Dear Ole Bob Berger You mention my suggesting that salivary metalloproteins could facilitate sublingual and alimentary assimilation of silver ions.
Might I remind you that in proposing my ammonia hypothesis, I pointed out that common fasting values of salivary ammonia are 10mg/100ml (100mg/L = 100ppm) (Ref. Documenta Geigy Scientific Tables). This is more than enough to liberate and render any silver ions soluble from complexion with chloride, even in the case of colloidal silver made with salt, as has been (needlessly) frowned upon by many on the list (provided it is freshly made). Same applies to the lumen, where silver chloride is rendered soluble by the relatively high concentration of ammonia at that critical juncture justprior to assimilation and where metalloproteins might conceivably form and incorporate Ag ions, especially as Cu substitutes. Also, the colon, unlike most organs, is "normally" exposed to high concentrations of ammonia, a weak base that exerts profound and diverse biological effects on mammalian cells. The colonic lumen normally contains up to 70 mM, actively inhibiting chloride secretion in the colon, the transport event which hydrates mucosal surfaces. (Prasad M, et al, J Clin Invest, 96(5), 1995; Hrnjes B, et al, Gastroenterol 110, Suppl, 1996; Mayol J, et al, Am J Physiol 273 (Cell Physiol 42), 1997; Miyata R, et al, Inflamm Res, 48(5), 1999) Cell membranes are generally highly permeable to small, lipophilic molecules such as ammonia (Walter F, et al, J Experiment Biol, 196(1), 1994). Further, ammonia is an endogenous inhibitor of intestinal chloride secretion and is equally effective mucosally and serosally (O'Brien T, et al, Digest Disease Week, 3355, 1998). Colon cells are subjected to high concentrations of NH3 and NH4+. A sizeable portion of this buffer is absorbed (Raminez M, et al, Pflugers Arch (Eur J Physiol), 438(4), 1999). Ammonia profoundly inhibits Cl secretion in human intestinal epithelia, with half-maximal inhibition at 4-6 mM. The lumen of the lower gastrointestinal tract is the setting for bacterial action on ingested protein and the colon consequently experiences concentrations of the protein degradation product ammonia that may reach 100 mM. (Hrnjez B, et al, Amer J Physiol, 277(3), 1999) Silver chloride complexation is not the death of ionic silver which it has been made out to be. Consider the recent Russian eference which I posted dealing with the management of patients with purulent infection with intravenous infusions of "silver chloride ammonia solutions" (Abrosimov I, et al, Khirurgiia (Mosk), 7, 1997). I am still waiting on Frank Key's commets on this paradoxicalphenomenon. I think it would be advantageous to consider my ammonia hypothesis along with the metalloprotein hypothesis for a more holistic approach to silver assimilation. I have brought much of this data together on my website which Frank considers with such horror that he needs to attack it. The specific URL is: http://www.gaiaresearch.co.za/silver.html Regards Stuart
