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PubMed1983

Selenium status of a rural (predominantly Amish) community living in a low-selenium area.

Selenium intake and blood selenium and selenium-dependent glutathione peroxidase concentrations were assessed in a rural, 71% Amish, sample of residents in a region with low availability of soil selenium and in urban (Columbus, OH) residents. Subjects were interviewed (24-h dietary recalls) on three separate occasions over an 18-month period, and blood and food samples were taken for analysis (maximum subject observations = 452). Mean selenium intake of the entire population was 82.8 +/- 4.4 micrograms/day. Rural and urban residents at 82.0 +/- 4.9 and 83.6 +/- 4.4 micrograms/day, respectively, did not differ significantly in intake. A breakdown by gender within location demonstrated that rural males consumed the most selenium (104.7 +/- 6.1 micrograms/day) and rural females the least (59.3 +/- 6.3 micrograms/day). Rural subject groups had significantly lower mean whole blood, plasma, and erythrocyte selenium levels (12.5 to 14.5%) as well as blood selenium-dependent glutathione peroxidase concentrations (5.6 to 10.8%) than urban groups. Subjects in both cohorts were in adequate selenium status as judged by blood parameters, even though about one-fourth of the dietary observations were below the safe and adequate range of selenium intake established by the Food and Nutrition Board. The rural diet was 18.3% lower in selenium density than the urban diet. High selenium grain products (greater than 0.2 micrograms/g) were the most important dietary selenium source in both groups, providing 29.3 to 41.6% of total intake.

Adolescent↗
PubMed1990

Selenium intake, age, gender, and smoking in relation to indices of selenium status of adults residing in a seleniferous area.

Duplicate meals, serum, whole blood, and toenails were collected every 3 mo for 1 y from a group of 44 free-living adults residing in high-selenium areas of South Dakota and Wyoming to assess the relation of selenium intake to indices of selenium status. The average selenium values for the group were as follows: dietary intake, 174 +/- 91 micrograms/d (mean +/- SD), 2.33 +/- 1.08 micrograms/kg body wt; serum, 2.10 +/- 0.38 mumol/L; whole blood, 3.22 +/- 0.79 mumol/L; and toenails, 15.2 +/- 3.0 nmol/g. Selenium intake (micrograms/kg body wt) was strongly correlated (all values, P less than 0.01) with selenium concentration of serum (r = 0.63), whole blood (r = 0.62), and toenails (r = 0.59). Men and women had similar mean values of serum, whole blood, and toenail selenium despite higher selenium intakes in men. Smokers had lower tissue selenium concentrations than did nonsmokers due, at least in part, to lower selenium intake. Age was not associated with tissue selenium content. Of the variables examined selenium intake was clearly the strongest predictor of tissue selenium concentration.

Adult↗
PubMed1994

Characterization of tissue selenium profiles and anticarcinogenic responses in rats fed natural sources of selenium-rich products.

The present report describes the biological effects associated with the feeding of three selenium-rich natural products in rats: high-selenium garlic, high-selenium onion and Brazil nut. The first two are experimental crops cultivated with selenium fertilization. Brazil nut is probably the only unadulterated high-selenium food that is available commercially. Tissue selenium profiles, liver glutathione concentrations and mammary cancer inhibition (in the dimethylbenz[a] anthracene model) were the endpoints of investigation. Parallel designs were set up to compare the three high-selenium products with selenite and selenomethionine. Previous studies have shown that treatment with seleno-methionine resulted in significantly greater tissue selenium accumulation, particularly in skeletal muscle, than treatment with selenite. In contrast, selenite, but not selenomethionine, induced a modest increase in liver glutathione concentrations. The objective was to determine whether the high-selenium natural products elicited responses that were similar to that of selenite or selenomethionine. Our experiments suggested that the high-selenium garlic and onion might have some unique attributes. First, their ingestion did not lead to an exaggerated accumulation of tissue selenium, a concern that was shared by both selenomethionine and Brazil nut. Second, unlike selenite, they did not cause any perturbation in glutathione homeostasis. Third, they expressed good anticancer activity that was equal to, if not better than, that of selenite. The chemical form(s) of selenium present in the high-selenium Allium vegetables will be discussed in relation to the manifestation of the above characteristics.

