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clinical & pathological effects of toxic plants.
Presented to - Dr. Divakaran Nair.
Prof. & HOD, Dept. of VPP. COVAS,
Pookode.
Course no. VPP-609.
Toxicopathology.
Presented by
Sindhu K.
M. V. Sc. Scholar,
Dept. Of VPT.
Overview
• Introduction
• Classification of toxic plants
• Clinical & pathophysiology of toxic plants
• Plants producing various poisoning
• Treatment & management of poisoning plants
Toxic plant may be defined as “one which
detrimentally affects the health of man or
animal when eaten in such amount as would
be taken normally or under special
circumstances like restriction of choice of diet
or extreme hunger”.
Etymology
TOXIN
 Toxon (Greek)  for bow & arrow
 Toxicon  poison dipped arrow
POISON
 Poi  to drink & becoming potare in Latin
(potion)
 Venomous nature derived from wen to win, &
led to venus/venerate through “love potions”
(venin)
Sec. plant Metabolites
• The toxic (active) principles present in the plants =
PHYTOTOXINS.
• Plant toxins may be referred as SPM.
• SPM  defense mechanism / survival adaptations.
Toxic plants are of 2 types
• Plant containing toxic ingredients & are known to be
toxic to animals.
• Plants which are normally not toxic to animals but
becomes so under unfavorable conditions.
Classification of toxic
plants
I. Alkaloids
II. Terpenes
III. Glycosides
IV. Proteinaceous compounds
V. Organic acids
VI. Resins & Resinoids
Tropane/atropine like alkaloids
Atropine
Datura (jimsonweed)
Erythroxylum (coca
tree)
Hyoscyamus
(henbane)
Mandragora
(mandrake)
Pyrrolizidine alkaloids
Retronecine
Senecio (ragwort)
Crotalaria sp.
Heliotropium sp.
Trichodesma sp.
Pyridine/Piperidine alkaloids
Conium (Hemlock)
Lobelia (Indian tobacco)
Pyrrolidine-pyridine alkaloids
Nicotine
Nicotiana sp. (Tobacco)
Equisetum sp. (Horse
tail)
Purine alkaloids
caffeine
Coffea sp. (Coffee)
Theobroma sp.
(Cocoa)
Camellia sp. (Tea)
Quinoline alkaloids
Quinine
Cinchona sp. (Quinine
tree)
Echninops sp. (Globe
thistle)
Isoquinoline alkaloids
Morphine
Papaver somniferum
(opium)
Sanguinaria sp.
Dicentra (Blood root)
Indole/
indolizidine alkaloids
Strychnine
Strychnus (strychnine)
Claviceps (Ergot)
Psilocybe (Magic
mushroom)
Astragalus sp. (locoweed)
Gelsemium sp.
Quinolizidine alkaloids
Anagyrine
Laburnum sp. (Golden
chain)
Baptisia sp. (False
indigo)
Cytisus sp. (Scotch
broom)
Steroidal glycoalkaloids
Solanidine
Lycopersicum sp.
(Tomato)
Solanum sp.
(Nightshades)
Steroidal alkaloids
Jervine
Veratrum sp.
Zigadenus sp.
Diterpenoid alkaloids
Aconitine
Delphinium sp. (Larkspur)
Aconitum sp.
(Monkshood)
Phenylamine alkaloids
Ephedrine
Lophophora sp. (peyote)
Ephedra sp.
Terpenes
 Biosynthesized by plants
 Contains the branched 5-carbon skeleton of isoprene.
 On the basis of number of isoprene units present in the
structure of the molecule, terpenes are categorized as
C-10 compounds  monoterpenes
C-15 compounds  sesquiterpenes
C-20 compounds  diterpenes
C-30 compounds  triterpenes
Monoterpenes
• Cantharidine  an animal
monoterpene from fly ash.
• Picrotoxin from Anamirta
cocculus (Fish berries).
Sesquiterpenes
• Coramyrtin from Coriaria myrtifolia
• Geigerin from Geigeria
• Helenalin from Helenium
microcephalum
Diterpenes
• Andromedotoxin
• Mezerein
• Aconitine from Aconitum sp.
Triterpenes
• Cicurbitacins (toxic principles of
bittergourd)
• Lantadenes from Lantana sp.
