Natural toxicants

TOXICOLOGY
 Toxicology is derived from greek words toxicos (poison) and logos (knowledge).
 “It is a study of adverse effects of chemicals on living organisms, in other words it is a study
of symptoms, mechanism , treatments and detection of poisoning especially the poisoning of
peoples. Chief criteria regarding the toxicity of the chemicals is dose.”

Toxicity Class
 Major Toxicity: These plants may cause serious illness or death.
 Minor Toxicity: Ingestion of these plants may cause minor illnesses such as vomiting or
diarrhea.
 Oxalates: The juice or sap of these plants contains oxalate crystals. These needle-shaped
crystals can irritate the skin, mouth, tongue, and throat, resulting in throat swelling, breathing
difficulties, burning pain, and stomach upset..
 Dermatitis: The juice, sap, or thorns of these plants may cause a skin rash or irritation. Wash the
affected area of skin with soap and water as soon as possible after contact. The rashes may be
very serious and painful..
 Introduction
 Poisonous plants
 A poisonous plant is one which, as a whole or a part thereof; under all or certain conditions, and in
a manner and in amount likely to be taken or brought into contact with an organism, will exert
harmful effects or cause death either immediately or by reason of cumulative action of the toxic
property, due to the presence of known or unknown chemical substances in it, and not by
mechanical action

Classification of poisonous plants

Poisonous plants can be classified in a number of ways,
however the most common classifications are:
Based on active chemical constituents
Based on physiological action
Based on taxonomical system
However they can also be classified based on the poisonous
parts (bark, root, leaves, seed etc) of the plant.
Classification on basis of physiological action
 Neurotic- Papaver somniferum
 Spinal- Strychnos nux vomica
 Cerebral- Cannabis sativa, Erythroxylon coca, Atropa balledonna, Dhatura fastuosa
 Cardiac- Nicotiana tabacum, Aconitum napellus, Digitalis purpurea
 Irritant -Abrus precatorius, Calotropis gigantea, Cytisus laburnum, Argemone mexicana,
Croton tiglium
 Miscellaneous- Cyanogenetic glycosides, Ergot, Oleander (Glycoside), Poisonous Mushroom
 Plant toxicities in humans and animals
 Pyrrolizidine alkaloids are among the most significant plant chemicals causing disease in animals and
humans.
 After absorption from the gut, the compounds are converted to electrophilic pyrroles in the liver
which, apart from causing damage to this organ, may escape to cause injury to extrahepatic tissues
such as the lungs, heart, and kidneys.
 A group of compounds more recently found to be associated with neurotoxicity are various
polyhydroxyalkaloids which are able to interfere with polysaccharide metabolism.
 They are able to inhibit lysosomal monosaccharidases by virtue of their structural resemblance to the
transition state of particular sugar molecules.
 The resulting lysosomal storage diseases have pathology identical to that of the respective congenital
and heritable lysosomal storage diseases which occur in animals and humans.
 Consumption of cycad plants by cattle may cause a neurotoxicity characterised mainly by a posterior
sensory ataxia.
 In recent years, cycads are considered to be a risk factor for a spectrum of progressive neuro
degenerative diseases of humans in the Western Pacific region.
 The known toxins in the plant are the methylazoxymethanol glycosides which are hepatotoxic and
carcinogenic, and the neurotoxic non-protein amino acid beta-methylaminoalanine.
 A plant carcinogen which can be of great abundance in the nutritional environment is the illudine-
nor-sesquiterpene glucoside ptaquiloside which is found in bracken fern.
 This is the only plant carcinogen which causes natural outbreaks of bladder and/or intestinal cancer
in livestock. Many legumes contain phyto-oestrogens, notably isoflavones.
 Consumption of these compounds at high levels by sheep can cause extensive lesions of the genitalia
of females and castrated males.
 Higher plant toxins

