Zinc metabolism and homeostasis were studied in young growing rats fed a 38 ppm zinc diet with added zinc levels ranging from 0 to 8400 ppm for 21 days. High dietary zinc did not cause toxicity symptoms. Stable zinc in feces increased linearly with dietary zinc intake but fecal 65Zn, from a single oral dose, did not increase above the 1200 ppm dietary level. Stable zinc in liver, kidney, and tibia increased two to three times with 2400 ppm added zinc, but was not further elevated until 8400 ppm was fed. Stable zinc in muscle and heart was not affected appreciably by dietary zinc level. In all tissues, 65Zn retention was drastically reduced with 1200 ppm added dietary zinc. Additional dietary zinc reduced 65Zn in muscle and heart but had little effect on liver and kidney 65Zn. The data indicate that rats have fairly effective homeostatic control mechanisms for tissue zinc below about 7200 ppm dietary zinc. Whereas, with dietary zinc up to about 1200 ppm, decreasing absorption is the main route of homeostatic control, above this level, more rapid zinc turnover rates and increasing endogenous zinc excretion appear to have major importance.