Hepatic Se Concentrations Research Articles

Tissue-specific modification of selenium concentration by acute and chronic dexamethasone administration in mice.

Several clinical reports have shown changes in plasma Se concentration with corticosteroid treatments, but the results have been inconsistent. Few experimental studies have been done on this subject. In the present study the effect of dexamethasone (DEX) treatment on Se concentrations and activities of Se-dependent glutathione peroxidase (EC 1.11.1.9; SeGPx) were examined in adult male ICR mice. In the first experiment, DEX was given via drinking water containing 5 or 50 mg DEX/l. At 1 or 3 weeks of DEX treatment, mice were dissected and the Se concentrations as well as SeGPx activities in various tissues, including plasma, were determined. At 1 week the DEX-treated groups had significantly lower hepatic Se concentrations and significantly higher plasma and cerebral concentrations than the control group. The DEX-treated groups showed lower SeGPx activities in the hepatic cytosol and higher SeGPx activities in the plasma than the saline (9 g NaCl/l)-treated group, in parallel with the changes in Se concentrations. At 3 weeks, neither hepatic nor plasma Se concentrations showed a significant change. In the second experiment, mice were injected subcutaneously with DEX and, thereafter, mice were food-deprived. The DEX-injected groups had higher plasma Se concentrations. A similar finding was obtained also when the DEX- or saline-injected mice were not food-deprived. Thus, the difference between the DEX-treated and control groups was possibly caused by redistribution of tissue Se. These results suggested that the effects of DEX on Se concentrations were tissue dependent and that the higher plasma Se observed in DEX-treated groups might be explained by the release of tissue Se into plasma as plasma SeGPx.

Metabolism of selenium and copper in sheep with and without sodium bicarbonate supplementation

The interrelationship in metabolism between dietary selenium (Se) and copper (Cu) was investigated in sheep receiving a diet with or without sodium bicarbonate (NaHCO3). A sheep finishing diet, containing 0·3 mg Se/kg DM and 7·4 mg Cu/kg DM, and supplemented with 1·0 mg Se (as Na2SeO3) and/or 15·0 mg Cu (as CuSO4) and/or 40 g NaHCO3 per kg feed, was fed to young ewes for a period of 64 days. Hepatic Cu concentration and net accumulation were not affected by NaHCO3 supplementation. Furthermore, no evidence was found in blood, tissues or faeces to show that NaHCO3 influenced Se metabolism. However, hepatic Cu concentration was raised from 354 to 422 mg/kg DM (P<0·05) when the diet was supplemented with 1 mg Se/kg DM, independent of the level of dietary Cu. Furthermore, hepatic Cu retention was significantly (P<0·05) influenced by a Se × Cu interaction, namely when the diet was supplemented with 15·0 mg CuSO4 or 1·0 mg Na2SeO3 /kg DM or both, 0·084, 0·081 and 0·088 of the dietary Cu respectively was retained in the liver, compared to 0·047 in the sheep on the basal diet. In addition, supplementation with Se and Cu together increased hepatic Se concentration to a greater extent (P<0·001) than when Se alone was added to the feed (3·65 v. 5·17 mg Se/kg DM respectively). The concentration of Se in both muscle tissue and in rumen bacteria was raised (P<0·001) by Se supplementation, but more so (P<0·05) in both cases when Cu was not added to the diet. Interactions between Se and Cu were not influenced by NaHCO3 supplementation in the conditions of this study.

Postnatal Selenium Repletion Protects Lungs of Neonatal Rats from Hyperoxia

We reported previously that Se-adequate neonatal rat pups born to Se-adequate dams were resistant to lung damage by hyperoxia. To assess whether early postnatal Se repletion could also protect developing pups reared under hyperoxia, female Sprague-Dawley rats (n = 20) were bred and fed a Sedeficient (0.04 μg/g) diet during pregnancy. On d 1 postpartum, dams were divided into two groups and fed either a Se-deficient diet or a Se-repleted (0.5 μg/g) diet. On d 4 postpartum, litters in each group were randomly assigned to either air or high oxygen (>95% O2) environments. Histologic evaluation of lungs from d-8 pups indicated that Se repletion significantly reduced the incidence of lung lesions caused by hyperoxia. Selenium-repleted pups also had significantly greater lung volumes and internal surface areas. The 7-d period of Se repletion resulted in significantly elevated maternal milk Se concentrations compared with a Se-deficient group, which was reflected in the pups by elevated plasma and hepatic Se concentrations and Se-dependent glutathione peroxidase (SeGPx) activities. Pulmonary glutathione concentration and SeGPx activity in pups were affected by oxygen exposure only, not by Se nutrition. Therefore, early postnatal Se repletion can protect the developing lung from oxygen-induced injury, a protection that is not entirely due to the effects of Se on pulmonary SeGPx activity and glutathione concentration.

Tissue selenium accretion in premature and full-term human infants and children

Development of supplementation guidelines for formulated diets and total parenteral nutrition requires knowledge of Se tissue accretion. To this end, the total organ Se content was calculated from the Se concentrations that were measured by neutron activation analysis in postmortem samples of liver (n=56), kidney (n=11), adrenal cortex (n=9), and pancreas (n=6) from infants and children from birth to 10 yr including 17 born prematurely. Hepatic Se concentrations were similar in full-term and premature newborns, decreased from birth to 1 yr, and then increased thereafter. The total hepatic Se content was significantly greater in full-term than in preterm newborns and increased with age and liver size after 1 yr. No significant differences were found between the concentrations of Se in kidney, pancreas, and adrenal tissues. Falling hepatic Se concentrations in the full-term infant concurrent with stable total organ Se content may indicate inadequate dietary intake or may reflect a normal redistribution of the nutrient. Premature infants are born with smaller stores than full-term infants and are at greater risk of developing a deficiency.