Allium↗
PubMedDate not supplied

The effect of selenium supplementation on selenium status of patients receiving chronic total parenteral nutrition.

Patients receiving long-term total parenteral nutrition (TPN) are at risk for selenium deficiency. The purpose of this study was to determine the effect of parenteral selenium as selenious acid on the selenium status of seven long-term TPN patients. Patients received a dosage of zero, 80, or 160 micrograms Se/day for 1 month each. The measures of selenium status used were selenium levels in plasma and glutathione-peroxidase activities in erythrocytes and platelets. Urinary selenium excretion was measured. Control subjects were selected to match the sex, age, and weight of the patients. With increasing levels of parenteral selenium, there was increasing plasma selenium concentration as well as erythrocyte and platelet glutathione-peroxidase activity. There was no statistical difference between the patients during the time they received the 160 micrograms parenteral selenium treatment and the control subjects for platelet glutathione-peroxidase activity. At the 160 micrograms Se/day level, patient plasma selenium concentrations increased from 28% to 58% of the control levels. Four patients were studied after they returned to the 80 micrograms parenteral selenium/day from the 160-micrograms Se/day treatment. With decreasing parenteral selenium, three patients had decreasing platelet glutathione-peroxidase activity, while plasma selenium concentration decreased in two patients. These data suggest that some patients receiving long-term parenteral nutrition should receive parenteral selenium.

Adult↗
PubMed1999

Selenium elimination in pigs after an outbreak of selenium toxicosis.

In May 1996, 150 grower pigs in 5 California counties were exposed to selenium-contaminated feed distributed by a single feed company. Feed samples from 20 herds had a mean selenium concentration of 121.7 ppm dry weight (range, 22.1-531 ppm). In San Luis Obispo County, 52 pigs in 24 herds were exposed to the feed, and 8 pigs died with signs of paralysis. Bilateral symmetrical poliomyelomalacia involving the ventral horns of the cervical and lumbar intumescence was evident on histologic examination of spinal cord from affected pigs. Of 44 surviving exposed pigs, 33 (75%) exhibited signs of selenosis, including anorexia, alopecia, and hoof lesions. Thirty-nine of 44 pigs (88.6%) had elevated (>1 ppm) blood selenium concentrations. Surviving exposed pigs were changed to a standard commercial ration containing approximately 0.5 ppm (dry weight) selenium. Blood selenium concentrations were determined weekly for 46 days following removal of the contaminated feed and were compared with values of 20 control pigs fed a standard commercial ration. Mean (+/-SD) blood selenium concentrations of exposed pigs were 3.2 +/- 2.6 ppm at the initial sampling and 0.4 +/- 0.1 ppm after 46 days. Mean blood selenium concentrations of < or = 0.3 ppm for control pigs at all samplings were significantly lower (P < 0.001) than concentrations for exposed pigs. Muscle and liver samples of 22 of the 44 exposed pigs were collected at slaughter approximately 72 days after withdrawal of the selenium-contaminated feed. Muscle samples had a mean selenium concentration of 0.36 ppm (wet weight). Liver samples had a mean selenium concentration of 1.26 ppm (wet weight). One liver sample had a selenium value in the toxic range for pigs (3.3 ppm wet weight; reference range, 0.4-1.2 ppm). A 1-compartment pharmacokinetic model of selenium elimination in exposed pigs was generated, and the geometric mean blood selenium elimination half-life was estimated to be 12 days. The 60-day withdrawal time recommended by the Food Animal Residue Avoidance Database was considered sufficient to allow safe human consumption of tissues from exposed pigs.

Animal Feed↗
PubMed1990

Elevation of rat liver mRNA for selenium-dependent glutathione peroxidase by selenium deficiency.