Essential oils,Phenly propanes,

Monoterpenes,Plant acids, Glycosides and
alkaloids
 Toxicity of Essential
oils
Terpene
Cineol
Botanical source : Eucalyptus glublus
Family : Myrtaceae
Part used: Leaves
Toxicity: Systemic toxicity can result from ingestion or topical application at higher than recommended doses.The
probable lethal dose of pure eucalyptus oil for an adult is in the range of 0.05 mL to 0.5 mL/per kg of body weight.
Severe poisoning has occurred in children after ingestion of 4 mL to 5 mL of eucalyptus oil.
 Terpene
Pine oil
Botanical source : Pinus sylvestris
Part used: Seed
Family: Pinaceae Bornyl
Borneol
Chemical composition: The main chemical constituents acetate
of pine oil are borneol, bornyl acetate and b-phallandrene,
alpha and beta - pinene and 3-carene.
Toxicity: Pine oil has a relatively low human toxicity level, a low
corrosion level and limited persistence; however, it irritates the skin and
mucous membranes and has been known to cause breathing problems.
Large doses may cause central nervous system depression.
Monoterpene
Thujone
Botanical source : Artemisia absinthium
Family: Asteraceae
Part used: Leaf & flowering top constituents
Chemical constituents:
The hydro distilled essential oil of the
aerial parts mainly contain caryophyllene oxide , p-cymene,1,8-cineole
and (Z)-lanceol acetate .
Toxicity: Thujone is reported to be toxic to brain, kidney, and liver
cells and could cause convulsions if used in too high dose. In
extreme quantities, thujone is toxic and may cause hyperactivity, P- cyamine
excitability, delirium, seizures or worse .
Monoterpene
Menthafuran
Botanical source : Mentha pulegium
Family: Lamiaceae
Common name: Pennyroyal
Menthafuran
Part used: Leaves
Common name : Pennyroyal
Toxicity: Menthofuran is an organic compound found in a variety of essential oils
including that of Pennyroyal. It is highly toxic and believed to be the primary toxin in
Pennyroyal responsible for its potentially fatal effect. After ingestion of menthafuran,
it is metabolically activated to chemically reactive intermediates that are hepatotoxic.
 Phenyl propane
Apiol
Botanical source : Petrosileum hortense
Family : Apiaceae
Part used: Leaves
Toxic effects: The toxic dose is difficult to define, because it depends on the mode of
preparation and
on the association with other substances that can enhance the toxicity of the product. But the
facts that patient ingests an exceedingly large dose of the drug in a short period of time may
help to enhance the severity of the symptoms.1.He reacts with cell membrane dissolving the
latter;2.Patients show a bleeding tendency associated to thrombocytopenia and an anemia
partly due to blood loss and partly on a hemolytic basis.3.Ematuria4.Fatty liver and
necrosis5.Demielinization of peripheral nerves. All the cases reported would tend to show that
the process is limited to the peripheral nerves and there is no involvement of the SNC.

Safrol
Botanical source: Pimpinella anisum
Family: Umbelliferae
Part used: Root bark or fruit
Toxic effects:
 Following the ingestion of sassafras oil symptoms can include vomiting, stupor,
vertigo and pallor which can appear within 10 to 90 minutes.
 Excessive consumption of tea prepared from the roots of the shrub sassafras
albidum has produced sweating.
Safrol
 In beverages and candy, sassafras was used in the past to flavor root beer.
 It was also used as a tea. But sassafras tea contains a lot of safrole, the chemical in
sassafras that makes it poisonous.
 One cup of tea made with 2.5 grams of sassafras contains about 200 mg of safrole.
That equates to a dose of about 3 mg of safrole per 1 kg of body weight. This is
about 4.5 times the dose that researchers think is poisonous. So, in 1976, the US
Food and Drug Administration (FDA) ruled that sassafras could no longer be sold as
sassafras tea.
Myristicin
Myristicin is found in spices and herbs such
as nutmeg, mace, black pepper, carrot,
parsley and celery
 Nutmeg abuse :
 tachycardia,
 salivation
 CNS excitation
 Nutmeg has been abused as a narcotic
Plant acids
Oxalic acid
The term "oxalic acid" is formed from the Latin word oxalis, which refers to plants
with leaves similar to clover. It is important to note that the leaves of a plant almost
always contain higher oxalate levels than the roots, stems, and stalks.
 Fruits - blackberries, blueberries, raspberries, strawberries, currants, kiwifruit, Oxalic acid
concord (purple) grapes, figs, tangerines and plums
 Vegetables - spinach, Swiss chard, beets (root part), beet greens (leaf part), collards, okra, parsley, leeks and quinoa
are among the most oxalate-dense vegetables. Celery, green beans, rutabagas and summer squash would be considered
moderately dense in oxalates
 Nuts and seeds - almonds, cashews and peanuts contain oxalic acid.

Toxicity: It has been reported that the lethal oral dose is 15 to 30 grams. The toxicity of oxalic acid is due
to kidney failure caused by precipitation of solid calcium oxalate, the main component of kidney stones.
Oxalic acid can also cause joint pain due to the formation of similar precipitates in the joint , there is a
possible risk of congenital malformation in the fetus; may be harmful if inhaled, and is extremely destructive
to tissue of mucous membranes and upper respiratory tract; harmful if swallowed; harmful to and destructive
to tissue and causes burns if absorbed through the skin or is in contact with the eyes
Symptoms and Effects:

• A burning sensation, cough,wheezing, laryngitis, shortness of breath, spasm, inflammation and edema of the
larynx, inflammation and edema of the bronchi, pneumonitis.

