Poisonous Plants
Poisonous Plants
This chapter is prepared for PharmD students in accordance with the officially endorsed curriculum in Pakistan.
September 13, 2023
Chapter outline
» Introduction
» Classification of poisonous plants
› Plants with anticholinergic (antimuscarinic) poisons toxicity
› Plants with calcium oxalate crystals toxicity
› Plants with cardioactive glycosides toxicity
› Plants with convulsant poisons (seizure) toxicity
› Plants with cyanogenic compounds toxicity
› Plants with mitotic inhibitor toxicity
› Plants with nicotine toxicity
› Plants with toxalbumin toxicity
Introduction
» A poisonous plant is one which, as a whole or its part, under all or certain conditions, and in a manner and in amount to be taken or brought into contact with an organism, will exert or cause death, either immediately or by reason of cumulative action of the toxic property due to the presence of known or unknown chemical constituent(s) in it, and not by mechanical method
» If a plant causes piercing/rashes/cuts (e.g., on the tongue while eating or on skin by contact) leading to abscesses and death will not be considered poisonous, as piercing is a mechanical process
» By the metabolic activity, the plants not only produce primary metabolites (food material) but also produce secondary metabolites (alkaloids, glycosides, tannins, saponins, terpenoids, etc.)
› Many of these constituents can be harmful to animal life, at least under certain conditions
› The plants containing these principles which are capable of producing harmful effects are known as poisonous plants
Classification of poisonous plants
» Poisonous plants have been classified in a number of ways
» One way of classification is described below
1. Plants with anticholinergic (antimuscarinic) poisons toxicity
Toxic mechanism
» These are competitive antagonists of acetylcholine at the muscarinic receptors
Examples
» Atropa belladonna whole plant (Family Solanaceae)
» Hyoscyamus niger (اجوائن خراسانی) seeds (Family Solanaceae)
Toxins
» Atropine, scopolamine, and other anticholinergic alkaloids
Intoxication / clinical findings
» Dry mouth with dysphagia and dysphonia
» Tachycardia
» Urinary retention
» Elevation of body temperature
» Flushed, dry skin
» Mydriasis
» Blurred vision
» Excitement and delirium
» Headache
» Confusion
Management
» Initially, symptomatic and supportive care
» If the severity of the intoxication warrants intervention (hyperthermia, delirium), an antidote ‘physostigmine’ is available
» Consult poison control center
2. Plants with calcium oxalate crystals toxicity
Toxic mechanism
» Crystalline calcium oxalate needles, bundled in needle-like raphides, release from their intracellular packaging in a projectile fashion
› These needles penetrate the mucous membranes and induce the release of histamine and other inflammatory mediators
» Calcium oxalate crystals are also deposited in the kidneys and induce harm
Examples
» Alocasia watsoniana leaves (Family Araceae)
» Philodendron bipinnatifidum leaves (Family Araceae)
Toxins
» Calcium oxalate toxins
Intoxication / clinical findings
» A painful burning sensation of the lips and mouth, on eating
» There is an inflammatory reaction, often with edema and blistering
» Hoarseness, dysphonia (disorders of the voice), and dysphagia (swallowing difficulties) may result
Management
» The pain and edema reduce slowly without therapy
» Use of cool liquids or demulcents in the mouth may bring some relief
» Analgesics may be indicated
» Consult poison control center
3. Plants with cardioactive glycosides toxicity
Toxic mechanism
» Cardioactive glycosides inhibit the cellular Na+/K+-ATPase
› The effect is to indirectly increase intracellular Ca2+ concentrations in certain cells, particularly myocardial cells
› Therapeutically, this enhances cardiac ionotropy (contractility) and slows the heart rate
» However, excessive elevation of the intracellular Ca2+ (that occurs in poisoning) also increases myocardial excitability, predisposing to the development of ventricular dysrhythmias
› Enhanced vagal tone, mediated by the neurotransmitter acetylcholine, is common with poisoning by these agents and produces bradycardia and heart block
Examples
» Digitalis purpurea and D. lanata leaves (Family Scrophulariaceae)
» Nerium indicum (کنیر) leaves (Family Apocynaceae)
Toxins
» Cardioactive glycosides, e.g., digoxin, digitoxin, etc.
