According to a theory of Knappwost's, fluoride's protection against tooth decay relies on a vagotonic influence on saliva quantity and quality. Therefore, we looked for signs of a vagotonic mechanism for the effect of fluoride. On the basis of the inhibition of acetylcholinesterase by fluoride we could show that this inhibition increases when the pH is shifted towards a more acidic level (up to pH 6-6.5). Elucidating this state of affairs showed that the HF molecule is the actual inhibitory agent. From this it could be deduced that in those areas of the organism where such pH shifts occur, an inhibition of AChE is possible at physiological F concentrations.
We could show that fluoride complexes of Al and Si are only partially hydrolyzed under "quasi physiological" conditions, and that in the case of Si the "residual complexes" have an inhibitory effect on AChE. The inhibitory capacity of fluoride could be increased this way by using fluorosilicates, which appear in the inanimate realm of nature and probably also in the human body. Even so called physiological fluoride concentrations could now trigger vagotonic effects.
With the help of model experiments on human red blood cells we could study the influence of fluoride on the permeability of erythrocyte membranes to electrolytes. We found that the permeability for K+ and Ca2+ increases at fluoride concentrations over 10-4M. In the case of Na+ permeability we could already detect an impact at 5 x 10-5 M NaF. A spontaneous influx of Na+, which showed a certain similarity to the circumstances at nerve cells upon stimulation by acetylcholine, occurred upon contact of erythrocytes with fluoride concentrations of 10-4 M. The Na+ that had penetrated began to be transported back out of the cell after only two minutes. The dependence of Na+ permeability on fluoride concentrations after a reaction time of 2-4 minutes showed a maximum permeability at 10-4 M NaF. The exchange of radioactive phosphate at the erythrocyte membrane was also already affected at concentrations between 5 x 10-5 M and 10-4 M NaF. Phosphoglycerate accumulation and a decline in ATP synthesis only developed above 2.5 x 10-3 M NaF.
With the help of radioactive fluoride (18F) we could show that fluoride exchange occurs very quickly at the erythrocyte membranes. At fluoride concentrations of 2.5 x 10-4 M the cells received half as much 18F as the serum.
Altogether these studies suggest that an effect of fluoride on the membrane permeability for the aforementioned cations can already develop at physiological F concentrations. This is especially true for sodium. If these studies can also be applied to other body cells (for example nerve cells), it would mean that fluoride could, by way of a slight rise in the "leaking flow" of K+ and especially Na+, affect the resting potential, and thereby the overall excitability, of the cells.
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