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OCR for page 431
silver
Silver (Ag), a white lustrous metal, is a rare element that is distributed
within the earth's crust at a concentration of about 0.1 ppm. It occurs
as native silver and in minerals such as cerargyrite, argentite, and
several complex sulfides. Most silver is found in association with
copper, lead, and zinc, and, therefore, the silver of commercial value
is primarily a by-product of the mining of nonferrous base metals.
Major industrial uses are in the manufacture of silverware, jewelry,
alloys, metallic coatings, coinage (formerly), and in photographic appli-
cations (Browning, 1969; Standen, 19691. Domestic silver production in
1978 amounted to about 39 million troy ounces (U.S. Department of the
Interior, 1979~. Industrial exposure to silver results in a peculiar disease
(argyria) in which there is a generalized precipitation of silver in the
skin and tissues. Accordingly, the skin assumes a permanent and irre-
versible pigmentation of a blue-gray color with other health disturb-
ances usually being absent. Research interest in the biological actions
of silver stems from its involvement with vitamin E, selenium, and
-copper metabolism.
ESSENTIALITY
No known biological function has yet been discovered for silver in
animals.
431
OCR for page 432
432 MINERAL TOLERANCE OF DOMESTIC ANIMALS
METABOLISM
Silver metabolism in rats was studied by Scott and Hamilton (19501.
Rats were killed at various intervals postdosing with tracer quantities
of radiosilver (mixed isotopes) given intramuscularly, intravenously,
and by stomach tube. Radiosilver analyses yielded similar results for
both the intramuscular and intravenous paths of administration. By 4
days postdosing, most of the administered silver (ca. 93 percent) had
been excreted via the feces with relatively little (ca. 0.3 percent) ap-
pear~ng in the urine. The radiosilver was distributed throughout the
tissues of the rats with the large intestine having the highest concentra-
tion and muscle having the lowest. Kidney and liver were found to
contain intermediate quantities. In contrast, stomach tube admir~istra-
tion did not result in appreciable quantities of radiosilver in tissues.
Most of the dose (ca. 99 percent) was excreted by the fourth day
postdosing. These findings were extended by an experiment in which
rats were treated with intramuscular doses of radiosilver and with
radiosilver plus silver nitrate at 0.4 and 4.0 mg per kg of body weight.
At 6 days postdosing, 97 percent of the administered dose appeared in
the feces of the rats given the radiotracer alone, whereas similar figures
for the 0.4 and 4.0 mg doses were 89 and 37 percent, respectively.
Tissue distribution was affected both quantitatively and qualitatively
by dosage. As dosage increased, the amount of residual radiosilver in
the tissues increased. At the highest dosage, liver and spleen contained
the highest concentrations of silver, whereas, with the tracer dose, the
gastrointestinal tract had the highest concentrations. It can be con-
cluded from these studies that, in rats, silver elimination occurs via the
feces and that silver administration results in a wide and variable tissue
distribution.
SOURCES
No data could be located concerning the silver content of common
feedstuffs. Bowen (1966) indicates that soils average 0.1 ppm silver and
that land plants in general average 0.06 ppm. Silver can enter feed-
stuffs, however, due to its natural distribution, its association with
mineral feeds, and its loss through environmental dispersion.
OCR for page 433
Silver
TOXICOSIS
LOW LEVELS
433
In a dose-response experiment with chickens grown to 3 weeks of age,
Hill et al. (1964) demonstrated that 10 to 100 ppm of dietary silver (as
Ag2SO4) was without adverse effects on growth rate, mortality, hemo-
globin concentration, and elastin content of the aorta.
HIGH LEVELS
In growing turkeys, 300 ppm of dietary silver reduced rate of weight
gain (Jensen et al., 1974~. At 900 ppm, the heart was enlarged, the
gizzard musculature was dystrophic, weight gain was severely de-
pressed, and the blood packed cell volume was decreased.
In growing chickens, the signs of silver toxicosis included reduced
weight gain, increased mortality, increased heart weight, decreased
aortic elastin content, reduced blood hemoglobin, and exudative di-
athesis (Hill e' al., 1964; Bunyan et al., 1968; Peterson and Jensen,
1975a,b).
