Internal bioavailability of zinc (Zn) in the liver and intestine of juvenile rainbow trout (Oncorhynchus mykiss) was investigated following exposure to 150 or 600microgl(-1) waterborne Zn, 45 or 135microg dietary Zng(-1)fishday(-1), and a combination of 150microgl(-1) waterborne and 45microgdietaryZng(-1)fishday(-1) for 40 days. At the organ/tissue level the concentrations of Zn in the intestine were 15-25 times those in the liver, and a transient partially additive accumulation was observed in the intestine. At the subcellular level Zn distribution was ubiquitous with the accumulation pattern in the liver being heat stable proteins (HSP)>mitochondria>nuclei-cell debris>heat denaturable proteins (HDP)>microsomes-lysosomes (M-L)=NaOH resistant fraction, while in the intestine it was nuclei-cell debris>HSP>NaOH resistant fraction>mitochondria>M-L=HDP. The majority of cellular Zn was biologically available in both tissues with the estimated putative metabolically active pools (MAP) being 65-78% in the liver and 59-75% in the intestine. We show, for the first time, preferential streaming of dietary Zn into the metabolically detoxified pool (MDP) and that of waterborne Zn to the MAP. Specifically, in the liver the cellular Zn load shifted to MAP in the waterborne Zn and combined exposures, and to the MDP in the dietary Zn exposures. In the intestine the proportion of detoxified Zn increased in the dietary Zn-exposed fish but was unchanged in the waterborne and combined exposures despite elevated concentrations. Under the experimental conditions used in the present study, uptake from the food drove the accumulation of Zn in the intestine while uptake from both sources was important in the liver, consistent with its central location. Further, additive accumulation in the MDP (hepatic and intestinal), intestinal HSP, and hepatic HDP was revealed. Overall these data suggest that fish are better insulated from dietary than waterborne Zn toxicity.