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Biomedical subjects

G F Combs

Publications and source records attributed to G F Combs.

At least 109 records · Page 6Linked to original sources
PubMed1978

Influence of ethoxyquin on the utilization of selenium by the chick.

Experiments showed that commonly used concentrations of dietary ethoxyquin (6-ethoxy-2,2,4-trimethyl-1,2-dihydroxyquinoline) spare the selenium requirement of the vitamin E-deficient chick according to the following function: log Y = -0.0011X - 0.7741, where Y = Se requirement (ppm) and X = dietary ethoxyquin (ppm). The basis of the sparing effect appeared to be metabolic; (a) ethoxyquin was effective in alleviating exudative diathesis when fed (physiologically and chronologically) separately from selenium, and (b) ethoxyquin was effective in promoting increases in the plasma of the selenium-containing enzyme, glutathione peroxidase.

Animals↗
PubMed1978

Studies on the utilization of vitamin E alcohol and esters by the chick.

Experiments were conducted to evaluate the utilization of d1-alpha-tocopherol, d1-alpha-tocopheryl acetate and a water-soluble ester, d-alpha-tocopheryl polyethylene glycol 1000 (TPGS), as dietary sources of vitamin E for the chick. Results showed that tocopheryl acetate is utilized with efficiency equal to that of vitamin E alcohol at dietary concentrations less than or equal to approximately 40 ml d1-alpha-tocopherol equivalents per kg. At greater dietary concentrations of the vitamin, the alcohol form appeared to be better utilized than the acetate when it was adequately stabilized in the diet. However, TPGS was poorly utilized at all dietary levels examined. Saponification of both esters improved the utilization of vitamin E from these sources. The utilization of all forms of vitamin E was depressed in hypervitaminotic A chicks and, to a lesser extent, in chicks fed ethoxyquin.

Animals↗
PubMed1976

Vitamin E and selenium interrelations in the diet of Atlantic salmon (Salmo salar): gross, histological and biochemical deficiency signs.

Either simultaneous or separate dietary deficiencies of vitamin E and selenium in Atlantic salmon during first 4 weeks of feeding caused twice the mortality shown in fish fed both supplemental vitamin E (0.5 IU/g dry diet) and selenium (0.1 mug/g). Subsequent dietary repletion with both vitamin E and selenium significantly reduced mortality during the following 2 weeks. Larger salmon (0.9 g initial mean weight), with vitamin E deficiency with or without selenium resulted in the following deficiency signs: extreme anemia, pale gills, anisocytosis, poikilocytosis, elevated plasma protein, exudative diathesis, dermal depigmentation, in vitro ascorbic acid-stimulated peroxidation in hepatic microsomes, yellow-orange liver color, yellow-brown intestinal contents, enlarged gall bladder distended with dark green bile, low vitamin E in carcass and hepatic tissue, muscular dystrophy, increased carcass fat and water, and a response to handling characterized by a transitory fainting with interruption in swimming. A deficiency of dietary selenium suppressed plasma glutathione peroxidase activity. Supplemental selenium with vitamin E significantly increased tocopherol activity in hepatic, but not carcass tissues. Supplements of both vitamin E and selenium were necessary to prevent muscular dystrophy.

Animals↗
PubMed1976

Influence of ascorbic acid on selenium nutrition in the chick.

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 scrobutic. Absorption 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.

Animals↗
PubMed1976

Differential effects of high dietary levels of vitamin A on the vitamin E-selenium nutrition of young and adult chickens.

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.

Age Factors↗
PubMed1976

Studies on the enteric absorption of selenium in the chick using localized coccidial infections.

Studies were conducted to determine the primary loci of gastrointestinal absorption of inorganic selenium in the chick using radiotracer techniques and Eimeria sp. infections of known site specificity for the gastrointestinal tract. Results showed that coccidial infections in the anterior regions of the small intestine reduced selenium absorption and potentiated selenium deficiency among chicks fed critical levels of the mineral. Absorption experiments showed that selenium absorption was greatest in the duodenum and anterior ileum, although selenium was bound at least transiently to tissues in the gizzard and crop. It is concluded from these experiments that dietary inorganic selenium is absorbed primarily in the duodenum and anterior ileum. Factors such as enteric disease which disrupt the integrity of the anterior intestinal mucosa can, therefore, reduce the absorption of selenium and other nutrients absorbed in that region, resulting in a potentiation of nutritional deficiencies.

