Zinc absorption and metabolism by isolated, vascularly perfused rat intestine.

An isolated vascularly perfused rat intestine system was utilized to examine various aspects of zinc absorption in an attempt to more clearly examine the mechanisms involved. The lumen was perfused with a modified tissue culture medium containing 65Zn. The vascular system was perfused from the superior mesenteric artery to the portal vein, with Krebs-Ringer bicarbonate buffer containing 5% rat serum. The criterion for absorption was the amount of radioactivity transferred to the vascular perfusate. When the intestines were obtained from rats that had consumed a zinc-deficient diet the amount of zinc absorbed increased markedly. Conversely, elevation of zinc status decreased the amount of 65Zn that could be transferred to the vascular perfusate. These data strongly suggest that the isolated, perfused rat intestine retains the ability to exercise homeostatic control over 65Zn absorption. Transfer of infused 65Zn to the vascular perfusate was significantly decreased by aspirin, phytate, and prostaglandin E2. Uptake of 65Zn from the lumen into the intestinal cells was significantly increased by histidine and significantly decreased by phytate and prostaglandin E2. Thus, the isolated, vascularly perfused rat intestine appears to be capable of differentiating between the cellular uptake and cell to plasma transfer phases of zinc absorption.

Biomedical responses of rats to chronic exposure to dietary cadmium fed in ad libitum and equalized regimes.

Forty 100 g male rats were fed, in groups of eight, either 0, 5, or 25 ppm cadmium in a purified diet for 14 wk. Three groups were fed each of the levels of cadmium on an ad libitum basis. Two other groups were fed either 0 or 5 ppm cadmium in amounts that were equalized to that consumed by the 25 ppm group fed ad libitum. Cadmium ingestion decreased daily diet consumption, weight gain, and terminal body weight. These parameters were not significantly different in rats whose diet consumption was equalized. Packed cell volume and serum iron as well as serum zinc were decreased in the rats fed 25 ppm cadmium. These effects were not related to diet intake. No major differences were observed in serum ceruloplasmin, glucose, protein, leucine aminopeptidase activity, or copper in any of the groups. Blood urea nitrogen and renal leucine aminopeptidase activity were decreased by cadmium ingestion in the rats fed ad libitum only. In contrast, serum alkaline phosphatase activity was elevated by cadmium in the equalized-intake groups only. Cadmium and zinc concentrations were elevated and the iron concentration was decreased in the kidney, liver, and intestinal mucosa of the cadmium-fed rats irrespective of level of diet consumption. The increased uptake of cadmium in these tissues was coincident with the increased content of the cadmium-binding protein, metallothionein, in the cytosol fraction. The results indicate that some parameters of chronic cadmium toxicity are associated with diet consumption whereas others are not.