Toxins and Enzymes

Option D

Toxins evoke a series of chemical processes after the initial event through specific action sites or through action at receptor sites throughout the body. The resultant effect is usually related to the concentration of the toxin. However, one must understand that the final biological result may not correlate to the specific property of the toxin and that different toxins can produce similar reactions. One example would be strychnine that acts on the central nervous system but resultant effects are skeletal muscle contractions.

Toxins can also affect the enzymatic system producing both reversible and irreversible reactions. Enzymes are catalysts that perform essential biochemical cellular functions. Enzymes are complex protein molecules with specific sites of action. Interference with these sites affects the function of the enzyme and interferes with the intended biological action. Nerve agents developed for chemical warfare are examples of these types of actions. Organophosphates form an irreversible bond at the site of action of acetyl cholinesterase, the principal enzyme in the breakdown of the neurotransmitter Acetylcholine. Other types of enzyme inhibitors include heavy metals such as lead, arsenic and mercury. Some toxins induce disease or injury, including lethal effects, by the development of by-products. For example, methanol is enzymatically degraded to formaldehyde, which has a predilection for the optic nerve thus inducing blindness.

Carbon monoxide poisoning results from the tighter and greater affinity that carbon
monoxide has for the binding site on the hemoglobin molecule. Other agents lead to
illness by enhancing natural processes and affecting the body’s ability for regeneration.

Agents such as p-aminosalicilic acid, nitrites, quinine and primaquine among others,
produce methemoglobin as a result of hemoglobin oxidation. In conditions such as Beta
thalassemia, with a diminished capacity for hemoglobin regeneration, and neonates that have a limited ability to regenerate hemoglobin, a build-up of methemoglobin diminishes the effective transport of oxygen.


Some toxins accumulate in the cells and depress cellular activity causing a narcotic or anesthetic effect. General anesthetics such as ether and halothane, as well as glues, organic solvents, gasoline and other halogenated compounds tend to produce an
anesthetic reaction. In the clinical setting these substances have a fairly wide safety range, however, this is not the case with workplace organic solvents, which carry a substantial risk of death. Naturally occurring substances like atropine, norepinephrine, nicotine and curare affect cellular function by their actions on neurotransmission. These agents affect the neurotransmitters acetylcholine or norepinephrine by mimicking or inhibitory actions at the receptor sites. Cholinergic receptors that use acetylcholine for their action have either muscarinic or nicotinic receptors; adrenergic transmission is mediated by either epinephrine or norepinephrine action. Atropine and nicotine are cholinergic receptor inhibitors and act at the neuromuscular junction to induce relaxation of the skeletal muscle. Other examples of this action include the effects of Botulinus toxin, shellfish poisoning, tetrodotoxin and puffer fish poisoning.

Yet others have different forms of action. Some will affect the DNA duplication process and inhibit cell division while others prevent RNA transcription. More commonly known products exert their effects by altering protein synthesis and affecting amino acid chain reconstruction: i.e., tetracycline and chloramphenicol interfere with ribosomal action; streptomycin and gentamycin interfere with mRNA translation.

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