Selenium-dependent glutathione peroxidase (Se-GSH-Px, GSH-H2O2 oxidoreductase EC 1.11.1.9) is the best characterized selenoprotein in higher animals, but the mechanism whereby selenium becomes incorporated into the enzyme protein remains under investigation. To elucidate the mechanism of insertion of selenium into Ge-GSH-Px further, we have systematically analyzed and compared the results of Western blot, in vitro translation immunoprecipitation, and Northern blot experiments conducted with liver proteins and RNAs obtained from rats fed on selenium-deficient and selenium-supplemented diets. The anti-serum employed in this study was raised against an electrophoretically pure Se-GSH-Px preparation obtained from rat livers by a simplified purification procedure involving separation by high performance liquid chromatography on a hydrophobic interaction column. Different forms of Se-GSH-Px, including apo-protein, cross-reacted with this antiserum and Western blot analysis found no Se-GSH-Px protein present in livers from rats fed on selenium-deficient diets. By contrast, a distinct protein band corresponding to purified Se-GSH-Px was detected in livers from selenium-supplemented animals, a result consistent with the finding that the Se-GSH-Px activity was reduced to undetectable levels in livers of selenium-deficient rats. The in vitro translation experiments, however, indicated not only that mRNA for Se-GSH-Px was present during selenium deficiency but also that its translation products contained 2-3-fold as much immunoprecipitable protein as the products of poly(A) RNA from livers of selenium-supplemented rats. This result suggests that the Se-GSH-Px mRNA may be increased in the selenium-deficient state. Elevated levels of Se-GSH-Px mRNA were directly demonstrated in Northern blot experiments employing cDNA clone pGPX1211 as a probe. A similar increase in Se-GSH-Px mRNA was observed in such other tissues as kidney, testis, brain, and lung tissue, in selenium-deficient states. The present data support the co-translational mechanism for the incorporation of selenium into Se-GSH-Px in rat liver.

Animals↗
PubMed1993

Plasma and liver selenium levels in the rat during supplementation with 0.5, 2, 6, and 15 ppm selenium in drinking water.

Plasma and liver selenium of Wistar rats were determined after 1, 3, and 6 mo supplementation with 0.5, 2, 6, or 15 ppm selenium as sodium selenite in drinking water. Plasma selenium was not different from control values at additional intake of 0.5 ppm but increased above usual levels at higher intakes. A highly significant correlation was observed between the total quantity of selenium ingested and plasma selenium after 1 mo treatment (r = 0.99, p < 0.01), but was less pronounced after 3 and 6 mo (0.94, p < 0.05, and 0.78, p < 0.05, respectively). The decrease in plasma selenium with time of treatment was more pronounced at higher intakes. There was also a highly significant correlation between total selenium intake and liver selenium concentration (r = 0.99, p < 0.01) after 1 mo of treatment, but this time liver selenium did not change with time, and the correlation remained highly significant throughout the investigation. Liver selenium therefore appears as a more sensitive and more representative measure of selenium intake than plasma selenium. Most supplements did not affect body weight and survival of animals, except when the diet was supplemented with 15 ppm for 6 mo; however, alterations in biochemical parameters concerning lipid status and hepatic function were observed at levels above 2.0 ppm.

Animals↗
PubMed1998

Plasma selenoprotein P levels of healthy males in different selenium status after oral supplementation with different forms of selenium.

OBJECTIVE: To assess changes in selenoprotein P levels in plasma from subjects who had received oral supplements of different selenium forms. DESIGN: The same study group participated in two similar selenium supplementation trials, Trial I in 1981 (Levander et al, 1983) and Trial II in 1987 (Alfthan et al, 1991). During Trial II the mean baseline intake of selenium in Finland was higher compared to that during Trial I (100 and 40 microg/d, respectively), due to a nationwide supplementation of fertilisers which started in 1985. SUBJECTS: Fifty healthy Finnish men, 36-60 y old. INTERVENTION: The study group received daily placebo or oral supplements consisting of 200 microg selenium as selenium-enriched yeast, sodium selenate or selenium-enriched wheat (Trial I) or selenium-enriched yeast, sodium selenate or sodium selenite (Trial II). The duration of supplementation periods was 11 (Trial I) and 16 (Trial II) weeks. RESULTS: In Trial I the mean plasma selenoprotein P values in all the supplemented groups increased significantly, approaching a plateau at 2 weeks and reaching maxima at 4 weeks (mean increase 34%, P < 0.05). In Trial II the mean selenoprotein P levels of the supplemented groups were not significantly different from each other or from the placebo group at the start or at any time point of the supplementation period. CONCLUSIONS: At a low selenium status the selenoprotein P levels increased in a similar fashion after supplementation with different forms of selenium, but at a high selenium status no significant effects of supplementation with the same amount of selenium were observed. No differences in selenoprotein P levels were observed for inorganic and organic selenium supplements.

