Search

Experiments were conducted to determine the nature of the effect of dietary ascorbic acid on selenium nutrition in the chick. Results showed that ascorbic acid resulted in increased activities of the selenium-containing enzyme glutathione peroxidase in plasma, accompanied by an apparent reduction in the dietary selenium requirement of the vitamin E-deficient chick. The ascorbic acid contents of plasma, liver, kidney and adrenals were not affected by selenium or vitamin E deficiencies, indicating that selenium-vitamin E deficient chicks are not rendered scorbutic. Ab sorption experiments using ligated duodenal loops or oral doses indicated that dietary ascorbic acid promoted the enteric absorption of selenium but did not affect the absorption of vitamin E. These results support the hypothesis previously reported that factors which inhibit the oxidation of dietary selenium promote its absorption and, perhaps, its post-absorptive utilization in metabolically active components of the cell. J. Nutr. 106: 958-966,1976.

Experiments were conducted to determine the nature of the interaction of high levels of vitamin A and vitamin E-selenium nutrition in the chicken. Results showed that chicks were protected from the vitamin E-selenium deficiency disease exudative diathesis (ED) by a high dietary level of vitamin A (1.0 X 10(6) IU/kg) which moderately depressed growth. A greater concentration (1.5 X 10(6) IU/kg) of vitamin A in the diets of hens fed a low vitamin E diet hastened their depletion of plasma tocopherols and increased plasma glutathione peroxidase (GSH-px) activity. At hatching the progeny of vitamin A-fed hens were severely depleted of plasma tocopherols but had normal plasma GSH-px activities. They showed increased susceptibility to ED when fed selenium-deficient, vitamin E-free diets for 2 weeks. Absorption studies using ligated duodenal loops or oral doses indicated that high-level dietary vitamin A promoted the enteric absorption of selenium but interfered with the absorption of vitamin E. The dual nature of these effects was related to the ED-protective influence of vitamin A when fed to chicks, and the ED-stimulative influence on progeny when vitamin A was fed to dams.