• Ingested oxalic acid has an oral LDLo (lowest published lethal dose) of 600 mg/kg. It has been reported that
the lethal oral dose is 15 to 30 grams.The toxicity of oxalic acid is due to kidney failure caused by precipitation
of solid calcium oxalate, the main component of kidney stones. Oxalic acid can also cause joint pain due to the
formation of similar precipitates in the joints. Ingestion of ethylene glycol results in oxalic acid as a metabolite
which can also cause acute kidney failure.
 Plant acids
Amino acids
 proteins are polymerized residues of amino acids
the number and proportion of AA vary from
protein to protein
when proteins are denatured, the AA remain
to study protein, you must study AA
at least 30 different AA, some essential others
Most AA are made using short-chain fatty acids
non-essential
(FA; such as acetic, proprionic or butyric acid)
naturally-occurring have L-configuration
synthetic have large proportion of D
configurations
“D” vs. “L”
Configuration Aromatic Amino Acids
Aliphatic Amino Acids
 AA
Quality Essential AA
Amino acids divided into two  lysine (LYS)
groups:  arginine (ARG)
essential: those the animal  methionine (MET)
cannot synthesize in sufficient  histidine (HIS)
quantity to support maximum
 isoleucine (ILE)
growth, typically dietary in nature
 leucine (LEU)
nonessential: synthesized by
animal body, typically non-dietary  threonine (THR)
in nature  tryptophan (TRY)
 phenylalanine
(PHE)
 valine (VAL)
Amino Acid Toxicity/Antagonism
Toxicity/antagonisms are result of dietary imbalances in EAA
when one EAA is fed in excess it can also increase the requirement for another, structurally-
similar EAA
Toxicity = overfeeding of one EAA and negative effects not mitigated by increasing other EAA
Gastrointestinal distress, such as bloating
Abdominal pain
Diarrhea
Increased risk of gout (build up of uric acid in the body, leading to joint inflammation)
Unhealthy drop in blood pressure
Changes in eating patterns
Need for your kidneys to work harder to maintain balance

Antagonism = one EAA regulates uptake of another

Growth depression can be overcome by supplementation with an amino acids structurally similar to
the antagonist Ex: lysine and Arginine. (structure similar) Excess of lysine→ growth depress
→improve by addition of arginine
Resin acid
• Resin acid refers to mixtures of several related carboxylic acids,
primarily abietic-type acid and pimaric-type acids
• It has three fused ring with the empirical formula C19H29COOH.
• Resin acids are tacky, water-insoluble, produce soaps for diverse
applications, protectants and wood preservatives.
Toxicity : It can cause :
• Carcinogenicity, Reproductive developmental toxicity, Neurotoxicity, Contact dermatitis,
• Eye irritation
• Nose irritation
• Throat irritation
• Asthma
• Changes in lung function.

Pimeric acid
 Glycosides
CARDIOTONIC GLYCOSIDES
Agents that have a strengthening effect on the heart or that can increase cardiac output.
Biological source: Digitalis purpuera
TOXICITY
 Diuretics medicine are given to heart failure patient. Many diuretics can cause
potassium loss. A low level of potassium in the body can increase the risk of cardiotonic
toxicity.
An irregular heartbeat that causes dizziness, feeling that the heart has skipped a beat,
shortness of breath, sweating or fainting.
 Hallucinations, confusion and mental changes like depression.
 Unusual tiredness or weakness.
 Trouble with eyesight, such as blurry eye sight, double vision, seeing yellow, green or
white halos around objects.
 A loss of appetite or an upset stomach.
Digitoxin may cause a variety of arrhythmias in patients.
 It frequently causes vomiting, anorexia and diarrhea.
Digitoxin has adverse effects potentiated by hypokalemia, reduced by hyperkalemia.
Cyanogenic glycosides
Widely distributed in the plant kingdom including many that are commonly
consumed by humans
 Cyanogenic glycosides serve as important chemical weapons in the defence
of the plant against herbivores because of the potential to generate toxic
hydrogen cyanide
Amygdalin is the most common of the cyanogenic glycosides
Present in abundance in the seeds and kernels of fruits such as apricot,
almond, apple, cherry, plum, peach and nectarine
 Peeling, washing in running water and cooking or
Toxicity occur in humans at doses between 0.5- 3.5 mg
kg-1 body weight
When cyanogenic plants are ingested by humans, enzymes
produced by the intestinal microflora are able to hydrolyse
intact cyanogenic glycoside to produce hydrogen cyanide
in vivo.
Symptoms :
Headache, nausea, vomiting, abdominal pain, dizziness,
weakness, mental confusion, convulsions, cardiac arrest,
circulatory and respiratory failure, coma and in extreme
cases death
Alkaloids
 Alkaloids form the most important group of vegetable base. These are complex heterocyclic nitrogenous
compounds having a basic nature and are mostly tertiary amines. These have profound physiological
action and in many cases are of intense poisonous nature.
 These plants contain bitter taste and sufficient protection from being eaten by cattle. Some of the
poisonous alkaloids are—aconitine from aconite root, morphine from poppy capsules, emetine from
ipecachuanha root, strychnine from nux vomica seeds, nicotine from tobacco leaves, curarine from
curare, etc
Imidazole
Biological source: Jaborandi leaves (Pilocarpus microphyllus and P. jaborandi)
Toxicity
 high level of amino transferase enzyme and hepatocellular toxicity
 Renal toxicity
 Eye toxicity by damaging cornea and retina.
 pyrrolizidine
Biological source: Senecio and Crotalaria spp
Pyrrolizidine alkaloids are among the most significant plant chemicals causing disease in animals
and humans. After absorption from the gut, the compounds are converted to electrophilic pyrroles
in the liver which, apart from causing damage to this organ, may escape to cause injury to
extraheptic tissues such as the lungs, heart, and kidneys
Tropane
 Biological source: Datura stramonium, Atropa belladonna
 Toxicity :
The toxicity (anticholinergic effects) of Solanaceae plants can be attributed to their
tropane alkaloids content and profile (i.e., the relative amount of atropine,
hyoscyamine, and scopolamine), which can differ greatly between species,
geographical regions, and harvesting stages . All parts of the plants are toxic, including
the flowers, seeds (fruits), leaves, and stems.
Tropane alkaloids compete with acetylcholine for binding sites on the muscarinic
receptors, producing both peripheral (e.g., dilated pupils, blurred vision, hyperthermia,
dry mouth, dry flushed skin, tachycardia, reduced bowel motility, and urinary
retention) and central (e.g., hallucinations, delirium, drowsiness, amnesia, ataxia,
seizures, and coma) antimuscarinic effects.
Their toxicity is dose-dependent, with more profound effects as the dose increases.
LOWER PLANT TOXIN