Glycosides
 Complex organic compounds having glycone attached to
aglycone/genin moiety by ether linkage
 Neutral in reaction
 Soluble in alcohol, less soluble in water & insoluble in ether
 They don’t combine with acids to form salts
 Names ends with suffix –in.
Eg: digitoxin, ouabin, scillarin, glycyrrhizin, senegin.
Cyanogenic glycosides
Amygdalin
Amygdalin (Almond seed)
HCN in Hydrangea, Linum
(Linseed)
Prunus (Wild cherry)
Sorghum vulgare (Jowar)
Sorghum sudanese (Sudan
grass)
Gossypol (cotton seed)
Steroidal (cardionilides/
cardiac glycosides)
Digitoxin
Digoxin from Digitalis sp.
Oubain from Strophanthus
Convallarin from
Convallaria
Ascleipas (Milk weed)
Nerium oleander
Steroidal (saponigenic
glycosides)
Argostemme (Corn
cockle)
Phytolacca (Poke weed)
Hedera (English ivy)
Coumarin glycosides
Esculin
Ausculus glabra
Moldy Meliolotus sp.
(White sweet clover)
Ipomoea sp. (Sweet potato)
Anthraquinone glycosides
Cassia fistula (Senna)
Aloe sp.
Mustard glycosides
Sinigrin
Thiocyanates/isothiocyan
ates of mustard oil.
(Brasssica nigra)
Proteinaceous compounds
 Plant proteins = harmless + beneficial agents.
 Plant protein + seed reserve proteins  important source of food.
 Ingestion  protein hydrolysis  enzymatic reactions in GIT 
absorption of amino acids  protein biosynthesis in the body.
 However; there are no. of proteins, peptides/amines which are of
toxicological importance.
Eg: toxalbumins, polypeptides, amines.
Toxalbumins
(proteins)
• Abrin from Abrus precatorius
• Ricin from Ricinus communis
Polypeptides • Amatoxins, phallotoxins &
phalloidin from Amanita sp.
Amines
• Aminotryptaline from seeds of Sativus odoratus
• Phoradendron sp. (Berries of mistle toe)
• Mimosine from Mimosa pudica
• Canavanine from Canavalia ensiformis (Jack
beans)
• Leucaena leucocephala (Subabul)
Organic acids
 Acids accumulated in plants, particularly in their fruits but are non-
toxic.
1. Malic acid
2. Tartaric acid
3. Citric acid
4. Ascorbic acid
 But other plant acids possess significant toxic property solely due to
their acidity
Eg: plant oxalic acid & its soluble Na, K or NH4 salts.
Oxalic acid & soluble salts
• Oxalic acid
• Potassium oxalate
• Sodium oxalate
Resins & resinoids
 Toxic plant resins = phenolic compounds
 Important naturally occurring phenolic resin in plants
 Exists as amorphous & brittle solids
 Insoluble in water, soluble in organic solvents (alcohol, chloroform &
ether)
I. Tetrahydrocannabinol
II. Hypericin
III. Urushiol
Tetrahydrocannabinol
• Cannabis sativa
(marijuana or hemp)
Hypericin • Hypericum perforatum
Urushiol
• Poison ivy
• Poison oak
• Rhus sp.
CLINICAL & PATHOLOGICAL EFFECTS
• Specific action of toxicants
Receptor mediated, ionic channels, enzyme mediated, carrier
molecules mediated events.
• Non specific action of toxicants
Physical toxicants, direct chemical injury, interference with
body metabolism, impairment of O2 transport, injury to vascular
system, altered Ca++ homeostasis, immunomodulations,
carcinogenesis, non-specific action on enzymes & proteins,
tissue residual effects.
General Clinical signs affecting systems
1. CNS:
ConvulsionCyanide, nitrate, strychnine, OP, Carbamates,
Picrotoxin.
Coma  Bromide, CO, Nicotine, Morphine, ZnP.
Ataxia  OP, carbamates, Thallium.
2. Digestive system:
Nausea, vomiting & diarrhoea  heavy metals, fluoride, paraffin,
muscarine, OP. Constipation  Opioids, Oxalate producing plants.
Hypersalivation  OP & Carbamates.
Dry mouth  Atropine, Opioids & Phenothiazines.
3. Respiratory system:
Dyspnoea  Opioids, OP, cyanide, nitrate & nitrite producing plants,
strychnine
Hyperpnoea aspirin, isoniazid, atropine, nicotine, apomorphine.