Adult↗
PubMed1988

Effect of dietary sodium nitroprusside as a source of cyanide on the selenium status of chicks given diets of varying selenium concentration.

1. The interaction between dietary cyanide, given in the form of sodium nitroprusside (SNP), and selenium has been studied in two experiments with growing chicks from 14 to 38 d of age. 2. In experiment 1, dietary selenium at 10 mg Se/kg reduced growth, food intake and efficiency of utilisation, and increased relative liver size and selenium content. All of these effects were eliminated by the addition of 0.1 g SNP/kg except for liver selenium content, which progressively declined towards control values as SNP was increased to 0.4 g/kg in increments of 0.1 g/kg. At 0.3 g SNP/kg, cyanide toxicity, as judged by decreased growth, reached significance. 3. In experiment 2, similar effects were observed with selenium at 10 mg Se/kg and SNP at 0.3 g/kg, but selenium deficiency was not evident from growth indicators when selenium supplementation of the diet was omitted completely, nor did these indicators suggest that deficiency was induced by cyanide. 4. In both experiments, plasma and liver glutathione peroxidase activity reflected the dietary selenium content. There was an interaction with dietary SNP content. With selenium intake at a toxic level, SNP increased enzyme activity, further evidence of alleviation of selenium toxicity, but when selenium intake was low and normal, SNP decreased activity in liver, an indication that cyanide could induce deficiency. 5. A possible mechanism for alleviation of selenium toxicity is proposed.

Animals↗
PubMed1985

Effect of selenium supplementation on selenium balance in the dependent elderly.

Although trace minerals are necessary constituents of enzymes, dietary requirements of these nutrients for the elderly are unknown. This study measured selenium balance in six dependent elderly men before and after five weeks daily administration of 200 micrograms organically-bound selenium; dietary selenium intake averaged 62.1 +/- 7 micrograms/day during both study periods. Selenium status was assessed not only chemically but also biologically as red cell and platelet glutathione peroxidase activities. Plasma selenium averaged 8.8 +/- 0.8 micrograms% (normal: 10 +/- 2 micrograms %) when intake derived from dietary sources alone and increased during medicinal supplementation to an average of 12.8 +/- 1.9 micrograms %. The rise in plasma selenium was not associated with an increase in red cell or platelet glutathione peroxidase activity. The effect of selenium supplementation on in vivo platelet aggregability was studied by measuring plasma levels of beta-thromboglobulin and platelet factor 4, two proteins secreted concomitant with aggregation. beta-thromboglobulin diminished 7.5 +/- 11.0 ng/ml and platelet factor 7.6 +/- 11.0 ng/ml during selenium supplementation despite no change in platelet glutathione peroxidase activity. These data support the concept that selenium nutritional status should be assessed not only by blood selenium content but also by selenium-dependent enzyme activity or selenium-dependent biologic effect.

Aged↗
PubMed1995

Selenium status of New Zealand infants fed either a selenium supplemented or a standard formula.

OBJECTIVE: New Zealand soils are deficient in the essential micronutrient, selenium. New Zealand infants have low selenium levels at birth and experience a further decline if fed cows milk based formula. This study examined the selenium status of infants fed with a new commercially available selenium supplemented formula. METHODOLOGY: Forty-four newborn infants, whose mothers wished to formula feed, were randomized in an open controlled trial to be fed a commercially available selenium supplemented cows milk formula (containing 17 micrograms Se/L) or an unsupplemented formula (containing 4.6 micrograms Se/L). Cord, 1 and 3 month blood samples were obtained for selenium status (plasma and red cell selenium and glutathione peroxidase) and thyroid function. RESULTS: Mean plasma selenium and glutathione peroxidase values were significantly higher in supplemented than unsupplemented infants at 1 month (unpaired t-tests; P < 0.0001 and P = 0.001 respectively) and 3 months (P < 0.0001 and P = 0.0005). Analysis within treatment groups between time points (paired t-tests) showed that selenium supplementation prevented the fall in plasma selenium from birth to 1 month seen in unsupplemented infants and was associated with a rise in levels between 1 and 3 months (P = 0.002). CONCLUSIONS: Supplementing cows milk formula with selenium to replicate the levels found in breast milk is nutritionally sound. Feeding from a few days of age with a formula containing 17 micrograms Se/L in infants with low selenium status at birth is sufficient to cause a rise to 80% of adult levels at 3 months of age.

