Wednesday, May 30, 2012

Biochemical Effects of Silicofluorides Enzymatic Inhibition

Enzymatic Inhibition: Professor Roger D. Masters 


That SiF and NaF have different enzymatic effects was shown long before Westendorf completed his laboratory studies in 1975.    In 1933, when reporting on his doctoral research, F. J. McClure reported that fluoride (in the form of NaF) can act as an enzyme inhibitor.[i]

      Experimental evidence has established the fact that there is also a specific
      influence of fluorides on certain enzymatic changes associated particularly
      with carbohydrates and fats. Thus, the results of a systematic study conducted by
      Kastle and Loevenhart on the effect of antiseptics on the reactions of pancreatic
      and liver extracts revealed an effect of most substances and also a particularly
      remarkable destructive action of NaF on the reaction of lipase...Dilutions of
      NaF as low as 1:15,000,000 [0.07 ppm] may inhibit the action of lipase on
      ethyl acetate as much as 50 per cent…Leake et al have obtained evidence that
      NaF inhibits the action of this enzyme in vivo.” [ii]

Two years later (in 1935), Kick et al. found the excretion pathways of fluoride differ depending on whether test animals have ingested NaF or SiF.[iii]   

Little additional work on the biological effects of these chemicals was conducted until Westendorf found that SiF inhibits AChE without a concentration threshold, whereas NaF inhibition of AChE starts at about 5 ppm of fluoride ion.  Moreover, at equal fluoride levels beyond the NaF threshold level, SiF is about 2-4 times more powerful an inhibitor of AchE than NaF. The kinetics indicated that NaF inhibition was only competitive (i.e., worked by blocking the enzyme active site), while SiF inhibition was both competitive and non-competitive.

Competitive inhibition is explained by the presence of hydrofluoric acid (HF), formed from free fluoride ion, which could find and occupy the active site in the enzyme molecule. That would occur whether inhibition were due to NaF or SiF, since both release free fluoride under physiological conditions at 1 ppm of fluoride. However, whereas NaF releases all of its fluoride ion by simple dilution/ionization, SiFs release fluoride ion in a complicated sequence of dissociation steps that depend on concentration and pH.

The chemical structures of likely SiF residues  -- [SiF2(OH)4]2-or SiF2(OH)2 --  would make each one a logical precursor for the creation of mono-silicic acid in the blood-stream.   Mono-silicic acid is not a commonplace form of hydrated silica in blood and according to the following hypothesis, has the potential for serious damage to health and behavior in a number of ways.


[i] McClure  FJ; “A Review of Fluorine and its Physiological Effects”; Physiological Reviews vol XIII, No. 3, July 1933, pp 277-300)

[ii] Ibid., p. 291. It should be noted that the fluoride level in this experiment was far lower than 1 ppm

[iii] Kick CH, Bethke RM, Edgington BH, Wilder OHM, Record PR, et al. 1935.  Fluorine in animal nutrition. Ohio Agricultural Experiment Station Bulletin 558:1-77.

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