Metabolism of cadmium, zinc and copper in the rat kidney: the role of metallothionein and other binding sites.

Studies were undertaken to determine the effect of host zinc deficiency upon the distribution of Cd, Zn and Cu between and within male rat kidney cytosol and unfractionated cell pellet. In the first experiment male rates were fed stock diets supplemented with 100 micrograms Cd/mL in the drinking water for 30 days. Then Cd-treated rats and controls were segregated into groups, which received semipurified diets adequate or deficient in zinc for 14 days. After this regimen there were comparable concentrations of total Cd and metallothionein bound Cd in cytosol and the supernatant of sonicated, unfractionated pellet on a microgram Cd/g protein basis. Although less than 5% of cytosolic Cd is not bound to metallothionein (MT), 3-5 times as much non-MT Cd is present in the particulate fraction. The zinc-deficient (Zn-) dietary regime increases the non-MT Cd in the pellet. Quantitations were done of the Cu and Zn distribution in high molecular weight, superoxide dismutase, and metallothionein regions of the profiles of metals from Sephadex G-75 chromatography. In animals exposed to Cd and fed a zinc-normal (Zn+) diet, supernatant and pellet metal contents only change in the MT fraction. Similarly, zinc deficiency affects primarily the complement of metals bound to metallothionein: zinc is markedly decreased and Cu is lowered to a smaller extent. Cadmium is unchanged. Control kidney, unexposed to Cd, normally contains a substantial amount of Zn,CuMT. Two-week zinc deficiency greatly reduces MT-Zn and -Cu content without altering the metal content of other cellular pools.(ABSTRACT TRUNCATED AT 250 WORDS)