Bacterial toxins and Algal toxins

Staphylococcus aureus
Bacterial toxins
• Staphylococcus aureus are Gram-positive bacteria
• Approximately 0.5-1.5 µm in diameter, non-motile, non-spore-
forming
• Part of human flora, and are primarily found in the nose and skin
groin, axillae(armpit), perineal area (males), mucous membranes,
mouth, mammary glands, hair, and the intestinal, genitourinary and
upper respiratory tracts.
Toxic compound:
• Leukocidin
• Alpha toxin, beta toxin, delta toxin,
• Enterotoxins (ETA and ETB)
• Toxic shock syndrome toxin (TSST-1)
• Exfoliatin toxin
• Enzyme, coagulase (clots plasma and coats the bacterial cell),
Hyaluronidase (breaks down hyaluronic acid and helps in spreading
it),  Deoxyribonuclease ( breaks down the DNA) ,lipase (digest
lipids), staphylokinase (dissolve fibrin and aid in spread),beta-lactamase
(drug resistance)
Symptoms: Septic shock, Toxic shock, Emesis, Scalded skin syndrome in
neonates(blisters, skin loss, pimples, furuncles(infection of the hair
Treatment:
Cloxacillin ,cephalexin,vancomycin and penicillin.

Clostridium botulinum Toxins

• Liberated during growth.
• Clostridum botulinum is a Gram – positive , rod-shaped
bacterium that produces several toxins.
• Seven types of toxins (A-G).
• The best known are its neurotoxins,subdivided in types
A-G, that causes the flaccid muscular paralysis seen in
• Antigen (light and heavy chain)
botulism.
• They are also the main paralytic agent in botox C.
• Most biological warfare agents .
• Botulinum is an anaerobic spore-former, which produces
oval, sub terminal endospores and is commonly found in
• Lethal dose=1-2 microgram.
soil.
 Neurotoxin types
Neurotoxin types production is the unifying feature of the species
C.botulinum. Seven types of toxins have been identified and
allocated a letter (A-G).Most strains produce one type of
neurotoxin but strains producing multiple toxins have been
described. The toxin type has been designated Bf as the type B
toxin was found in excess to the type F. Similarly strains
producing Ab and Af toxins have been reported. There is evidence
that the neurotoxin genes have been the subject of horizontal gene
transfer possibly from a viral source. This theory is supported by
the presence of integration sites flanking the toxin in some strains
of C.botulinum. However, these integration sites are degraded
indicating that the C.botulinum acquired the toxin genes quite far
into the evolutionary past.