In growing rats, observed signs of silver toxicosis, in addition to
reduced weight gain, liver necrosis, and increased mortality, were a
generalized deposition of silver in the tissues (Shaver and Mason, 1951;
Diplock et al., 19671. For a further characterization of the effects of
long-term administration of silver to rats, the papers of Olcott (1948,
1950) on experimental argyrosis are particularly useful. Essentially,
Olcott found that the life term administration of silver at 1,000 ppm in
the drinking water of rats produced an intense pigmentation of many of
the tissues. More pronounced pigmentation occulted in the basement
membrane of the giomeruli, the portal vein and other parts of the liver,
the choroid plexus of the brain, the choroid layer of the eye, and in the
thyroid gland.
FACTORS INFLUENCING TOXICITY
Shaver and Mason (1951) were the first to demonstrate that silver (as
AgNO3 in the drinking water) was more toxic, as evidenced by mor-
tality, to rats when administered in conjunction with a vitamin E-
deficient diet, as compared to a vitamin E-adequate diet. Similarly,
Dam et al. (1958) noted that 20 ppm silver as silver acetate in the diet
promoted exudative diathesis in chickens fed diets deficient in vitamin
E. In rats, Diplocket al. (1967) noted a vitamin E-defcient diet coupled
OCR for page 434
434 MINERAL TOLERANCE OF DOMESTIC ANIMALS
with 0.15 percent silver acetate in the drinking water produced a high
incidence of liver necrosis and moronity that could be totally prevented
by tocopherols, partially prevented by selenium at 1 ppm, and only
marginally prevented by 0.15 percent D~-methionine. These experi-
ments were extended to chickens by Bunyan et al. (1968), who found
0.15 percent silver as silver acetate in the drinking water produced an
exudative diathesis that was responsive to treatment with a combina-
tion of vitamin E and methionine. The addition of lard to the basal diets
of chicks simultaneously treated with silver gave rise to green exudates
that were prevented by either vitamin E or selenium. It was concluded
that silver and selenium have an antagonistic relationship in rats and
chickens.
More recent studies of the silver-selenium antagonism in chicks
(Peterson and Jensen, 1975a) compared the effectiveness of vitamin E,
selenium, and cystine in preventing the adverse effects of excessive
dietary silver. Nine hundred parts per million of silver (as AgNO3) in a
diet marginal in vitamin E and selenium resulted in depressed chick
growth and caused a high mortality, largely from exudative diathesis.
Either 1 ppm selenium or 100 flu vitamin E per kilogram of diet was
effective in preventing the growth depression and mortality. Adding
0.15 percent cystine stimulated growth but failed to prevent the mor-
tality. In these studies, all diets were fortified with 50 ppm copper in
order to prevent the appearance of a silver-induced copper deficiency.
These studies were extended by Jensen (1975) to reveal the effects of
supplementary silver in chickens treated with toxic quantities of sele-
nium. Accordingly, chickens were reared for 2 weeks on diets contain-
ing 0, 5, 10, 20, 40, and 80 ppm supplemental selenium with and without
1,000 ppm of silver (as AgNO3~. The higher levels of selenium produced
a growth depression and an increased mortality that were mitigated by
the silver supplement. Radiotracer studies conducted with 75Se in these
experiments showed that dietary silver interferes with selenium absorp-
tion, a finding that could explain the antagonistic relationship between
silver and selenium.
Studies were also conducted in turkeys (Jensen et al., 19741. Accord-
ingly, 900 ppm of silver depressed growth rate, reduced packed cell
volume, and caused cardiac enlargement. There was a varying inci-
dence of-degeneration of the gizzard musculature that could be com-
pletely prevented by dietary additions of 1 ppm selenium or partially
prevented by 50 flu vitamin E per kilogram of diet. The observed micro-
cytic, hyperchromic anemia was prevented by the addition of 50 ppm
of copper but not by the addition of 5 ppm of copper to the diets. The
silver-induced cardiac enlargement was also responsive to the copper
treatments.
OCR for page 435
Silver
435
HE e' al. (1964) found that copper could reverse the toxic effects of
silver in growing chicks as evidenced by growth rate, mortality, hemo-
globin, and aorta elastin content. In these studies, 25 ppm of dietary
copper were totally effective in preventing the adverse effects of 200
ppm of dietary silver. The silver-copper antagonism was studied
fi=her by Peterson and Jensen (1975b) in chickens grown to 4 weeks
of age. Adding 900 ppm of silver (as AgNO3) to practical diets signifi-
cantly depressed growth, increased heart weights, increased mortality,
and decreased aorta elastin content. Supplemental copper (50 ppm) was
effective in reversing adverse effects except for the growth depression
that was only partially corrected.
