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Sign in with your library card Please enter your library card number. Clearly, the difference between the action of botulinum and tetanus toxins is the location where the light chain is released and destroys the vesicle docking mechanism.
Transport to the different sites of action is carried out by the heavy chains of these toxins. These effects occur only at high concentrations and are masked by the peripheral paralysis. The reason for this lies in the localization of the receptors for these toxins on the luminal side of the synaptic vesicle.
Only after the synaptic vesicle merges and becomes incorporated into the cell membrane do the receptors become accessible to the toxins. However, the dependence of uptake on synaptic activity is only valid if the peripheral effects are involved.
Systemic TeNT, which is transported axonally, enters neurons by a different mechanism; it is endocytosed independent of synaptic activity 10, TeNT enters vesicles which transport peripheral metabolites via the retrograde route into the soma, for reuse or introduction into other metabolic pathways. TeNT travels on this route as a stowaway. BoNT serotypes and TeNT are believed to be derived from an ancient toxin that has adapted to different targets in the course of evolution.
An adaption allowing the toxin to readily reach a different destination in the nervous system is probably responsible for disguising the toxin. Question: Why is TeNT not absorbed orally? Answer: A complex of several proteins protects BoNTs from proteolytic degradation in the upper small intestine, this complex is responsible for the oral availability of botulinum toxins. During its further passage in the digestive system, as soon as the pH changes from acid to basic, neurotoxin leaves the complex and is able to enter the circulatory system.
SinceTeNT has no protective complex proteins, like all other proteins, it is destroyed in the course of the gastrointestinal passage. Answer: Clostridium botulinum also grows in poorly perfused tissue injury and can form and release BoNT. Recently, such intoxications have been observed in drug addicts who use injectables contaminated with clostridial spores BoNT is also formed in the intestine of infants when they consume spore-contaminated food, like honey.
Answer: At least under laboratory conditions, TeNT is produced from bacteria in fermenters. Whether Clostridium tetani naturally produce the toxin under oxygen deficiency outside living organisms is a good question.
Tetanus toxin, without a protective coating, is more vulnerable to the environment than botulinum toxin complex. It does not survive the digestive process when ingested.
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