Botulinum neurotoxin
 Botulinum toxin
• The toxin is synthesized as a single polypeptide chain.
• Botulinum toxin is nicked by a bacterial protease (or
by gastric proteases) to produce two chains
A light chain (the A fragment )
A heavy chain (the B fragment).
Both are connected by a disulphide bond.
The A fragment of the nicked toxin, becomes the most
potent toxin found in nature.
• Absorbed in GIT , blood , prepheral neuromuscular
synapse.
• Presynaptic block Acetylcholine release (by proteolysis
of SNARE proteins in neuron which is important in
Ach release)
Botulism symptoms
Symmetric, descending (cranial nerves first then upper
extemeties then respiratory muscles and lower extremities)
flaccid paralysis with prominent bulbar palsies particularly:

Diplopia- double vision

Disarthria-difficulty in speech articulation
Dysphonia-difficulty in voice production
Dysphagia –difficulty in swallowing
Patient sensibilitis are intact , cognitive functions are
unaffected.

Treatment
Trivalent (A ,B ,E) antitoxin must be administered intravenously.
Recovery make takes several weeks.
Mechanical respirator is administered if necessary.
 Treatment
• Antitoxin action • Prevention
Food borne botulism • Natural disease
• Neutralizing antibody levels exceed toxin Boil home –caned foods for 10
levels. minutes.
• Single dose adequate. Follow USDA instructions on
Large exposure (e.g biological weapon) home- canning
• Can confirm adequacy of neutralization. Restrict honey from less than 1
(Recheck toxin levels after treatment) year old
• Antitoxin adverse effects: Seek medical care for wounds.
Serum sickness (2-9%) , anaphylaxis (2%). Avoid injectable street drugs
 Algal toxin
Microcystis aeruginosa
Species of fresh water cyanobacteria
Source of natural butylated hydroxytoluene (BHT), (an antioxidant, food additive, and
industrial chemical).
Hepatotoxins (microcystin, cyanopeptolin)
Neurotoxins (lipopolysaccharides-LPSs), anatoxin-a, saxitoxin, neosaxitoxin
Toxicity:Gastroenteritis and related diseases, allergic and irritation reaction, and liver
diseases, diarrhea, vomiting, piloerection (involuntary erection or bristling of hairs due to a
sympathetic reflex ), weakness.
Cyanobecteria :
Cyano toxins are toxins produced by bacteria called cyanobacteria. Blooming cyano
bacteria can produce cyanotoxins in such concentrations that they poison and even kill
animals and humans. Cyanotoxins can also accumulate in other animals such as fish and
shellfish, and cause poisonings such as shellfish poisoning.Among cyanotoxins are some of
the most powerful natural poisons known, including poisons which can cause rapid death
by respiratory failure.The toxins include potent neurotoxins, hepatotoxins, cytotoxins, and
endotoxins. Recreational exposure to cyanobacteria can result in gastro-intestinal and hay
fever symptoms or pruritic skin rashes.
Treatment: Oral administration of cholestyramine, in combination with supportive
therapy, could significantly reduce hospitalization time, cost-of-care and mortality for
cyano bacterial -poisoned animals .
Gonyaulax cantenella
 Scientific name : Alexandrium catenella
 Synonym: Red tide dinoflagellate
 Alexandrium catenella is a marine photosynthetic dinoflagellate. Alexandrium catenella forms
chains of 2, 4 or 8 cells that swim together like a snake. Individual cells are almost round,
slightly longer than wide (Olenina and Olenin 2006). It has a large U-shaped nucleus .
Harmful effects
 This species produces neurotoxins that cause deadly paralytic shellfish poisoning (PSP) events
in the Pacific Ocean .The PSP toxins can cause human illness . Symptoms of PSP include
numbness around the lips, muscular paralysis, choking sensation and death .
 Mycotoxins

Fungal toxins and Mushrooms

 Fungal Toxins
Aspergilus spp.
Four group of toxins are produced: Aflatoxin , Ochra toxin , Apatulin Fusarium.
Aflatoxin:
 Toxic metabolites produced by fungi in food and goods
 Produced by A.flavus, A.niger and Aspergilus porosities
 13 different aflatoxin are produced mostly A,B,G and M
 Milk, cheese, corn, peanut, cotton seed, almond, cereals, rice and figs
 Potent human carcinogens especially cause hepato-cellular carcinoma
 Immune suppression
 Mutagenic Teratogenic
 Detected in blood of pregnant woman, neo-natal umbilical cord blood and breast
milk
Ochratoxin:
• Produced by aspergilus and pencillium species
 Found in cereals, coffee, bread and food of animal origin
 Most common is ochratoxin A
 Fatigue, headache, loss of weight, pale skin, Aplastic anemia
 Nephrotoxic, Immuno-suppresent, carcinogenic and teratogenic.
 Ergot(Cleviceps purpurea)

Ergot
 grain is toxic to animals. There are four forms of toxicity: Convulsions ,
Gangrene , Hyperthermia (increased body temperature) in cattle , agalactia (no
milk) and lack of mammary gland development, prolonged gestations and early foal
deaths in mares fed heavily contaminated feed .
Ergot toxicity symptoms depend on:
Type
 of ergot consumed
Ratio of major toxic alkaloids present in the ergot: ergotamine, ergotoxine, and

ergometrine
Frequency and quantity of ingestionClimactic conditions when ergot was growing

Species of ergot

Other impurities in the grain such as histamine and acetylcholine

Claviceps purpurea is usually associated with gangrenous ergotism.


