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Silver, an element of the II(B) Group, is in the second transition series of the periodic table. It is a white, lustrous, relatively soft and very malleable metal. Silver has high thermal and electrical conductivity and resists oxidation in air that is devoid of hydrogen sulfide. Silver is insoluble in water although it can exist in an aqueous environment in three cationic forms, Ag(I), Ag(II), and Ag(III), in addition to its metallic state (AgO). Most silver compounds are made from silver nitrate, which is prepared from silver metal. The toxicological properties of many substances depend on the particular chemical species of that substance, and silver is no exception. Although silver exists in its elemental state and many references within the scientific literature are simply to “silver,” it is important to stress that speciation is critical to understanding the potential for toxicity and subsequent health effects. As with many substances, a discussion of each silver species' toxicological properties would appear rather incomplete due to the lack of information available. Given these factors, it is more logical to discuss silver based on specific target organs or endpoints of concern (i.e., irritation, carcinogenicity) and to provide information on relevant silver species within this context. An explanation for the apparent lack of toxicity information on numerous species of silver is that many of the commonly used forms are insoluble in aqueous media and therefore are not readily tested in laboratory animal species. This property of many silver species may, in part, also explain its apparent lack of acute or chronic toxicity in humans based on years of occupational and workplace experience. Gold is a dense, yet malleable, lustrous, yellow metal widely found in nature as elemental gold or in combination with sulfides in igneous rocks and ores. Gold is very stable and nonreactive and does not burn or oxidize in air. Other than in its atomic state, the metal does not react with oxygen, sulfur, or selenium at any temperature. Gold does react with various oxidizing agents at ambient temperatures provided a good ligand is present to lower the redox potential below that of water. Therefore, gold is not attacked by most acids under ordinary conditions and is stable in basic media. Early uses of gold were in medicinal, antibacterial, and dental applications dating back to the ancient Chinese and Egyptians. Gold salts have been used therapeutically, without notable success in treating several diseases, including asthma, leprosy, syphilis, and tuberculosis. Presently, gold salts have therapeutic usefulness (chrysotherapy) limited to treating rheumatoid arthritis of the peripheral joints and in certain rare skin diseases. Gold salts are most efficacious in the early stages of arthritic disease and reduce the inflammatory process but without inducting any repair process in the joints. Two generally recognized disadvantages to chrysotherapy include relapse following discontinuation of treatment and potential toxicity associated with gold salts. Because of its distribution in the body and short half‐life, colloidal radioactive gold, has been used as a radiation source in treating cancer. As noted for silver, a discussion of the toxicological properties for each gold compound is not practical from the standpoint of available information. Therefore, this discussion on gold and its toxicity potential centers on particular aspects of gold toxicology, and within this framework, where a particular gold compound has been evaluated, it are discussed.
Silver, an element of the II(B) Group, is in the second transition series of the periodic table. It is a white, lustrous, relatively soft and very malleable metal. Silver has high thermal and electrical conductivity and resists oxidation in air that is devoid of hydrogen sulfide. Silver is insoluble in water although it can exist in an aqueous environment in three cationic forms, Ag(I), Ag(II), and Ag(III), in addition to its metallic state (AgO). Most silver compounds are made from silver nitrate, which is prepared from silver metal. The toxicological properties of many substances depend on the particular chemical species of that substance, and silver is no exception. Although silver exists in its elemental state and many references within the scientific literature are simply to “silver,” it is important to stress that speciation is critical to understanding the potential for toxicity and subsequent health effects. As with many substances, a discussion of each silver species' toxicological properties would appear rather incomplete due to the lack of information available. Given these factors, it is more logical to discuss silver based on specific target organs or endpoints of concern (i.e., irritation, carcinogenicity) and to provide information on relevant silver species within this context. An explanation for the apparent lack of toxicity information on numerous species of silver is that many of the commonly used forms are insoluble in aqueous media and therefore are not readily tested in laboratory animal species. This property of many silver species may, in part, also explain its apparent lack of acute or chronic toxicity in humans based on years of occupational and workplace experience. Gold is a dense, yet malleable, lustrous, yellow metal widely found in nature as elemental gold or in combination with sulfides in igneous rocks and ores. Gold is very stable and nonreactive and does not burn or oxidize in air. Other than in its atomic state, the metal does not react with oxygen, sulfur, or selenium at any temperature. Gold does react with various oxidizing agents at ambient temperatures provided a good ligand is present to lower the redox potential below that of water. Therefore, gold is not attacked by most acids under ordinary conditions and is stable in basic media. Early uses of gold were in medicinal, antibacterial, and dental applications dating back to the ancient Chinese and Egyptians. Gold salts have been used therapeutically, without notable success in treating several diseases, including asthma, leprosy, syphilis, and tuberculosis. Presently, gold salts have therapeutic usefulness (chrysotherapy) limited to treating rheumatoid arthritis of the peripheral joints and in certain rare skin diseases. Gold salts are most efficacious in the early stages of arthritic disease and reduce the inflammatory process but without inducting any repair process in the joints. Two generally recognized disadvantages to chrysotherapy include relapse following discontinuation of treatment and potential toxicity associated with gold salts. Because of its distribution in the body and short half‐life, colloidal radioactive gold, has been used as a radiation source in treating cancer. As noted for silver, a discussion of the toxicological properties for each gold compound is not practical from the standpoint of available information. Therefore, this discussion on gold and its toxicity potential centers on particular aspects of gold toxicology, and within this framework, where a particular gold compound has been evaluated, it are discussed.
The Cu concentration was about 40 times higher in the liver of LEC (Long-Evans with a cinnamon-like coat color) rats aged 77 days (227.5 +/- 21.6 micrograms/g liver) than in Fischer rats (5.2 +/- 0.1 microgram/g liver). However, in the kidney and brain of the LEC rats, Cu concentrations were lower than in these organs of the Fischer rats. Cu concentration in the hepatic metallothionein fraction was about 130 times higher in the LEC rats than in the Fischer rats. The LEC rats showed markedly low concentrations of Cu in the serum and bile. It seems likely that excretion of Cu from the liver into the bile and blood (as ceruloplasmin) is inherently lacking in the LEC rat.
Fischer rats were a fed diet supplied with copper chloride (150-600 ppm) for 60 d from weaning. Serum (glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) activities were increased with the increase of Cu concentration in the diet. Biliary excretion of Cu was related to the dietary Cu level. Depositions of hepatic and renal Cu were also related to the dietary Cu level in a dose-dependent manner. In particular, hepatic (155.2 +/- 13.3 micrograms/g) and renal (44.9 +/- 4.4 micrograms/g) Cu concentrations increased abruptly in the Cu-600 ppm group. In the liver, about 60% of Cu was distributed in the soluble fraction (100,000 g supernatant). In the Cu-600 ppm group, 25% of cystosolic Cu was bound to metallothionein (MT). Our results suggest that chronic exposure to Cu appears to have a deleterious effect on the hepatic function, and further, that even in rats with normal biliary Cu excretion, clearance of Cu from the liver may be marginal when dietary Cu is near the 600-ppm level. Although Cu is an essential nutrient, an overload of Cu should be avoided.
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