TOXIC EFFECT OF
PLANT by Sanskriti
Nausheen
Shubhshree
Amit
Why do plants release toxins ?
Why do plants release toxins ?
In the course of evolution,
plants have been attacked by
viruses, bacteria, and fungi, and
have been eaten by animals of
many kinds. In response, plants
have developed various defense
mechanisms, including
synthesis of antimicrobial
chemicals and chemicals
designed to repel animals by
various means
Apple seeds contain a toxic compound called
amygdalin, which can release cyanide, a poisonous
substance, when ingested. While the seeds
themselves are not typically fatal, consuming large
quantities can cause serious health problems.150-
200 apple seeds must be consumed to be fatal which
is about 18-25 apples
Cherry, Peach, and Apricot Pits – Cyanide
Poisoning Risk
The seeds (pits) inside cherries, peaches, apricots,
and similar fruits contain amygdalin, a natural
compound that can break down into hydrogen
cyanide (HCN) when metabolized in the body.
Cyanide is a highly toxic substance that can interfere
with oxygen transport in the blood, leading to
serious health effects or even death in large
amounts. Amygdalin itself is not highly toxic, but
when the pit is chewed, crushed, or ground,
enzymes in the body convert it into cyanide
Toxic effects by
organ
I. Skin
II. Respiratory tract
III.Gastrointestinal tract
IV.Cardiovascular system
V. Liver
VI.Bone & bone marrow
VII.Kidney and bladder
VIII.Nervous system
IX.Skeletal muscle and
neuromuscular junction
X. Reproduction and teratogenesis
XI.Bone and tissue calcification
Factors affecting plant toxicity
There may be marked variability in the amount of a toxic chemical
produced by a plant. The reasons for variability in concentration of toxic
chemicals are several:
1. Different portions of the plant may contain different concentrations of a
chemical. An example of localization of bioactive compounds is found in the
bracken fern (Pteridium aquilinum) in which the carcinogenic terpene,
ptaquiloside, is found in high concentrations in the fronds compared with the
roots .
2. The age of the plant contributes to variability. Peak concentrations of
bioactive compounds often are found at different periods of growth. For
example, in lettuce (Lactuca species) the concentration of lactucin and other
sesquiterpenes increases with maturation, reaching a peak in the latex when the
flower stalk is forming.
3. Climate and soil influence the synthesis of some chemicals. For example,
lichens produce carotenoids in direct relation to the amount of sunlight,
with the advantage to the plant that carotenoids protect from excessive
ultraviolet light.
4. Genetic differences within a species alter the ability of plants to synthesize a
chemical.
SKIN
1. Contact Dermatitis
Contact dermatitis is a type of skin inflammation that occurs when the skin comes
into contact with an allergen or irritant. It is a common condition that can be
caused by a variety of substances, including plants. Several plants that are common
to the temperate regions worldwide contain compounds that produce irritation on
contact with the intact plant.
Example : The genus Euphorbia (Euphorbiaceae, spurge family) contains
hundreds of species in the temperate and tropical regions. Characteristically, the
stems and leaves exude milky latex when damaged. The latex contains diterpene
esters that are irritating to the skin.
2. Allergic Dermatitis
Allergic dermatitis is a type of skin inflammation that occurs when the skin reacts to an allergen. It is a common
condition that can be caused by a variety of substances, including plants.
Example : Most people are familiar with allergic dermatitis caused by contact with some plants, such as poison ivy.
These allergens tend to be located in the outer cell layers of plant organs.
Blisters from contact with poison ivy
Poison ivy is a type of allergenic plant in the
genus Toxicodendron native to Asia and North
America.
3. Photosensitivity
Not all cases of dermititis from plants are
due to skin contact. Poisoning of livestock
from Hypericum perforatum has been
reported from several countries. The toxic
principle is hypericin (a bianthraquinone),
present throughout the plant. Sheep are the
most commonly affected animals,
ingesting the plant in pasturage. The effect
in sheep is development of edematous
lesions of the skin in areas not well
covered with hair, including the ears, nose,
and eyes. Hypericin causes
photosensitization and the lesions appear
from exposure to sunlight
St. John's wort plant
Respiratory Tract
Allergic Rhinitis:
Rhinitis from inhalation of plant pollens, also
known as “hay fever” or pollinosis, is a seasonal
problem for many individuals. Many plant species
contribute to airborne pollen, especially grass
pollens. Poa and Festuca species are major
contributors to the allergic response. It is cause due
to the overreaction of the immune system to certain
substances in the air, such as pollen, dust, and mold.
Castor bean
Castor bean is a plant that contains a toxic compound called ricin.
Ricin is a potent toxin that can cause respiratory distress, including
coughing, wheezing, and shortness of breath.
How Ricin Affects the Respiratory Tract
When ricin is inhaled, it can cause damage to the lining of the lungs
and airways. This can lead to inflammation and scarring of the
lungs, making it difficult to breathe.