Ergot control:
Harvest
 before the heads are mature
Deep plouhing

Control grassy weeds

 Mushroom poison
 Cause severe and deadly effects
 Produce two different group of toxins
 First group known as anatoxin that block the production of DNA so
cause the death of rapidly producing cells such as liver, intestine and
kidney
 Second group effects the muscle contracting proteins so inhibit the
function of certain protein
Symptoms occur at different phases
 1st phase abdominal cramping, nausea, vomiting, watery diarrhea that leads
to dehydration and decrease the blood pressure
 2nd phase lasts for two days
 Blood test show the evidence of liver and kidney damage
• 3rd stage liver and kidney failure increases that lead to death in a weak or
recovery with in two weak
 Weakness, Internal bleeding, decrease muscle formation and paralysis
 Treated either by removal of poison or preventing the absorption of poison
 Gastric levage
 MUSHROOM TOXINS
General principles Eating mushrooms may be connected with
various hazards:
Real mushroom poisoning:
a) With persistently toxic mushrooms. Many mushrooms lose
their toxicity during processing.
b) With old mushrooms. Toxic substances are formed during
the decomposition of the mushrooms.
 Poisonings by environmental toxicants, bioaccumulated in
mushrooms.
 Allergic-supersensibility reactions against mushroom
constituents
Two mushrooms of the genus Amanita—the green death cap (A.
phalloides) and the white death cap (A. virosa)—are really fatally
toxic, which contain amatoxins (α-, β-, and γ-amanitins) and
phallotoxins such as phalloidin, phalloin, phallacidin, and
phallolysin. In addition, A. virosa contains virotoxins.
Amatoxins are thermostable and insoluble in water; they cannot
be destroyed either by boiling or by cooking as well as by drying
of the mushrooms.
 Phallotoxins induce severe gastroenteritis, appearing 4–8 h after
the ingestion of the white death cap; but, owing to negligible
absorptivity, this group of toxins has no essential role in
mushroom poisonings.
Amatoxins or amanitins are divided into five subtypes—α and β
subtypes being the most important ones.
 Amatoxins are cyclic octapeptides (MW ≈ 900) that after absorption via
amatoxin-transporting system block the synthesis of mRNA in the
eukaryotic cells by the inhibition of the enzyme RNA polymerase II. This
inhibition causes a continuous fall of the mRNA concentration and rate
of protein synthesis in the cell and the cell death during the first 24 h
after the ingestion of the mushroom.
These processes take place first in the digestive tract, and thereafter in
the liver and kidneys.
 Liver necrosis (the most critical injury) and decomposition of the renal
tubular cells may also occur. Thionic acid is used for curing the
amatoxin-caused intoxication. The toxin of Amanita pantherina damages
the nervous system.
NATURAL TOXICANTS (PLANTS)
ABRUS PRECATORIUS:
 Toxic part of plant: Seed
 The most important 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.
Abrus Precatoriuos
PHARMACOLOGICAL ADVERSE REACTIONS
ACTIONS
Antibacterial Ingestion of abrus seeds
Anthelmintic
resulted in pulmonary
Anti-viral
Anti-inflammatory
edema and hypertension.
Anticancer/Anti-tumour Abrine can cause
Antiplatelet coma,confusion,convulsion
Antiprotozoal s,dehydration,gastroentero
Antioxidant
sis and hypertension.
Immunomodulatory
Antiplasmodial
Antitubercular
 CANNABIS SATIVA:

• Scientific name: Cannabis Sativa

• Family : Cannabinaceae
• Common name(s):
• Marijuana, hashish, hemp, marihuana, pot
• Family:Cannabaceae
CANNABIS SATIVA:

Description of the plant:

 Indian hemp is an annual dicotyledon herb that can reach up to 3 metres
high or more with suitable humidity and soil. The stem is covered by
rigid hairs, rough to the touch. Species are male and female; the latter has
more leaves. The leaves are long-stalked, palmate, with 3-7 narrow and
toothed leaflets. The upper leaves are alternate and the low ones,
opposite.
 Flowers are very small, green and have axillary branches (Hardin &
Arena, 1974). The fruit is oval, flat, 5 to 6 mm long and 4 mm wide, with
a light green colour. It has an herbaceous strong smell and taste.
CANNABIS SATIVA:

Habitat: It grows in well-irrigated lands with warm weather,

blooming in the spring and summer.
Distribution :The plant is originally from the Caspian and Black
Sea area, and was taken to Persia and India eight centuries ago.
 The Cannabis sativa native to Central Asia has a world wide
distribution. It is cultivated in North, Central and South America, in
Asia, Europe and North and Central Africa. Major producers include
Mexico, Brasil, Paraguay, Colombia, Peru, New Zealand and Arabia.
The Indian variety is cultivated in the Orient, Asia and North Africa.
Poisonous part:All parts, but greatest toxicity in flower stalks.
CANNABIS SATIVA:

Poison Delivery Mode:

 Ingestion and inhalation
Symptoms:Exhilaration, hallucinations, delusions, blurred vision, poor
coordination, stupor, and coma.
Toxic Principle:Resins
The common "street" marihuana is usually a mixture of dried flowers,
leaves and ocassionally seeds. It has a brownish green colour, depending
on dryness and maturity of the plant.
The toxin(s):
Indian hemp contains more than 60 cannabinoids including: cannabinol,
cannabidiol, cannabinolic acid, cannabigerol, cannabicyclol, and various
tetrahydrocannabinol isomers, the most important is delta-9-
tetrahydrocannabinol (delta-9-THC).
CANNABIS SATIVA:

Chemical Constituents:
Cannabis consist of 15 to 20% resin, the resins are
amorphous,
semisolid, brown coloured, soluble in ether, alcohol,and
carbon disulphide.
The most important active constituents present in cannabis
are:cannabidiol, cannabidolic acid, cannabinol,
cannabichromene, and trans-tetrahydrocannbinol.
Cannabis also contains Cannabidiolic acid, cannabidiol A 9,
tetrahydrocannabinol, cannabinol A9, Tetrahydrocannabinol
(THC), volatile oil, trigonelline,and cholene.
CANNABIS SATIVA:

Treatment:
Intoxication within 4-6 hrs.
In case of over dose medical supervision is neede.
Side Effects:
Drowsiness, dizziness and lethargy are common. feeling of loss of control, impaired
memory,hallucinations, blurred vision,muscle weakness.
others include; Euphoria,Moodalterations,Anxiety,Hypotension,Hypertension, Tachycardia,
Increased appetite, Nausea,Vomiting
Contraindications:
Acute psychosis and other unstable psychiatric conditions
Severe cardiovascular, immunological, liver, or kidney disease, especially in acute illness §
Cannabis may exacerbate arrhythmia or a history of arrhythmias.
 DATURA STRAMONIUM
• Common Name(s):Jamestown weed, Jimsonweed, datura, stinkweed, thorn-apple
• Family:Solanaceae
• Categories:Perennials, Poisonous Plants
Description:Annual herb, stem green to purplish, ill-scented, with alternate, simple, coarsely toothed leaves;
flower solitary, large, tubular with 5 shallow lobes at top, white or lavender. Egg-shaped seed capsule can be
spiny or smooth, with many glossy black seeds. Flowers open at night and are quite
fragrant and fed upon by nocturnal moths.
Height:2-5 feet
Flower Color: white to lavender purple
Poison Part: All parts, mainly seeds and leaves
Poison Delivery Mode: Ingestion
Symptoms: Hot, dry, and flushed skin, hallucinations, pupil dilation, headache, delirium,
rapid and weak pulse, convulsions, and coma
Toxic Principle: Tropane alkaloids
Found in: Weedy in disturbed areas, along roadsides, old fields, pastures, waste places;
landscape as weed in gardens.
Dose: Accidentally or intentionally ingesting even a single leaf could lead to severe side
effects
DATURA STRAMONIUM

Treatment:
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.
DIGITALIS PURPUREA

Common Name(s):Annual foxglove, Foxglove

Family:Scrophulariaceae
Categories:Annuals, Perennials, Poisonous Plants
Description:Biennial herb with alternate, simple, toothed leaves; flowers in a
showy, terminal, elongated cluster, each tubular, pendent, purple, pink, rose,
yellow, or white and spotted inside bottom of the tube; fruit a capsule.
Height:24-60 in.
Flower Color: Purple, white
Poison Part: Leaves, flowers, seeds; overdoses of the drug digitalis.
Poison Delivery Mode: Ingestion, confusion with Symphytum (comphrey) and
brewed into a toxic tea.
Symptoms: Nausea, vomiting, diarrhea, stomach pain, severe headache, irregular
and slow pulse, tremors, unusual color visions, convulsions.
Toxic Principle: Cardiac or steroid glycosides
DIGITALIS PURPUREA
Treatment:
Treatment involve drugs that would be used to traet an
overdose of the cardiac medication.
Thismay include;
Potassium chloride
Atropine
Phenytoin
Oxygen
Cardiac drugs such as propranolol or procainamide are also
used.
PAPAVER SOMNIFERUM
Opium is the dried juice of papaver
somniferum ripe and dry poppy capsule –
trace of opium
– used as sedative.
Poppy seeds (Khas Khas) harmless.
PROPERTIES
 Smells like raw flesh.
 Taste bitter when fresh plastic & moist
internally
on keeping becomes hard, brittle &
dark brown.
Active Principle
Two groups of alkaloids
1. Phenanthrene group

