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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 knowledge of the cellular molar concentration of a drug is an extremely important parameter for the discussion and interpretation of its efficacy and bioavailability. Concerning metal complexes, electrothermal atomic absorption spectroscopy (ETAAS) offers a valuable analytical tool. However, matrix effects often hamper proper quantification of the metal concentration in biological tissues. This paper describes the development of an ETAAS method for the quantification of the molar gold concentration in HT-29 colon carcinoma cells. ETAAS analytical conditions were optimised and a factor was developed which allows the calculation of the molar cellular gold concentration from the measured gold per cellular biomass value. The method was used to quantify the gold content in HT-29 cells after exposure to the gold drug auranofin. Results indicated a strong cellular uptake of auranofin (compared to other metal anticancer drugs), which significantly correlated with the antiproliferative effects triggered by this agent.
The novel cisplatin analogue D-17872 was studied for its anticancer activity using in vivo and in vitro preclinical models. The compound at the sublethal dose of 215 mg/kg (ca. 50% of the approximate LD50) induced no nephrotoxic effect strong enough to increase the blood urea level in rats. It had good in vivo antitumor efficacy against murine P388 (max. ILS: D-17872 132%, cisplatin 55%) and L1210 leukemia (max. ILS: D-17872 43%, cisplatin 38%), L5222 leukemia of the rat (max. ILS: D-17872 163%, cisplatin 163%) and murine B16 melanoma. Activity against P388 leukemia substantially exceeded that of cisplatin. Moreover, the M5076 reticulum cell sarcoma implanted into the subrenal capsule and the DMBA-induced mammary tumor of the rat were inhibited by D-17872 to a greater extent than by cisplatin (min. T/C: D-17872 -3%, cisplatin 11%). Using clonogenic microassays, D-17872 was active in vitro against a variety of human and rodent tumor cell lines, albeit at higher concentrations than cisplatin (IC50 values: D-17872 2.6-12.7 mumol/l, cisplatin 0.13-0.42 mumol/l). Apart from its cytotoxic action it was able to induce in vitro differentiation of the human HL-60 and K562 and of the murine M1-T22 cell lines, while cisplatin induced differentiation only in the HL-60 cell line. Thus D-17872 exhibited a pharmacological and toxicological profile different from that of the parent compound. The results suggest that induction of differentiation contributes to the antineoplastic efficacy of this novel cisplatin derivative.
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