Surviving the streets.
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Biomedical subjects
Publications and source records attributed to M Nordberg.
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Cadmium-induced nephrotoxicity develops at cadmium concentrations in the renal cortex of 10-300 micrograms/g wet weight. The actual concentration at which it develops depends on a number of factors, e.g., exposure route, chemical species of cadmium administered, rate of administration and simultaneous exposure to other metals. The role of these factors can be explained by a mechanism of cadmium nephrotoxicity in which both extracellular and intracellular metallothionein binding play an essential role. In reindeer used for human food, cadmium was shown to be bound to metallothionein-like proteins. If cadmium bound to such proteins enters the blood plasma via the gastrointestinal tract, this is of special toxicological significance. Metallothionein-bound cadmium in the plasma of experimental animals is efficiently transported to the kidney. Tubular dysfunction in the kidney following a normally tubulotoxic dose of cadmium bound to metallothionein was prevented by preinduction of metallothionein synthesis by small non-toxic doses of cadmium.
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Concentrations of metallothionein and metals, i.e. cadmium, copper and zinc, were determined in six rejected transplanted human kidneys and one kidney prepared for transplantation. Tissue samples separated by gel chromatography showed that almost all of cadmium in tissue was in the form of firmly bound cadmium-metallothionein.
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