin and balsams

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Effect and symptom

 Allergy e.g. epoxy resin(powerful irritant)

 weakness, depression, labored breathing,

elevated temperature, staggering,

degeneration of kidneys, dilation of pupils
 Irregular heartbeat, hypotension, collapse,

coma and death…….

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Treatment
 Provide breathing support to manage
breathing difficulty
 administer activated charcoal or laxative to

eliminate
 surgical treatment is used to remove the

burnt part ( if severe)

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4. Proteinaceous Compound
4.1 Toxalbumin and Amines

Ricin
 It is most widely used toxalbumin,
as biochemical warfare agent and as
bio terrorizing poison
 It is isolated from a caster seed

Use
 It attacks CD5 T-cell antigen and

interleukin-2 receptor, prevent cellular

protein synthesis, treatment of cancer
 commercial mole repellant

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Route and Mechanism of intoxication

 If ingested or if ocular or dermatologic exposure

happen it is toxic
 It has disulfide linked A chain and B chain.
 B chain bind to galactose containing receptor

allow entry into the cytosol and facilitate GI wall

penetration and A chain bind irreversibly 28s sub
unit of ribosome  inhibit protein synthesis
 adrenal cortex, spleen, bone marrow and liver are

primary organs to be affected

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 Sign and Symptom
 abdominal burning, anaphylaxis,
bronchospasm, contact dermatitis, diarrhea,
fever, hematuria, hypotension, GI
hemorrhage, GI irritation, nausea,
oropharyngeal burning, seizures, shivering,
tachycardia, thirst, vomiting
Treatment
 Supportive: Replace fluid/electrolyte loss
 Aggressive gastrointestinal decontamination

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Abrin
 Same with ricin but originated
from abrus
precatorius.
 75 times potent rodenticide but

no report found of its use during

war and terrorism
 Intoxication is from ingestion of

the seed
 It has no specific treatment so

management is symptomatic and

supportive
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Amines (Aminopropionitrile)
 Toxic amino acid derivative from lathyrus
plant
 It interfere with lysyl oxidase which cross

links collagen with elastin

 results in impairment of connective tissue

stability and causing osteolathyrism (bone

deformity) and angiolathyrism (aortic
aneurisms).

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 4.2 Polypeptide proteins
( Amotoxin, Phallodin, Phallotoxin and Lectin )

Amatoxin
 It is major component of mushroom specifically

in the amanita species.

 If ingested it bind non-covalently

to and inhibit RNA polymerase II

and protein synthesis in
hepatocyte.

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Treatment and complications
 Decontamination with activated charcoal is
possible if patient reaches hospital on time.
 No antidote exists so supportive treatment is

given.
 encephalopathy, neuropathy, pancreatitis,

dehydration and renal liver toxicity are major

complications of amatoxin.

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Phallotoxin
 It is also mushroom(phalloid)poison accounting for
90% toxicity
 The mechanism of their action is inhibiting F-actin
and attacking the plasma membrane.

Phallodin
 It is primary member of phallotoxin it is different
from phallotoxin because it is taken up by liver only
through bile salt membrane transporter, but the
mechanism is the same. 20
Treatment
 no specific antidote for both
 The initial treatment is supportive care with

adequate intravenous fluid and electrolyte

replenishment
 For the injured liver, N-acetyl cysteine

administration is beneficial.

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 Lectin
 These plant proteins are
dose dependent poisons
 It is found in raw legumes

and whole grains like wheat

and kidney beans
Mechanism of action
 It impairs membrane repair.
 It also give favorable

environment for harmful

bacteria then causing many
complications.

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Symptoms
 skin rush, joint pain, general inflammation,

nausea vomiting, diarrhea

Prevention
 Eat the grains after boiling at least for 10

minutes.
Possible complications
 Obesity, diabetes, autoimmune disease and

so on.

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 5.Alkaloids
 Old assumptions
◦ Thought to be found only in higher plants.
◦ plant component that show only basic properties and
strong biological effect.
 both central and peripheral effect.
 small dose activate the central nervous system.
 larger doses first depression followed by

delirium and finally coma.