Analysis of Variance↗
PubMed1975

Distribution of selenium in egg white and yolk after feeding natural and synthetic selenium compounds.

Practical diets containing various selenium levels, with and without selenite supplementation, were fed to hens. Eggs were then collected over a 14-day period to determine how quickly changes in dietary selenium affected egg white and yolk selenium. Changes in egg white selenium content were rapid and essentially completed seven days after changing the selenium content of a practical diet. Changes in egg yolk were not yet completed by 14 days. When selenium from practical feedstuffs was fed, the selenium content of dried egg white was about equal to or greater than the selenium content of dried egg yolk. When selenite was fed, the selenium content of dried yolk was higher. Feeding selenomethionine resulted in more selenium in egg white than in egg yolk. Feeding selenocystine resulted in more selenium in egg yolk than egg white, a pattern similar to that from feeding selenite. The data suggest that selenocystine is not incorporated into protein but is metabolized to an inorganic selenium compound.

Animal Feed↗
PubMed1978

[Distribution pattern, statistical analysis and correlation of selenium levels in swine selenium-indicating organs].

There is a potential risk of excessive selenium levels in organs of swine, resulting in toxicity and residues in pork, or selenium deficit. Therefore, random selenium mean values in "selenium-indicating" organs of pigs selected from suspicious populations were compared with mean and limiting values (reference or normal values) recorded from animals with intact metabolism. Prerequisites required for such comparative assessment included the availability of estimated variance values and knowledge of the presence of abscence of agreement between normal distribution and empirical frequency distribution for the population concerned. Knowledge must be available also on the informative value of measured selenium data in blood plasma and their relevance to the general selenium situation in the organism and muscle at large. These were some of the problems studied by determining selenium levels in the liver, kidneys, blood plasma, and M. longissimus dorsi. Organic selenium concentrations were found to be distributed with right axis deviation but almost normal. The parameters established were typical of the majority of data known from literature. Those date, however, are quite variable, so that the need for independently prepared reference values cannot be abandoned. Correlation analysis showed reciprocal relationships between selenium levels in blooc plasma, liver, and muscles but much less correlation between these, on the one hand, and selenium in kidneys, on the other. The correlations between blood plasma and muscle selenium were close enough to take blood plasma values recorded from the living animal as reference from which to draw conclusions as to the muscular selenium state.

Animals↗
PubMed1977

Sulphur-selenium studies in sheep. I. The effects of varying dietary sulphate and selenomethionine on sulphur, nitrogen and selenium metabolism in sheep.

Sulphur, selenium and nitrogen metabolism were studied in Merino wethers fed for 35-day periods on semipurified diets in which the sulphur content was increased to either 0-07 or 0-20% by the addition of sodium sulphate. At both levels of sulphur, additions of selenium as DL-selenomethionine increased the basal level of selenium (0-02 microgram/g) to 0-06, 0-09 and 0-67 microgram/g. Both levels of dietary sulphur supported positive sulphur balances but a reduction in sulphur intake per se resulted in a significant depression in dry matter digestibility (P less than 0-05), apparent nitrogen digestibility (P less than 0-05), nitrogen balance (P less than 0-01), sulphur balance (P less than 0-05) and plasma sulphate-sulphur (P less than 0-05) and wool (P less than 0-01) selenium levels. Selenium balance was not affected by differences in sulphate-sulphur intake. Selenium balances (P less than 0-001), plus the selenium levels in plasma (P less than 0-001), and wool (P less than 0-001) were significantly different at the different levels of selenium supplementation. A positive selenium balance was achieved when the selenium intake was approximately 37 microgram/day, regardless of sulphur treatment. The validity of using plasma and/or wool selenium levels as indices of the selenium status of sheep is questioned.

