Venoms, toxins, poisons and herbs

It is important to note that the scientific discovery of new medicines has often been derived from venoms, toxins, poisons and chemicals derived from plants. It is therefore important to understand how such molecules affect physiology. (Page et al., Integrated Pharmacology, 2nd ed, Chapter 29, Chapter 30 provide an expansion on this topic which is condensed below.)

Toxicity and target organ damage

Exposure to venoms occurs through direct contact with a venomous animal, whereas ingestion is a common route of exposure for toxins and poisons from both animals and plants. Acute toxicity often arises from brief exposure to venoms or toxins, whereas chronic low-level exposure to chemicals in the environment (or food) can induce long term toxicity.

Organs that are particularly susceptible to damage from toxins and venoms include the kidneys, lungs and liver ( Fig. 35.1 ). The reversibility of damage depends on the repair and regenerative potential of the target tissue. Liver damage is often reversible, whereas damage to the central nervous system (CNS) is more likely to be irreversible.

Fig. 35.1

Physiological mechanisms that expose the kidney, lung and liver to poisons.

From Page C, Curtis M, Walker M, Hoffman B. Integrated Pharmacology . 3rd ed. Philadelphia: Elsevier; 2006.

Medical procedures for treatment of poisoning and toxicity

Effective procedures involve removal of the source of exposure; limitation of absorption and increasing speed of elimination; and the use of antidotes, antivenoms and antitoxins to pharmacologically inhibit the mechanism of action by which the toxin or venom is thought to cause organ damage ( Table 35.1 ).

Table 35.1

Principles for the Treatment of Poisoning

From Page C, Curtis M, Walker M, Hoffman B. Integrated Pharmacology . 3rd ed. Philadelphia: Elsevier; 2006.

  • Remove the source of poison or the victim from the source (e.g. rescue)

  • Remove and limit the absorption of the poison (e.g. fresh air, wash, emesis, limit contact)

  • Supportive therapy (e.g. ventilation, external cardiac massage, saline/oxygen, drugs)

  • Specific therapies:

    • Antivenins for animal venoms

    • Antitoxins for bacterial toxins

    • Chelators for heavy metals

    • Gases (e.g. oxygen for carbon monoxide)

  • Other drug therapies:

    • Ethanol for methanol

    • Digoxin antibodies for digoxin

    • Pyridoxine for isoniazid

    • Nitrite and thiosulfate for cyanide

    • N -acetylcysteine for acetaminophen

  • Specific antagonists:

    • Atropine and oximes for organophosphate anticholinesterase inhibitor poisoning

    • Flumazenil for benzodiazepine overdose

    • Opioid antagonists (naloxone) for opiate overdose

    • Anticholinesterases for neuromuscular blocking drugs

Natural sources

Venoms occur in all animal groups, and these are usually proteins or polypeptides. Furthermore, serious anaphylaxis can occur after repeated exposure. Examples are shown in Table 35.2 . Plant toxins and poisons are usually small organic molecules and can be very diverse, as expected of a diverse and wide phylum. Examples are shown in Table 35.3 , and the list reveals common names that students will recognize as forerunners to drugs described elsewhere in this book, because the active substances from plants has led to the serendipitous discovery of many important medicines that are either extracted directly from plants or synthetic derivatives of extracts.

Table 35.2

Sources and Mechanisms of Action of Various Animal Venoms and Toxins

From Page C, Curtis M, Walker M, Hoffman B. Integrated Pharmacology . 3rd ed. Philadelphia: Elsevier; 2006. CNS, central nervous system, ATPase, Adenosine triphosphatase enzyme.

Toxin Source Mechanisms of action
Small molecules
Cardiac glycosides
Domoic acid
Puffer fish, octopus, salamander
Shellfish contaminated with dinoflagellates
Large tropical fish contaminated with dinoflagellates
Toad skin
Frog skin
Shellfish (mussels)
Sea anemone
Na + channel blocker
Na + channel blocker
Actions on Na + channel
ATPase inhibitor
Na + channel activator
CNS toxin
Proteins and polypeptides
α bungarotoxin
β bungarotoxin
α conotoxin
μ conotoxin
ω conotoxin
Elapid snakes (kraits)
Elapid snakes (kraits)
Elapid snakes
Many snakes
Nicotinic receptor blocker
Presynaptic cholinergic nerves
Skeletal muscle Na + channel blocker
N-type Ca 2+ antagonist
Direct acting cardiotoxin
Cell membrane destruction
Bacterial toxins
Botulinum toxin
Cholera toxin
Pertussis toxin
Tetanus toxin
Staphylococcal toxin
Clostridium botulinum
Cholera vibrio
Bordetella pertussis
Gram-negative bacteria
Clostridium tetani
Staphylococcus spp.
Synaptin in cholinergic nerve endings
Activation of G 2 protein
Inactivates G 0 /G 5 protein
Cell membranes
Cell membrane ionophore

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Mar 31, 2020 | Posted by in PHARMACY | Comments Off on Venoms, toxins, poisons and herbs

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