 Here they are according to their chemical

structure into:
◦ tropanes, pyrrolizidines, pyridine, purines,
isoquinoline, steroid, and diterpines.

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A. Tropanes
 commonly known as Belladonna alkaloids.
 mainly known to occur in solanaceae and

erythroxylaceae families.
 Common ones; (-)-hyoscyamine, (-)-scopolamine,

and atropine.
Mechanism of Intoxication
• Are competitive antagonists at muscarinic
acetylcholine receptors.
• Tropane alkaloids can modulate the functions of
smooth muscles, heart rate, rate of respiration, and
our central nervous system.

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Sign and Symptoms Treatment
 2-step toxicity; delirium
followed by coma.
• Washing the stomach
 bitter taste followed by with a weak solution of
dry mouth and throat, tannic acid.
aphasia, dysphagia, • Prostigmine in 0.5-
thirst, face flushing, 1mg dose or
dilated pupils, pilocarpine in 5-15mg
hyperthermia, dry and
dose. (physiological
hot skin, tachycardia,
tachypnea..
antidote)
 The usual fatal dose is • Barbiturates are given
50-100 seeds and has a for the delirium
fatality period of 24
hours.
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B. Pyrrolizidine Alkaloids

 Named senecio alkaloids ;S. vulgaris and S. pierotti.

 also found in asteraceae, borainaceae, and

fabaceae.
 Contains common pyrrolizidine nucleus, an amino-

alcohol known as necine unit, and a fatty acid chain

necic acid. ( variety of Pyrrolizidine alkaloids)

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 Mechanism of Intoxication
 could be either saturated or unsaturated.
 unsaturated ones are responsible for their

toxicity, metabolized to pyrroles in the hepatic

parenchymal cells.
 Toxicity follows three mechanisms these are:

◦ their ester group is hydrolyzed to necine base,

◦ the necine base is oxidized to N-oxide, and
◦ the necine bases are dehydrogenated to
didehydropyrrole.
 The metabolites formed have different toxicity

level on the liver.

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 Sign and Symptoms Treatment
 The toxic substances are  Primary care is based
carcinogenic, mutagenic, on supportive care.
and teratogenic.  Prevention of
 Nausea, elevated liver exposure is our only
enzymes, fever, acute option since no
upper-gastric pain, specific antidote or
distended abdomen with medication exists for
dilated veins on the it.
abdomen.
 Rate of mortality is

higher in the acute

phase as it can cause
liver failure. 29
 C. Purine
 naturally found in our genetic makeup, DNA and
RNA.
 Our body decompose them into uric acid, cause of

gout.
 The xanthine derivatives caffeine and theobromine

are the most common purine alkaloids.

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 Caffeine
 Safety varies between individuals.
 MTC 15mg/L, toxic 50mg/L, fatal >80mg/L

Sign and Symptoms

 GI-nausea, vomiting, and diarrhea;
 NS-hallucinations, anxiety, headache, and

sometimes coma.
 There are also feelings of weakness, rigidity,

tremor, hyperventilation, diuresis, and death.

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 Mechanism of Intoxication
 Target ->adenosine receptors, PDE-I, calcium channels,
GABA(A) receptors.
 Main target-adenosine receptors, as a non-selective
antagonist, catecholamine release  vasospasm
HTN,MI
 PDE-I when potentially lethal doses have been ingested.
 Activation calcium channels IC calcium release (250
μmol).
 The above actions result in the most often cause of
death, ventricular fibrillation.
 GABA(A) increase catecholamine levels and inhibit
acetyl-cholinesterase.

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Treatment
 Supportive care depending on symptoms and
physical conditions of the patient.
 mild side effects, and irritability; mild

intervention or benzodiazepine.
 massive overdose might require numerous

interventions like hemodialysis.

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Theobromine

 Methylxanthine alkaloid is the main toxic

component of chocolate, Theobroma cacao.
 toxic in dogs, slow absorption and longer half-life.
 Mechanism of intoxication and sign and symptoms

are similar with caffeine’s.

Treatment-> emetics, activated charcoal admin.,
urinary catheterization and other symptomatic
therapies.

