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To determine if zinc homeostasis occurs by zinc output from bile-pancreatic secretions, the bile-pancreatic duct and intestine of rats were surgically cannulated, and bile-pancreatic fluid was collected 2 h/d from the day of surgery to 8 d after surgery. The rats were fed diets containing 10, 100 or 1000 micrograms Zn/g diet before and after surgery. The effect of surgery itself was significant; food intake was initially lower than presurgery levels, but returned to presurgery levels by d 5. Protein and zinc concentrations, and carboxypeptidase A (CpA) and carboxypeptidase B (CpB) activities in bile-pancreatic fluid increased after surgery and leveled off at approximately d 6. Among the dietary zinc groups, the concentration of zinc in bile-pancreatic fluid varied significantly, whereas concentrations of calcium and copper did not. Zinc concentration in bile-pancreatic fluid for d 1-8 postsurgery averaged 1.8, 3.2 and 4.4 micrograms Zn/g, in the groups fed 10, 100 and 1000 micrograms Zn/g diet, respectively. Because the percent of zinc ingested that was secreted in bile-pancreatic fluid, estimated to be 57, 9.5 and 1.2% for the groups consuming the diets containing 10, 100 and 1000 micrograms Zn/g diet respectively, was not similar in the three groups, the quantity of zinc in bile-pancreatic fluid is not proportionally related to the amount of zinc ingested. Our results therefore suggest that zinc secretion in bile-pancreatic fluid does not play a major role in zinc homeostasis. Molecular localization of zinc in bile-pancreatic fluid and measurement of activity of CpA and CpB indicated that zinc in bile-pancreatic fluid is associated primarily with these digestive enzymes.

The interaction between zinc and copper in the pregnant rat was investigated by feeding Sprague-Dawley rats, from mating to term, diets that varied in zinc and copper concentrations. A factorial design was used with diets containing 1, 10, 100 or 1000 micrograms zinc/gram and 0.5, 5, 10 or 100 micrograms copper/gram. Malformations were found only in fetuses from rats fed the zinc-deficient diets (1 microgram/g), and the frequency of malformed fetuses increased as concentration of dietary copper increased. Maternal and fetal tissues of rats fed diets deficient in either zinc or copper were significantly lower in these elements than were those of rats fed a control diet. An antagonistic effect of dietary zinc on maternal and fetal tissue copper concentration was observed. The concentration of fetal liver zinc from rats fed a copper-deficient diet was significantly higher than controls. The concentration of iron in maternal and fetal tissues was significantly affected by the level of dietary zinc, with values highest in the zinc-deficient groups. Maternal plasma cholesterol and triglyceride levels were significantly lower than normal in the zinc-deficient animals. These data show that when the concentration of zinc in the diet is deficient an interaction can occur between dietary zinc and copper such that high levels of copper potentiate the teratogenicity of zinc deficiency.