Slow respiration atropine late stage
4. Skin. Hair & nails:
Cyanosis (metHb.) nitrite producing plants
Photosensitisation  Lantana camara,
Alopecia alkali sulphide, X-radiation
5. Urogenital tracts
Urinary retention  atropine, opioids
Micturation & incontenance OP & Carbamates
Crystalluria  oxalates, amaranthus.
Poisonous plants
• Cyanogenetic plants
• Plants producing lathyrism
• Plants producing thiamine deficiency
• Plants producing Photosensitization
• Datura & related plants
• Oleander & Cardiotoxic plants.
• Plants containing toxic lectins/ castor bean poisoning.
• Ipomoea poisoning
• Cotton seed/gossypol poisoning
• Nux vomica poisoning.
Cyanogenetic plants
• Eucalyptus, kappa/ tapioca, sorgum/corn, linseed cake, bitter almond.
• MOA: HCN + trivalent iron of cytochrome oxidase  inhibits ETC
• Tissue anoxia in brain
• Peracute & acute toxicity, chronic toxicity.
• restless, laboured & quick breathing, stumbling gait, tachycardia,
salivation, lachrymation, mydriasis, cyanotic mucus membrane & bitter
almond smell.
• Sodium nitrite & Sodium thiosulphate.
Cattle & sheep @ 20 mg/kg slow IV followed by sod.
Thiosulphate @ 500 mg/kg slow IV as 25% soln.
Dogs & cats @ 25 mg/kg slow IV as 1 % soln. followed
by sod. Thiosulphate @ 1.25 g/kg slow IV as 25% soln.
Horses @ 16 mg/kg slow IV as 1 % soln. followed by
sod. Thiosulphate @ 30-40 mg/kg slow IV as 20 %
soln.
Plants producing lathyrism
• Legume lathyrus / wildpea / Khesari dal
• Osteolathyrism – BAPN (irreversible inhibition of lysyl
oxidae)
• Neurolathyrism – ODAP (symmetrical axonal
degeneration)
Osteolathyrism & Neurolathyrism
Plant producing thiamine deficiency
• Braken fern/ pteridium aquilinum
• Toxic principles – Thiaminase, aplastic anaemia
factor, Ptaquiloside, haematuria factor,
Quercetin.
• Cattle: bleeding from body orifices Urogenital,
Nostrils, GIT, severe BM depression,
thrombocytopenia, HYPHEMA, enzootic
haematuria, death due to anaemia.
• Horses: emaciation, lethargy, wt. loss,
recumbancy followed by muscular tremors,
clonic spasms & Opisthotonus, colic, braken
staggers, haemolytic crisis.
Oxalate accumulated plants
• Sarcobatus, rheum, beet.
• Ruminants/ Cattle
• Soluble potassium & sodium
oxalates.
• MOA- form complex with serum
Ca++  hypocalcemia 
muscular weakness, CNS
depression, CVS collapse.
Plant producing
photosensitisation
• Primary  Hypericin, fagopyrin
• Secondary  senecio sp. Lantana sp.
Plants producing
allergic stomatitis
• Lantana
• Acacia
• Dracula stromonium
• Jatropa leaves/ cake
• Abrus spp
Strychnos nux vomica poisoning
• Alkaloid – strychnine & brucine
Treatment of poisoning
• Preventing continuous absorption of toxicant
• Preventing distribution of toxicant to target site
• Increasing threshold level of toxicity
• Hastening elimination of absorbed toxicant
• Enhancing metabolic conversion of absorbed toxicant.
Preventing continuous absorption of
toxicant
• Gastric lavage
• Adsorption theraphy
• Purgation/ cathartics
• Enema
• Cleansing of eyes/ skin/ hairs
• Gastrotomy/ rumenotomy
• Dilution
• Complex formation
Preventing distribution of toxicant to
target site
• Ion-trapping
• Alternate binding site
• Complex formation
Increasing threshold level of toxicity
• Rx for resp. depression
• Monitoring cardiac disturbances
• Control of shock
• Control of acidbase disturbances
• Maintenance of uresis
• Rx of Hypo/Hyper thermia
Hastening elimination of absorbed
toxicant
• Ion-trapping
• Dialysis
• Diuresis
• Specific treatment
Clinical pathophysiology f toxic plants

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