Symptoms of Ricin Exposure
The symptoms of ricin exposure can include:
1. Coughing: A persistent and severe cough that can produce
blood or mucus.
2. Wheezing: A high-pitched sound when breathing out.
3. Shortness of breath: Difficulty breathing or feeling like you
can't catch your breath.
4. Respiratory failure: In severe cases, ricin exposure can cause
respiratory failure, which can be life-threatening.
Gastrointestinal System
Antimitotic Effects
• Podophyllum peltatum (May apple, Berberi-daceae) contains the toxic purgative,
podophyllotoxin, especially in foliage and roots. Overdose results in nausea and severe paroxysmal
vomiting. Podophyllotoxin inhibits mitosis by binding to micro-tubules, and this property has made
the toxin of interest in treatment of cancer .
• Colchicine is best known in western medicine for its antimitotic effect, resulting from block of
formation of microtubules and failure of the mitotic spindle, for which it is useful in attacks of
gout. Colchicine is the major alkaloid in the bulbs of Colchicum autumnale (autumn crocus,
Liliaceae), native to Asia Minor. Severe gastroenteritis (nausea, vomiting, diarrhea, and
dehydration) follows ingestion of the bulbs that may be mistaken for wild garlic. Systemic effects
(confusion, hematuria, neuropathy, and renal failure) may develop in severe poisoning. Bone
marrow aplasia results from block of mitosis in bone marrow. Additional toxic effects may be due
to lectins in the plant. In southern Europe, hay for cattle may contain the wild autumn crocus, and
deaths occur if contamination is heavy.
• Tubers of Gloriosa superba (glory lily): This ornamental lily also contains colchicine. The plant
grows wild in Sri Lanka and poisoning by Gloriosa tubers has been reported as the most common
plant poisoning in that country. Poisoning has also been reported in India .
Protein Synthesis Inhibition
Some of the most toxic plant proteins act through inactivating protein systhesis.
1.Ricinus communis (castor bean) is a member of the family Euphorbiaceae, which contains several
genera that produce toxic chemicals.
• The castor bean is an ornamental plant introduced from India. If the attractive, mottled seeds are
eaten, children and adults experience no marked symptoms of poisoning for several days. In this interval
there is some loss of appetite, with nausea, vomiting, and diarrhea developing gradually..
• With fatal doses the gastroenteritis becomes severe, with persistent vomiting, bloody diarrhea, and
icterus. • Death occurs in 6–8 days. The fatal dose for a child can be five to six seeds; it may be as low as
20 seeds for an adult.
• However, fatality is low—less than 10% when a “fatal” dose is consumed—because the toxic protein is
largely destroyed in the intestine.
• Death from castor beans is caused by two lectins in the beans: ricin I and ricin II. The more toxic is ricin
II. Ricin II consists of two amino acid chains. The A-chain (molecular weight 30,000) inactivates the 60s
ribosomal subunit of cells by catalytic depurination of an adenosine residue within the 28s rRNA (Bantel
et al., 1999) and blocks protein synthesis. The A-chain is endocytosed into the cell cytosol after the B-
chain (molecular weight 30,000) binds to a terminal galactose residue on the cell membrane. The two
chains are linked by disulfide bonds. Details of binding properties of ricin to glycoproteins have been
investigated (Wu et al., 2006).
Skeletal Muscle and Neuromuscular Junction
Toxic Effects on the Neuromuscular Junction (NMJ)
• The NMJ is a synapse where motor neurons transmit signals to skeletal muscles via acetylcholine (ACh).
• Plant toxins can interfere with neurotransmitter release, receptor binding, or enzyme activity, disrupting muscle
control.
• Block of the neuromuscular junctionof skeletal muscle may result from either block of postsynaptic
acetylcholine receptors (nicotinic receptors) by an antagonist or by an agonist causing excessive stimulation of
the receptor followed by prolonged depolarization.
• Nicotine stimulates autonomic,as well as the neuromuscular junction.
• An isomer of nicotine ,anabasine, present in Nicotiana glauca (tree tobacco, Solanaceae),produces prolonged
depolarization of the junction.
• Consumption of the leaves of the plant has caused flexor muscle spasm and gastrointestinal irritation,
followed by severe, generalized weakness, and respiratory compromise (Mellick ..,1999).
• Poisoned cattle show muscle tremors and ataxia followed by prostration and respiratory arrest in fatal
cases.
• The compound has a high affinity for the acetylcholine receptor at the neuromuscular junction like
curare.
• Physostigmine has been used successfully as an antagonist in some cases of methyllycaconitine
poisoning .
Mechanisms of Toxic Effects on NMJ
a) Inhibition of Acetylcholine (ACh) Release
• Some plant toxins block calcium entry into nerve terminals, preventing ACh release.
• Result: Muscle paralysis and weakness.
• Example:
• Coniine (from Poison Hemlock - Conium maculatum): Blocks ACh release, causing respiratory
failure.
B) Toxins Mimicking Acetylcholine
Some plant toxins directly stimulate ACh receptors, causing uncontrolled muscle contractions.
