Juvenile rainbow trout were exposed to 25–400 μg copper∙L−1 for 24 h. Water hardness, pH, and alkalinity were varied independently at a constant [Na+]. Net and unidirectional sodium fluxes were measured in hard and soft, low-alkalinity water and in hard, high-alkalinity water at neutral pH and pH 5.0. In low alkalinity water, Na+ uptake (Jin) was inhibited at copper concentrations as low as 25 μg∙L−1, and sodium efflux (Jout) was stimulated above 100 μg∙L−1. High-alkalinity water significantly reduced the effects of copper on Jin and Jout, but there was no significant effect of increasing water hardness. The effects of pH 5.0 and copper were additive from 25 to 100 μg∙L−1, but a pure copper effect was found from 200 to 400 μg∙L−1. Fish died when they had lost about 50–55% of their exchangeable Na+ pool. Water hardness and alkalinity had no effect on the apparent uptake of copper, but copper uptake was reduced by about 50% at pH 5.0.

No abstract

Whole body, gill, and liver copper uptake, gill Na+-K+-ATPase specific activity, and gill and liver acid-soluble thiols (AST), glutathione, and cysteine of rainbow trout (Salmo gairdneri) were measured during 28 d of exposure to 55 μg copper∙L−1. Na+-K+-ATPase specific activity was inhibited by 33% within 24 h of copper exposure, but this was compensated by a significant increase in microsomal protein so that the total Na+-K+-ATPase activity per milligram of gill tissue returned to normal by day 14. There was no accumulation of copper and no increase in AST, glutathione, or cysteine in the gill. However, after 7 d of exposure, hepatic AST and glutathione had increased by about 2 times, and a sulfhydryl-rich, acid-soluble protein, tentatively identified as metallothionein, increased by 2.8 times. Copper accumulation was highest in the liver, but other tissues also accumulated copper.

Juvenile rainbow trout (Salmo gairdneri) were exposed to 55 μg copper∙L−1 for 28 d and then transferred to uncontaminated water for 7 d. Whole body sodium concentration and sodium uptake (Jin) were measured at weekly intervals; Jin was measured at various Na+ concentrations and kinetic parameters estimated. After 24 h of copper exposure, the maximum rate of sodium uptake (Jmax) was inhibited by 55%, the affinity for sodium (Km) reduced by 49%, and whole body Na+ decreased by about 12.5%. After 7 d of exposure, whole body Na+ had returned to control values, but Jmax was still inhibited by 41%. Recovery of whole body Na+ occurred largely by a reduction of sodium efflux (Jout). Both Jmax and Km continued to recover until day 28, at which time Jin had returned to control values. We conclude that acclimation to sublethal copper depends on changes in both Na+ transport and permeability.

The intrahepatic biliary system was studied in the rainbow trout (Salmo gairdneri), a teleost known to form liver neoplasms after exposure to various carcinogens. Normal adults (N = 25) were examined using light microscopic, enzyme histochemical, and transmission and scanning electron microscopic methods. In light micrographs, longitudinal arrays of hepatocytes appeared as double rows incompletely divided by elongated darkly stained cells. Electron micrographs showed tubules of five to nine pyramidally shaped hepatocytes with their apices directed toward a central biliary passageway and their bases directed toward sinusoids. Sequentially, beginning with hepatocytes, biliary passageways included canaliculi, preductules, ductules, and ducts. Canaliculi were short and joined transitional passageways (preductules) formed by junctional complexes between plasma membranes of hepatocytes and small, electron-dense cells with a high nuclear to cytoplasmic ratio. Ductules, completely lined by biliary epithelial cells, occupied central regions of hepatic tubules. Relatively elongated, ductular cells were intimately associated with surrounding hepatocytes, separated from them by only a thin extracellular space devoid of a basal lamina. Epithelium of bile ducts included cuboidal through mucus-laden columnar cells, surrounded by basal lamina and, in larger ducts, by fibroblasts, smooth muscle cells, and a capillary plexus. Bile ducts and hepatic arterioles, but not venules, were distributed together. The ultrastructure of biliary epithelium, periductular, and periductal cells is presented.