Animals↗
PubMed1999

The influence of supplements of selenite, selenate and selenium yeast on the selenium status of dairy heifers.

The aim of the study was to define possible differences between selenite, selenate and selenium yeast on various aspects of selenium status in growing cattle. Twenty-four Swedish Red and White dairy heifers were fed no supplementary selenium for 6 months. The basic diet contained 0.026 mg selenium/kg feed dry matter (DM). After the depletion period the animals were divided into 4 groups; group I-III received 2 mg additional selenium daily as sodium selenite, sodium selenate, and a selenium yeast product, respectively. Group IV, the control group, received no additional selenium. The total dietary selenium content for groups I-III during the supplementation period was 0.25 mg/kg DM. After the depletion period the mean concentration of selenium in blood (640 nmol/l) and plasma (299 nmol/l) and the activity of GSH-Px in erythrocytes (610 mukat/l) were marginal, but after 3 months of supplementation they were adequate in all 3 groups. The concentration of selenium in blood and plasma was significantly higher in group III than in groups I and II, but there was no significant difference between groups I and II. The activity of GSH-Px in erythrocytes did not differ between any of the supplemented groups. The animals in the control group had significantly lower concentrations of selenium in blood and plasma and lower activities of GSH-Px in erythrocytes than those in the supplemented groups. The activity of GSH-Px in platelets was also increased by the increased selenium intake. There was no difference in the concentration of triiodothyronine (T3) between any of the groups, but the concentration of thyroxine (T4) was significantly higher in the unsupplemented control group.

Animals↗
PubMed1988

Dose-dependent distribution of injected selenium in rat blood. Effect of previous selenium intake in drinking water.

The effect of an administered dose of 75Se-selenite and a previously increased selenium intake in drinking water (0.1 mg/l) on the distribution of injected selenium in rat blood was studied. In a dose range of 0.01-1.6 mg Se/kg body weight the ratio of injected selenium in blood plasma and in blood cells decreased from 3.20 in rats with increased selenium intake and 4.60 in rats without this intake, to 0.13 and 0.10, respectively. After injection of high selenite doses, 85-88% of the selenium present in the blood was localized in blood cells irrespective of increased selenium intake by drinking water. Possible relationship between accumulation of selenium in blood cells and its toxic effect in the organism is discussed. Previously increased intake of selenium had no effect on the levels of selenium in blood cells but affected significantly its plasma levels. The results indicate that the previously increased selenium intake in drinking water increases the capacity of the plasma for selenium injected in the form of selenite.

Animals↗
PubMedDate not supplied

Selenium administration does not cause thyroid insufficiency in subjects with mild iodine deficiency and sufficient selenium intake.

Selenium is a trace element essential for the activity of type I 5'-deiodinase which converts thyroxine (T4) to 3,5,3'-triiodothyronine (T3). In iodine deficient hypothyroid children at low selenium dietary intake the supplementation of selenium induced a significant decrement of serum FT4 and T4 concentrations and an increase of serum TSH concentrations. Since in western countries selenium tablets begin to be largely consumed as a diet integrator, we have administered 100 micrograms/day of selenium as selenium methionine to 8 euthyroid female subjects with a positive iodine-perchlorate discharge test who had a previous episode of subacute or postpartum thyroiditis. We have studied subjects with positive iodine-perchlorate discharge test since the test indicates the existence of a subtle defect of thyroid hormone synthesis and therefore these subjects are prone to develop thyroid dysfunction. In contrast to previous findings in hypothyroid children at low iodine and selenium dietary intake, the supplementation of selenium did not decompensate thyroid hormone synthesis of euthyroid subjects with reduced thyroid iodine organification. The lack of any effect of selenium on thyroid hormone synthesis even in subjects with subtle thyroid hormone synthesis defect may be due to the fact that these subjects had a sufficient selenium dietary intake before selenium supplementation and an only marginally reduced dietary iodine intake.

Adult↗