Abstract
In 1966 it was observed that Cu2(acetate)4 was an effective antiinflammatory agent in the carrageenan paw model of inflammation (1). In pursuing this observation it was found that arthritics had elevated serum Cu levels, and that chelation and subsequent excretion of Cu had been proposed as a mechanism of action of the antiarthritic drugs. This was consistent with the facts that all antiarthritic drugs are chelating agents and the serum Cu level returns to normal with disease remission. However, the administration of Cu leading to an antiinflammatory effect, on the one hand, and promoted excretion of Cu leading to an arthritic effect, on the other, were inconsistent.
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Sorenson, J.R.J. (1982). Copper Complexes as the Active Metabolites of Antiinflammatory Agents. In: Sorenson, J.R.J. (eds) Inflammatory Diseases and Copper. Experimental Biology and Medicine, vol 2. Humana Press. https://doi.org/10.1007/978-1-4612-5829-2_28
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DOI: https://doi.org/10.1007/978-1-4612-5829-2_28
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