The biological effects of silver are apparently due to reversible bonds with enzymes and other active molecules on the surface of cells. Due to its sulphydryl binding propensity, biologically-available silver disrupts membranes, disables proteins and inhibits enzymes. The ionic form of silver is necessary for biological activity and the lipid phase of the membrane appears to be important in adsorbing silver ions to living cells. The active sites on enzymes which are affected by silver are apparently the electron-rich functional groups such as-SH groups. Silver was similar in toxicity to mercury in in vitro experiments on the activity of glutamic oxaloacetic transaminase (GOT), and lactic dehydrogenase (LDH), obtained from the blood plasma of the white sucker, Catostomus commersoni. The GOT was the most sensitive and was completely inhibited at 50mg/L (Cooper and Jolly 1970, Christienson 1971/72). Interference with active transport and cyclic adenosine monophosphate are reported, as is binding to bases, riboses and phosphates on DNA (Klein 1978).
Silver combines with plasma proteins, is removed by the liver and over 90% is eliminated in the bile; most of this in the feces with very little in the urine. That which is not excreted is deposited in the skin and mucous tissues (MRI 1975, Cooper and Jolly 1970). In 1986, George et al. reported a metallothionein which complexes silver and copper.
Tissue deposition of silver results from precipitation of insoluble salts such as silver chloride and silver phosphate. These may be transformed to soluble silver sulphide albuminates and bind with amino or carboxyl groups in proteins and nucleic acids. They may also be oxidized to metallic silver by ascorbic acid or catecholamines.
Experiments with radiosilver indicate that it is mainly associated with the reticulo-endothelial system. The silver is concentrated in the basement membrane of the skin, in the elastic fibres around sweat glands and the eyes; generally in areas of the skin exposed to the sun. The discoloured skin in argyric patients exposed to ultraviolet radiation is likely caused by photoreduction of silver chloride to metallic silver, which is then oxidized to black silver sulphide and bound by tissues. If the diet is high in selenium, the silver sulphide is converted to silver selenide which may result in higher silver deposition rates than with silver sulphide (Danscher 1981, Berry and Galle 1982, Buckley et al. 1965).