The effect of dietary silver on the tissue distribution patterns of 64Cu
in rats has been studied by Van Campen (1966~. Liver content of copper
was increased as dietary silver increased. No effects on the copper
content of heart, kidneys, and spleen were found attributable to the
dietary silver.
TISSUE LEVELS
No data were found concerning the tissue levels of silver which result
from dietary administration.
MAXIMUM TOLERABLE LEVELS
The minimum level of silver observed to have an adverse effect on
animals reared under conditions of adequate nutntion is 300 ppm. In
this regard, the maximum tolerable level for poultry and swine is set at
100 ppm.
SUMMARY
The toxicity of silver has been relatively well studied in poultry and
rats. In these animals, silver accentuates and/or causes a multiple defi-
ciency of vitamin E, selenium, and copper with the resulting toxic signs
approximating the respective deficiency signs. Acute signs of intoxica-
tion in rats include increased pigmentation of tissues such as the base-
ment membrane of glomeruli, the portal vein, and the liver.
OCR for page 436
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OCR for page 440
440 MINERAL TOLERANCE OF DOMESTIC ANIMALS
REFERENCES
Bowen, H. J. M. 1966. Trace Elements in Biochemistry. Academic Press, New Yorlc and
London.
Browning, E. 1969. Toxicity of Industrial Metals. Butterworths, London.
Bunyan, J., A. T. Diplock, M. A. Cawthorne, and J. Green. 1968. Vitamin E and stress.
8. Nutritional effects of dietary stress with silver in vitamin E-deficient chicks and
rats. Br. J. Nutr. 22:165.
Dam, H., C. K. Nielsen, I. Prange, and E. Sondergaard. 1958. Influence of linoleic and
linolenic acids on symptoms of vitamin E deficiency in chicks. Nature 182:802.
Diplock, A. T., J. Green, J. Bunyan, D. McHale, and I. R. Muthy. 1967. Vitamin E and
stress. 3. The metabolism of D+-tocopherol in the rat under dietary stress with
silver. Br. J. Nutr. 21:115.
Hill, C. H., B. Starcher, and G. Matrone. 1964. Mercury and silver interrelationships
with copper. J. Nutr. 83:107.
Jensen, L. S. 1975. Modification of a selenium toxicity in chicks by dietary silver and
copper. J. Nutr. 105:769.
Jensen, L. S., R. P. Peterson, and L. Falen. 1974. Inducement of enlarged hearts and
muscular dystrophy in turkey poults with dietary silver. Poult. Sci. 53:57.
Olcott, C. T. 1948. Experimental argyrosis. Am. J. Pathol. 24:813.
Olcott, C. T. 1950. Experimental argyrosis. Arch. Pathol. 49:138.
Peterson, R. P., and L. S. Jensen. 1975a. Induced exudative diathesis in chicks by dietary
silver. Poult. Sci. 54:79S.
Peterson, R. P., and L. S. Jensen. 1975b. Interrelationship of dietary silver with copper
in the chick. Poult. Sci. 54:771.
Scott, K. G., and J. G. Hamilton. 1950. The metabolism of silver in the rat with radio-
silver used as an indicator. Univ. Calif. Publ. Pharmacol. 2:241.
Shaver, S. L., and K. E. Mason. 1951. Impaired tolerance to silver in vitamin E deficient
rats. Anat. Rec. 109:382.
Standen, A., ed. 1969. Kirk-Othmer Encyclopedia of Chemical Technology, vol. 18.
John Wiley & Sons, New York.
U.S. Department of the Interior. 1979. Bureau of Mines Mineral Industry Surveys, Gold
and Silver, March.
Van Campen, D. R. 1966. Effects of zinc, cadmium, silver, and mercury on the absorp-
tion and distribution of copper 64 in rats. J. Nutr. 88:125.
Wagner, P. A., W. G. Hoekstra, and H. E. Ganther. 1975. Alleviation of silver toxicity
by selenite in the rat in relation to tissue glutathione peroxidase. Proc. Soc. Exp. Biol.
Med.148:1106.
Representative terms from entire chapter:
exudative diathesis
