Zinc Uptake in the Rainbow Trout, Salmo Gairdneri (Richardson), as Affected by Dietary and Waterbone Zinc and Waterborne Calcium
Rainbow trout took up Zn from both the diet and the water. Trout on a low Zn diet became Zn-deficient, based upon mortality, lack of growth, and depressed plasma protein and hematocrit. Both plasma and whole body [Zn] were also depressed. Elevated [Zn], in either diet or water, reversed all symptoms of Zn deficiency. At high [Zn], Zn was taken up in excess of requirements, but in an attenuated fashion. These results support a relative homeostasis for Zn for both plasma and whole body, but also indicated that Zn uptake from water and diet were partially independent. There was no overt toxicity. Metal-binding proteins, important in mineral metabolism, were induced by this exposure in gill and intestine but not in liver.
The gill was identified as the major site of Zn uptake from the water by the use of an in vitro preparation which directly measured flux rates. Pre-exposure of trout to soft water for 5 days gave considerably higher influx rates than occurred in tapwater-acclimated trout, probably by stimulating proliferation of gill chloride cells. Zn influx in soft water, studied from 0.4 to 7.5 mg Zn/L followed saturable, first-order kinetics, suggesting a restricting pore or carrier mediation. Influx was studied in vivo for 24 h using a novel technique which overcame the limitations of non-specific adsorption found with traditional methods. Influx rates measured with this technique confirmed the saturable nature of influx, but were much higher. Waterbone Ca interacted with Zn influx in two separate ways. Acute increases in [Ca] up to 5 fold showed a competitive interaction, suggesting that Zn and Ca compete for the same mechanism of branchial entry. Acute removal of Ca however revealed in addition, a large influx with increasing [Zn], indicative of opening of a paracellular leak pathway across the gill.