Intoxication / clinical findings
» GIT symptoms
› Nausea, vomiting, abdominal pain, and diarrhea
» Hyperkalemia (elevated level of K+)
» Generalized weakness
» Drowsiness
» Cardiotoxicity
› Bradycardia and heart block, dysrhythmias
Management
» Assessment of the severity of the toxicity and its etiology (e.g., accidental ingestion, unintentional or deliberate overdose, altered digoxin metabolism due to diminished renal clearance or interaction with other drugs)
» Consideration of factors that influence treatment, including age, medical history, chronicity of digoxin intoxication, existing heart disease and/or renal insufficiency, and ECG changes
» Prompt measurement of electrolyte levels, including potassium and calcium, and of serum creatinine and digoxin levels
» Intensive care unit (ICU) admission
» Activated charcoal is indicated for acute overdose or accidental ingestion
» Digoxin-specific antibody antigen-binding fragments (DSFab) are an effective antidote that directly binds digoxin
› DSFab is indicated for life-threatening toxicity
» Consult poison control center
4. Plants with convulsant poisons (seizure) toxicity
Toxic mechanism
» A convulsion is the rhythmic, forceful contraction of the muscles
› One cause of convulsion is seizures
» Seizures are disorganized discharges of the central nervous system that generally, but not always, result in a convulsion
» These poisons (e.g., strychnine) result in hyperexcitability of the motor neurons, which manifests as a convulsion
Examples
» Strychnos nux-vomica (کچلہ) seeds (Family Loganiaceae)
Toxins
» Alkaloids (strychnine and brucine)
Intoxication / clinical findings
» Restlessness
» Anxiety
» Dizziness
» Neck and back stiffness
» Spasms of jaw and neck muscles
» Convulsions
» Seizures
» Breathing problems
Management
» Shift the patient to a quiet dark room
» Artificial respiration
» Gastric lavage with tannic acid
» Administer barbiturates (e.g., phenobarbitone)
» Administer muscle relaxants
» Consult poison control center
5. Plants with cyanogenic compounds toxicity
Toxic mechanism
» These plants contain cyanogenic glycosides
» Cyanogenic glycosides release cyanide (cyanide causes poisoning)
» Cyanogenic glycosides must be metabolized to release cyanide
» Cyanide inhibits the final step of the mitochondrial electron transport chain
› Resulting rapidly in cellular energy failure
Examples
» Malus domestica (apple سیب) seeds (Family Rosaceae)
» Prunus armeniaca (apricotsخوبانی ) seeds (Family Rosaceae)
» Prunus avium (cherriesچیری ) seeds (Family Rosaceae)
» Prunus persica (peaches آڑو) seeds (Family Rosaceae)
» Prunus domestica (plums آلو بخارہ) seeds (Family Rosaceae)
Toxins
» Cyanogenic glycosides (e.g., amygdalin and prunasin)
Intoxication / clinical findings
» Apple seeds that are swallowed whole or chewed and eaten in small quantities are harmless
» A case of fatal cyanide poisoning has been reported in an adult who chewed and swallowed a cup of apple seeds
» Because the cyanogenic glycosides must be hydrolysed in the gastrointestinal tract before cyanide ion is released, several hours may elapse before poisoning occurs
» Abdominal pain, vomiting, lethargy, and sweating typically occur first
» In severe poisonings, coma develops and may be accompanied by convulsions and cardiovascular collapse
Management
» Gastric lavage
» Symptomatic and supportive care should be given
» Cyanide antidote (hydroxocobalamin and sodium thiosulfate and sodium nitrite) given intravenously
» Consult poison control center
6. Plants with mitotic inhibitor toxicity
Toxic mechanism
» These plants contain alkaloids (vincristine and vinblastine) which are cytotoxic, i.e., capable of inhibiting microtubule formation
» They also impair axonal transport and are neurotoxic
Examples
» Catharanthus roseus (سدا بہار) whole plant (Family Apocynaceae)
Toxins
» Alkaloids (vincristine and vinblastine)
Intoxication / clinical findings
» Ingestion may cause initial oropharyngeal pain followed in several hours by intense GIT symptoms
