Botulinum toxin is a chemical toxin that is formed by the bacterium Clostridium botulinum. This toxin affects the neurons and is considered as one of the most poisonous biological substances. It works by preventing the release of neurotransmitters particularly acetylcholine from the endings of the motor neurons (Nigam & Nigam, 2010).
Botulinum toxin can easily be absorbed from mucous membranes, eyes, non-intact skin, or respiratory tract. Blood is not found to cause metabolism or change the bioavailability of the toxin. The toxin remains unmodified and affects the nerve endings in the same condition. Researchers have found that the elimination half-life for native (nonmetabolized) toxin in the blood and serum ranges from 230 to 260 min (Ravichandran et al., 2006).
Chemically, botulinum toxin has a heavy chain and a light chain. Heavy chain helps the protein in binding to the neuron. After binding, it enters into the neuron, and the light chain helps in cleaving the proteins that would help in the release of neurotransmitters from the cell. This is considered as the disruption of the process of exocytosis or the release of neurotransmitters, i.e. acetylcholine. Usually, acetylcholine is related to the transmission of nerve impulses to muscles, but its blockage due to botulinum toxin results in muscle paralysis. This paralytic effect reaches to its peak in four to seven days (Nigam & Nigam, 2010).
The toxin takes from 24 to 72 hours to produce some effect showing the time required to destroy the synaptosomal process. In some circumstances, it may take up to five days for the toxin to take effect. The effect of this toxin remains for eight to twelve weeks (Nigam & Nigam, 2010).
Function of the neurons can be recovered by the fresh development of nerve terminals and production of new synaptic contacts; however, this process takes from two to three months (Nigam & Nigam, 2010). An equine antitoxin can be used to remove the problem of toxicity and food-borne illness. Artificial ventilation can also be used until the excretion or metabolism of neurotoxins.
References
Nigam, P. K., & Nigam, A. (2010). Botulinum toxin. Indian J Dermatol, 55(1), 8-14. doi: 10.4103/0019-5154.60343
Ravichandran, E., Gong, Y., Al Saleem, F. H., Ancharski, D. M., Joshi, S. G., & Simpson, L. L. (2006). An initial assessment of the systemic pharmacokinetics of botulinum toxin. Journal of Pharmacology and Experimental Therapeutics, 318(3), 1343-1351.