2. Isoquinoline group
ALKALIODS OF OPIUM
 Phenanthrene
group Morphine 9-14 %
1. Codeine 2- 4
2. %
3.used inThebaine 0.5 % anti
analgesic, euphoriants,
tussives anti diarrheal.
 Isoquinoline group
1. Papaverine 1 %
2. Narcotine 6 %
ABSORPTION & EXCRETION

Absorbed through GIT

excreted in stomach, intestine, bile &
milk eliminated mainly as morphine in
urine & faeces
it is excreted in the stomach & small
intestine even after parental use.
MODE OF ACTION

Acts as agonists on different opiate

receptors sites
in CNS .
There are 3 sub species of opiate receptors
e.g Kappa,(OP2) Sigma
Delta(OP1) It acts by depression of cortex
Respiration and cough centers are
stimulated Vagal reflex and vomiting is
stimulated
 SIGN AND SYMPTOMS
2.STAGE OF STUPOR
1.STAGE OF EXCITEMENT
Headache, Nausea, Vomiting
( may be absent if a large dose is taken)
Uncontrollable desire to sleep
 Euphoric feeling of well being
Pupils contracted
 Restlessness and hallucination
Cyanosis
 Increased pulse rate
Itching sensation
 Flushing of face
Pulse respiration normal
 In children convulsions may occur
3. STAGE OF NARCOSIS
 Patient is in deep coma
 Muscles relaxed and reflexes lost
 Secretions are suspended except of skin
 Blood pressure falls pulse is week and slow
 Cheyne – stroke breathing (R. rate 2-4/m)
 Lower jaw drops
 Pin point pupils
 Bladder distended
UNUSUAL SYPTOMS

 Vomiting
 diarrohea

 Convulsions

 Increased Temperature

 Dilated Pupils
 FATAL DOSE
Crude 1-2 grams
Opium 200-400 mg
Morphine 8-16 ml
Tincture 1-3 drops
In childrenFATAL PERIOD
6-12 hours in extreme case 45
minutes
 TREATMENT

 Gastric lavage
First with warm water then with potassium permagnate or tannic acid
Magnesium sulphate 15 grams as enema Oxygen in halation
ANTITODE
Naloxone hydrochloride is antidote for opiate poisoning .01 - .02mg /kg /
body weight i.v
Nalorphine hydrochloride 10 mg i.v (total of 40 mg can be given)

rest of the treatment is symptomatic

 MEDICO LEGAL
ASPECTS
 Suicidal
 Accidental

 Homicidal (rare) but used for

infanticide
 Cattle poisoning

 Drug addiction
Many products, marketed for adults and children, were sold for pain and
cough relief. they all contained opium.
EUCALYPTUS SPP
Common Name(s):Eucalyptus, gum, lemon scented gum,
silver dollar tree.
Categories:Poisonous Plants, Shrubs
Family:Myrtaceae
EUCALYPTUS SPP
Description:Evergreen trees with alternate or opposite, simple,
smooth- margined leaves; flowers in small clusters, top- or bell-
shaped, 4-petaled with many stamens; fruit a many-seeded capsule.
Height:6-25 ft.
Foliage:Paired, opposite blue-green leaves
Poison Part: Leaves, bark
Poison Delivery Mode:Ingestion, dermatitis
Symptoms: Nausea, vomiting, diarrhea, coma. Skin redness,
irritation, and burning from handling leaves and bark. Eucalyptus oil
is extremely toxic if eatenToxic
Principle: Eucalyptus oil and cyanogenic glycoside
NICOTIANA TOBACCUM

Common Name(s):Tobacco
Category: Poisonous Plants
Family:Solanaceae
Description: Stout, annual herb; leaves large, alternate, simple, with sticky hairs; flowers
tubular, cream, pink, or green-white, 5-lobed at top; fruit a capsule with many, minute seeds
Poison Part: All parts
Delivery Mode: Ingestion
Toxic Principle: Nicotine and other alkaloids
Side-effects:Nausea,vomiting,salivation,diarrhea,convuluions, muscle twitching ,weakness.
If large amounts are consumed and the nervous system is depresssed,difficult breathing and
a low heart rate may preced heart failure,coma and death.
Treatment:It involves removal of the plant material from the digestive tract,along with
supportive care to ensure breathing and cardiac function until the toxin is eliminated from
the body.
 Tropane
alkaloids
Phenanthrene and
isoquinoline alkaloids

Cyanogenic glycoside