» Abdominal pain along with severe, profuse, and persistent diarrhea may develop causing extensive fluid depletion
» May subsequently produce peripheral neuropathy, bone marrow suppression, and cardiovascular collapse
Management
» Gastric lavage
» Extracts of crude drugs rich in tannins can be given (because tannins precipitate alkaloids)
» Symptomatic and supportive care is critical
» Hyaluronidase is found an effective antidote in several studies
» Consult poison control center
7. Plants with nicotine toxicity
Toxic mechanism
» These agents are direct acting agonists at the nicotinic subtype of the acetylcholine receptor in;
› The ganglia of both the parasympathetic and sympathetic limbs of the autonomic nervous system (NN receptors)
› The neuromuscular junction (NM receptors)
› The brain
Examples
» Nicotiana tabacum (tobacco تمباکو) whole plant (Family Solanaceae)
Toxins
» Alkaloids (nicotine)
Intoxication / clinical findings
» Acute intoxications result from
› Ingestion of the leaves
› Use of N. tabacum infusions in enemas as a home remedy
› The cutaneous absorption of the alkaloid during commercial tobacco harvesting
› The ingestion of cigarettes or purified nicotine
» Initial gastrointestinal symptoms may be followed by those typical of nicotine poisoning
› Hypertension, large pupils, sweating, and perhaps seizures
» Severe poisoning produces coma, weakness, and paralysis
› That may result in death from respiratory failure
Management
» Gastric lavage
» Extracts of crude drugs rich in tannins can be given (because tannins precipitate alkaloids)
» Symptomatic and supportive care should be given, with attention to adequacy of ventilation and vital signs
» Atropine may reverse some of the toxic effects
» Consult poison control center
8. Plants with toxalbumin toxicity
Toxic mechanism
» The protein toxins derived from these plants work specifically by inhibiting the function of ribosomes
» The toxins typically have two linked polypeptide chains
› One of the chains binds to cell surface glycoproteins to allow endocytosis into the cell
› The other chain, upon cell entry, binds the 60S ribosomal subunit and impairs its ability to synthesize protein
Examples
» Ricinus communis (castor seeds ارنڈ کے بیج) seeds (Family Euphorbiaceae)
» Abrus precatorius (رتی) seeds (Family Fabaceae)
Toxins
» Toxalbumins (abrin in abrus seeds and ricin in castor seeds)
» The toxin is contained within the hard, water-impermeable coat of the seeds
» The toxin is not released unless the seed coats are broken (e.g., chewed) and the contents digested
Intoxication / clinical findings
» Ingested seeds that remain intact as they pass through the GIT, generally do not release toxin or cause toxicity
» However, if the seeds are chewed, pulverized, or digested (i.e., if passage through the gastrointestinal tract is delayed)
› Then the toxin is absorbed by intestinal cells causing mild to severe GIT toxicity
» Effects depend upon the amount of toxin exposure and include
› Nausea, vomiting, abdominal cramping, diarrhea, and dehydration
» Variations in the severity of toxicity may be related to the degree to which the seeds are ground or chewed before ingestion
» Parenteral administration (even with small quantities) or perhaps a large ingestion may produce life-threatening systemic findings, including multisystem organ failure
Management
» Ingestion of intact seeds does not cause toxicity in the majority of cases and requires no therapy
» Cases associated with GIT effects need to be assessed for signs of dehydration and electrolyte abnormalities
» Activated charcoal should be administered
» Intravenous hydration, antiemetics, and electrolyte replacement may be necessary in severe cases, particularly in children
» Consult poison control center
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Reading References
» Shah BN, Seth AK. Textbook of pharmacognosy and phytochemistry, Elsevier, 1st edition, 2010.
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