Animals↗
PubMed1975

Effects of dietary polychlorinated biphenyls on vitamin E and selenium nutrition in the chick.

Experiments were conducted to determine the effects of polychlorinated biphenyls (PCBs) on vitamin E-selenium nutrition in the chick. Results showed that 10 p.p.m. Aroclor¿ 1254 in the diets of breeding S.C.W.L. hens increased the susceptibility of progency to vitamin E-selenium deficiency when those chicks were reared on a diet deficient in vitamin E and supplemented with a marginal level of selenium. Susceptibility to this deficiency, as measured by the incidence of exudative diathesis, was also increased when PCBs were added to chick diets. Dietary PCBs were shown to induce hepatic microsomal benzopyrene hydroxylase and induction of this activity was associated with decreased biological utilization of dietary selenium. PCBs were shown to increase the apparent requirements of the chick for vitamin E and selenium for prevention of exudative diathesis. However, discrimination between effects on vitamin E function and effects on selenium function was not possible in these experiments.

Animals↗
PubMed1975

Polychlorinated biphenyl-stimulated selenium deficiency in the chick.

Experiments were conducted to determine individually the effects of dietary PCBs on the physiologic functions of vitamin E and selenium. Results showed that dietary PCBs did not affect the function of vitamin E in protection of biological membranes. However, PCBs did decrease the biological utilization of dietary selenium as measured by glutathione peroxidase activity in plasma and by the protection of biological membranes from peroxidation. These results indicate that dietary PCBs potentiate vitamin E-selenium deficiency in the chick by interference with the biological utilization of dietary selenium. An hypothesis for the mechanism of this effect is offered.

Animals↗
PubMed1975

Dieldrin dilution in visceral fat of field-contaminated broilers.

Broilers aged 4, 5 and 6 weeks were selected from 8 commercial flocks which had been accidentally exposed to dieldrin in feeds. The birds were given a dieldrin-free ration and were reared to 10 weeks of age. Dieldrin residues in visceral fat were determined weekly. Results indicated that dieldrin residues are rapidly diluted in the growing chick with a half-time for dilution of approximately 12 days.

Adipose Tissue↗
PubMed1975

Mechanisms of action of selenium and vitamin E in protection of biological membranes.

Opinions vary as to the mode of action of vitamin E and selenium. Some argue that they act as nonspecific biological antioxidants. Others propose that the functions of the two substances are distinct and that vitamin E acts as a true vitamin in addition to functioning as a lipid-soluble antioxidant. Support for the "Biological Antioxidant Theory" is largely circumstantial. However, lipoperoxides have been detected in adipose tissues of vitamin E-deficient animals, and increased rates of in vitro peroxidation have been demonstrated in homogenates of several tissues of selenium and vitamin E-deficient animals. The basis of the antioxygenic role of selenium in these systems was elucidated by the discovery of Rotruck et al. (1973) that selenium is a component of rat erythrocyte glutathione peroxidase. Further studies in this laboratory have demonstrated the important role of glutathione peroxidase in protection against the vitamin E- and selenium-deficiency disease of chicks, exudative diathesis, which results from increased capillary permeability. Also shown were the activities of both dietary selenium and vitamin E in prevention of ascorbate-induced peroxidation in mitochondrial and microsomal preparations from chick liver. Recent results demonstrate that both selenium and vitamin E are required to protect hepatic mitochondria and microsomes from peroxidative degradation. Dietary requirements of the chick for both nutrients for this function have been determined: approximately 0.06 ppm selenium in the presence of adequate vitamin E; 30-50 IU vitamin E per kg in the presence of adequate selenium.

Aging↗