Selenium readily binds with silver to form silver selenide.  Selenium is 
necessary for a properly functioning liver.

A deficiency of selenium, or vitamin-E. causes liver necrosis which will shut 
down the biliary excretion path. The potential for selenium deficiency is 
increased by silver combining with selenium and forming silver selenide and 
reducing the bioavailable selenium.  Some excerpts:

"Wagner et al. (1975) did not find any growth depression or liver necrosis when 
Holtzman rats (10 per group) were given silver acetate in drinking water at 7.6 
mg/kg/d for 52 d while ingesting a diet that had the recom mended 
concentrations of selenium and vitamin E. In another study by Diplock et al. 
(1967), no effects were seen in Holtzman rats given silver at 97 mg/kg/d as 
silver acetate in water for 50 d when the diet was complete.
Liver necrosis was seen only in rats fed a vitamin-E deficient diet."

..." Silver has also been reported to inhibit glutathione (GSH) peroxidase, a 
seleno-enzyme. Administration of silver acetate at 751 parts per million
(ppm) (silver at 484 mg/L or 73 mg/kg/d) in water for 15 wk to young Holtzman 
rats (fed a diet adequate in vitamin E and selenium) reduced liver GSH 
peroxidase activity to 5% of controls. In the erythrocytes and the kidneys, the 
enzyme activities were reduced to 37% of controls (Wagner et al. 1975). The 
same authors reported that when the rats were exposed to silver in drinking 
water at 76 mg/L (7.3 mg/kg/d) for 52 d, GSH peroxidase was only at 30% of the 
levels in control rats fed selenium at 0.5 ppm in the diet. These effects are 
probably due to the selenium deficiency caused by silver."

..." Diplock et al. (1967) reported that vitamin E and selenium in the diet 
could significantly influence the toxicity of silver. When weanling Norwegian 
hooded rats fed a basal vitamin-E deficient diet were provided drinking water 
containing silver at 970 mg/L (as silver acetate), all rats developed liver 
necrosis within 2-4 wk and died. In another group, when selenium was added at 1 
ppm to the vitamin-E deficient diet, and the drinking water contained silver 
acetate, only four of nine rats died. In another group that was fed a diet 
containing vitamin E and was sacrificed after 50 d of silver exposure, no liver 
necrosis was found. Bunyan et al. (1968) reported similar observations in rats 
exposed to silver at 650 mg/L (as silver acetate) in drinking water. Liver 
necrosis was seen when the dietary selenium was reduced. Necrosis was induced 
at much lower doses of silver (80 mg/L).
Vitamin E appeared to reverse that effect. Also, Grasso et al. (1969) reported 
that when silver (silver acetate) was fed either in the diet (at 130-1,000 ppm, 
or 4-33 mg/kg/d) or in drinking water (97.5 mg/kg/d) to vitamin-E deficient 
rats, fatal necrosis was noted. Alexander and Aaseth
(1981) reported that depletion of liver GSH by diethyl maleate decreased 
biliary excretion of silver into the bile. Selenite also inhibited the biliary 
excretion of silver and increased its retention in the tissues. It was 
suggested that selenite formed an insoluble complex with silver that retarded 
biliary excretion. It is not clear if that is in any way related to the effect 
of selenium-containing diets in reducing the GSH peroxidase (see Wagner et al. 
1975, described above)."

Some good news is that vitamin-E helps protect the liver and may even help 
protect against liver necrosis when selenium is low but probably not when 
selenium is missing. 
Please note in the quotes above the following:

"Alexander and Aaseth (1981) reported that depletion of liver GSH by diethyl 
maleate decreased biliary excretion of silver into the bile.
Selenite also inhibited the biliary
excretion of silver and increased its retention in the tissues."

On one hand selenium is necessary to prevent liver necrosis and causing 
decreased biliary excretion of silver into the bile. On the other hand selenium 
forms selenite with silver and can inhibit the biliary excretion of silver and 
increase silver's retention in the tissues.  



Modification of a Selenium Toxicity in Chicks by Dietary Silver and Copper
(http://jn.nutrition.org/cgi/content/abstract/105/6/769)

"The results of these experiments suggest that silver modifies selenium 
toxicity both by interfering with selenium absorption and by causing the 
accumulation of a nondeleterious selenium compound in the tissues.
Copper modifies selenium toxicity primarily by causing the accumulation of a 
nondeleterious compound in the tissues."



The selenomethionine form of selenium does not cause an accumulation of silver 
in the tissues and still provides the necessary support of the liver. That is 
document in the following document.

Agricultural and Biological Chemistry, Vol.47 
 Bioavailability of Selenite, Selenomethionine and Selenocystine in Rats with 
Silver Loading

To view study select the full text option at: 
http://www.journalarchive.jst.go.jp/english/jnlabstract_en.php?cdjournal=bbb1961&cdvol=47&noissue=4&startpage=807


"Nevertheless, selenomethionine was the most effective for synthesis of 
glutathione perioxidase in the rat liver with silver. This is presumably 
because selenomethionine would be hard to combine with accumulating silver in 
the liver unless metabolized."

Remember that silver is excreted in the bile by using glutathione (GSH) as a 
carrier molecule. And the study determined that selenomethionine provides for 
synthesis of glutathione without combining with silver.

 - Steve N



-----Original Message-----
From: MaryAnn Helland [mailto:[email protected]] 
Sent: Tuesday, September 28, 2010 6:48 PM
To: [email protected]
Subject: Re: CS>Patents on CS and Generators

Hi Steve.  Thanks for the info on their patent.  Would appreciate any 
reference/substantiation regarding imbalance with selenium.  Thanks.
MA




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