Abstract
Three experiments were conducted to determine whether vitamin E deficiency (−E) and/or the oral administration of lead (300 mg/kg body weight) to mallard ducks would affect hepatic xanthine dehydrogenase (XDH) activity and tissue lead deposition. Although there was a significant difference between the +E and −E plasma α-tocopherol (PαT) and liver α-tocopherol (LαT) concentrations in Experiment 1, XDH activity was unaffected. In Experiment 2, 1-day-old ducklings were fed the experimental diets for 14 days and then given lead (Pb). Forty-eight hours after dosing with Pb the results obtained were similar to those in Experiment 1 except that LαT was distinctly elevated and XDH activity per gram wet weight of liver was significantly depressed in the Pb-treated groups. With Pb treatment the whole blood and liver Pb content was markedly increased. After 96 hr, whole blood, liver, kidney, and spleen Pb concentrations in the +E+Pb group were significantly greater than that in the −E+Pb group. In Experiment 3, 30-week-old, vitamin E-depleted drakes fed diets similar to those above showed normal XDH activity but marked differences in PαT and LαT were observed. Again the liver Pb content of the +E+Pb group was signficantly greater than of the −E+Pb group. It appears that XDH activity is not responsive to vitamin E deficiency. Also tissue Pb content, with the exception of drake whole blood lead concentrations, seems to be positively related to vitamin E status.
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