By Albert E Pohland; Vulus R Dowell; J L Richard; Richard J Cole; Milven W Eklund; All authors
Read Online or Download Microbial Toxins in Foods and Feeds : Cellular and Molecular Modes of Action PDF
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Extra resources for Microbial Toxins in Foods and Feeds : Cellular and Molecular Modes of Action
In a railroad wreck discovery of misaligned rails does not tell us that the true cause of the wreck was the inefficiency of an alcohol besotted supervisory engineer in charge of the laying of the track. Thus discovery of a neurophysiological or neurochemical change is not necessarily discovery of primary cause, the initiating event. Nervous system activity takes place through catenary series, some single path distaxic, and other complex branching pathways. Blockage at one point can lead to pile up at one or more preceeding points near or far on a main branch or side branch.
One for each function. The pipe and valve hypothesis does not make a choice between these possibilities. Whether toxin prevents exocytosis by masking a trigger or blocks channel translocation of acetylcholine either process can be nonenzymatic. Toxin may frustrate an enzymatic event such as exocytosis without itself acting as an enzyme. Enzyme inhibitors can be nonenzymatic. The nonenzymic aspect of the pipe and valve hypothesis satisfies the rule of Ockham's razor, namely, that entities should not be multiplied unnecessarily.
Toxins may have their actions far from the vicinity of producing bacteria and thus are in no position to affect the immediate environment of the bacteria. Such is certainly the reality of the food poisoning caused by Staphylococcus and C. botulinum. Toxins act on anatomophysiological systems of the host not present in the parent bacterium. This is the case 22 for botulinal neurotoxins which interfere with acetylcholine releasing systems unique to nerve cells. These kinds of observations do not reveal any useful role for the toxicity of toxins in the economy of bacteria.