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.
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 ).
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.
|Toxin||Source||Mechanisms of action|
|Puffer fish, octopus, salamander |
Shellfish contaminated with dinoflagellates
Large tropical fish contaminated with dinoflagellates
|Na + channel blocker |
Na + channel blocker
Actions on Na + channel
Na + channel activator
|Proteins and polypeptides|
|α bungarotoxin |
|Elapid snakes (kraits) |
Elapid snakes (kraits)
|Nicotinic receptor blocker |
Presynaptic cholinergic nerves
Skeletal muscle Na + channel blocker
N-type Ca 2+ antagonist
Direct acting cardiotoxin
Cell membrane destruction
|Botulinum toxin |
|Clostridium botulinum |
|Synaptin in cholinergic nerve endings |
Activation of G 2 protein
Inactivates G 0 /G 5 protein
Cell membrane ionophore