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D. Steroidal alkaloids
 Solanum type and the Veratrum type.
Solanine
 found in all nightshades, including tomatoes,

potatoes, and eggplant.

 “Potato plant poisoning”
 Toxic even when small amount is ingested,

degree of signs and symptoms vary among

individuals.

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Mechanism of Intoxication
 acts as a cardiac glycoside and inhibits

cholinesterase activity due to structural

resemblance.
Sign and Symptoms
 fever, headaches, NVD, stomach cramp,

arrhythmia, headache, and dizziness. In more

severe cases fever, hallucination, paralysis, loss of
sensation, dilated pupils, hypothermia, and
jaundice.
Treatment
 depends on the consumed amount, time interval,

severity of symptoms, and personal condition.

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 E. Isoquinoline
 Found in Argemone, Chelidonium, Corydalis,
Dicentra, Papaver, and Sanguinaria species.
 Smoked for their stimulant and hallucinogenic

effect.
Treatment
 Activated charcoal for any ingestion of

isoquinoline plant within one hour.

 For patients experiencing seizure

Benzodiazepines can be used and opiate

antagonists like Naloxone might also be used to
reverse the effect.

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6. Glycoside
 organic compounds found in Scrophulariaceae,
Oleceae, and Liliaceae.
 selective steroidal glycosides (purine).

Mechanism of Intoxication
 action on Na-K ATPase pump increase cardiac

output and rate of myocardial contractility.

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 Treatment
 If ingested baseline ECG and electrolyte is a must.
 signs of toxicity without ingestion should be

admitted to ICU over 24 hour period for

observation and treatment.
 Gastric lavage, activated charcoal, IV fluids are to

be given within an hour post-ingestion.

 Serum potassium measurement- hyperkalemia is

common infestation of cardiac glycoside.

 Atropine for sinus bradycardia and AV block.
 Anti-arrhythmic should be given for the

tachyarrhythmia.

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Veratrum alkaline esters and their glycosides

 structurally and chemically similar to steroids.

 used as antihypertensive agents but seized due to

their narrow therapeutic.

 Veratridine-most potent

Sign and Symptoms

 nausea, vomiting, abdominal distention,

salivation, respiratory depression, yellow or green

scotomata, muscle hypertrophy, and rarely
seizures, bradycardia, hypotension, and cardiac
conduction abnormalities.

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 Mechanism of Intoxication
attach to a limited number of voltage-sensitive
sodium channels in conductive cells increase
sodium permeability  raising intracellular sodium
concentration  increased automaticity, enhanced
vagal tone without hyperkalemia, and occasional
neurotoxicity.
Treatment
• Initial management-activated charcoal if the
ingestion has occurred within the last 2 hours.
• Atropine for bradycardia.
• Hypotension- crystalloid fluids or vasopressors
are used.
• May also require mechanical ventilation and
cardiopulmonary resuscitation.
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7. Clinical Study of Plant Poison
 Phytotoxicology is the study of plant poisons
that includes the use of plant toxins in
laboratory settings to detect different
properties.
 With all the other parameters in mind dose is

often the aspect that causes a substance to

be toxic.
 It must be a focus of research, in order to

understand and set limits on how a plant

constituent causes toxicity.

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 Benefits
 It aids in the identification of dangerous plants an
d harmful chemicals.
 When substances are discovered to be hazardous,

elucidate the biological and molecular mechanism

of action.
 When poisoning happens, develop diagnostic and

prognostic procedures.
 Develop loss reduction management strategies

and therapies.
 their bioactive compounds are suitable for usage

in clinical setting in a safe manner.

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 Applications
 In cancer therapy, paclitaxel, effective in the
treatment of breast, lung, and other
malignancies. It has also been demonstrated to
be effective in avoiding coronary artery re-
narrowing in stent recipients.
 Natural poisons have been utilized for medical

purposes for millennia. The pain of operation

was eased by small dosages of opium, mandrake,
henbane, and hemlock.

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Conclusion
 The number of innovative and clinically
relevant plant remedies and medical items
will undoubtedly increase as our
understanding and characterization of plant
poisons and their mechanisms of action
grows as a result of technological
advancements in chemical purification and
identification.

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