Example:
Nicotine (from Tobacco plant - Nicotiana tabacum): Mimics ACh, causing muscle tremors, seizures, or
paralysis.
c) Ion Channel Disruption
• Some toxins alter sodium (Na⁺), potassium (K⁺), or calcium (Ca²⁺)
channels, affecting nerve impulse transmission.
• Result: Seizures, tremors, or paralysis.
• Example : Grayanotoxin (from Rhododendron species): Disrupts
sodium channels, leading to paralysis
Toxic Effects on Skeletal Muscle
Skeletal muscle contraction relies on ACh signals, calcium regulation, and ATP energy
supply. Plant toxins can weaken muscles, induce spasms, or damage muscle tissues
directly.
Skeletal Muscle Direct damage to skeletal muscle fibers has been demonstrated in some
plant poisonings.
Seeds of the poisonous species of Thermopsis contain quinolizidine alkaloids,
principally anagyrine and thermopsine.
The symptoms are abdominal cramps, nausea, vomiting, and headache lasting upto 24
hours. Serious poisoning has occurred in livestock grazing on thermopsis montana (false
lupine). The animals develop locomotor depression and recumbancy.
Microscopic areas of necrosis in skeletal muscle are found on autopsy .
Seeds of Cassia obtusifolia (sicklepod, Leguminosae) have been found as a
contaminant of animal feeds. Consumption of the seeds in cattle, swine, and chickens
causes a degenerative myopathy in cardiac and skeletal muscle.
Clinical Manifestations of Plant Poisoning Neuromuscular Symptoms:
Muscle weakness Respiratory distress (due to diaphragm paralysis)
Drooping eyelids (ptosis)
Difficulty swallowing or speaking
Flaccid or spastic paralysis
Skeletal Muscle Symptoms:
Severe muscle cramps
Uncontrolled twitching or spasms
Muscle stiffness or rigidity
Muscle fatigue and weakness
Mechanisms of Toxic Effects on Skeletal Muscle
a) Muscle Paralysis (Flaccid Paralysis) Toxins that prevent ACh release or block ACh receptors cause
muscle relaxation and weakness. Result: Respiratory paralysis, inability to move. Example: Curare (from
Chondrodendron tomentosum): Blocks ACh receptors, causing paralysis.
b) Muscle Spastic(Spastic Paralysis) Toxins that increase ACh levels or disrupt calcium homeostasis cause
continuous muscle contractions. Result: Muscle cramps, seizures.
c) Disruption of Calcium Regulation : Calcium imbalance prevents proper contraction and relaxation
cycles. Result: Muscle fatigue, cramping, or paralysis.
Example: Aconitine (from Monkshood - Aconitum spp.): Alters calcium ion channels, causing muscle
overactivity.
d) Energy Depletion and Muscle Necrosis : Some toxins damage mitochondria, reducing ATP production,
which muscles require for contraction.
Result: Muscle fatigue, cell death, or tissue necrosis.
Example: Taxine (from Yew plant - Taxus baccata): Impairs mitochondrial energy production, causing muscle
and cardiac failure.
Bone and Soft Tissue Calcification
Solanum malacoxylon (Solanaceae):
Causes "enteque seco", a wasting disease in cattle in South America's eastern coastal plains.
Symptoms include:
1. Decreased bone calcification
2. Calcification of the vascular system (especially heart and aorta)
3. Severe cases affect lungs, joint cartilage, and kidneys.
4. Resembles vitamin D intoxication.
Toxin: 1,25-dihydroxycholecalciferol glycoside (water-soluble vitamin D-like compound). Cestrum
diurnum (Day-blooming jasmine, Solanaceae): Causes hypercalcemia and extensive soft tissue
calcification. Found in grazing animals in Florida.
Toxin: Dihydroxyvitamin D3 glycoside. Cestrum laevigatum:
Causes calcium deposition in chickens. Occasionally contaminates hay in Europe.
Mechanism of Toxicity : All these plants contain vitamin D-like compounds that promote
excessive calcium absorption and deposition. Leads to mineralization in soft tissues, resembling
vitamin D overdose. Impacted Species are Cattle ,Sheep, Chicken . Important for diagnosing
unexplained cases of soft tissue calcification in livestock. Mimics the clinical signs of
hypervitaminosis D.
Quiz
1)Which toxic lectin found in castor beans is more dangerous?
a) Ricin I
b) Ricin II
c) Abrin-a
d) PAP-S
2) What is the primary mechanism by which ricin II inhibits protein synthesis?
a) Binding to DNA and preventing replication
b) Blocking ribosomal RNA function through catalytic depurination
c) Preventing the attachment of amino acids to tRNA
d) Interfering with mRNA translation
3) What is the primary function of the defense mechanisms developed by plants?
a) To attract animals for pollination
b) To protect plants from viruses, bacteria, and fungi
c) To produce colorful flowers for aesthetic purposes
d) To increase plant growth and development
Reference
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(Keeler and Baker, 1990)
