Cadmium, metallothionein and renal tubular toxicity.
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.
Nordberg
M
M
Department of Environmental Hygiene, Karolinska Institutet, Stockholm, Sweden.
Jin
T
T
Nordberg
G F
GF
D000818:Animals; D002104:Cadmium / Q000378:metabolism / Q000493:pharmacokinetics / Q000633:toxicity*; D002105:Cadmium Poisoning / Q000378:metabolism*; D005506:Food Contamination; D007674:Kidney Diseases / Q000139:chemically induced* / Q000378:metabolism; D007684:Kidney Tubules / Q000187:drug effects* / Q000378:metabolism; D008668:Metallothionein / Q000378:metabolism* / Q000633:toxicity; D011485:Protein Binding; D012053:Reindeer; D014018:Tissue Distribution
C004203:cadmium-binding protein; D002104:Cadmium; D008668:Metallothionein