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Selenium supplementation of Chinese women with habitually low selenium intake increases plasma selenium, plasma glutathione peroxidase activity, and milk selenium, but not milk glutathione peroxidase activity.

Twenty-one pregnant women living in Xichang County, China, a selenium-deficient area, were divided into two groups and given either a placebo (n = 10) as yeast or selenium-enriched yeast tablets (n = 11) to provide 100 microg selenium per day. This supplementation was begun the last trimester of pregnancy and continued for 3 months after parturition. Plasma selenium levels and glutathione peroxidase (GPX) activity steadily declined in supplemented women, but a curvilinear response occurred in milk selenium and GPX activity in both supplemented and deficient women and in plasma selenium and GPX activity in deficient women. The milk selenium levels were higher in supplemented women but there were no differences in the milk GPX activity between the two groups of women. The plasma alpha-tocopherol concentrations declined after parturition in both groups but no differences were found between the two groups of women. Plasma thiobarbituric acid reactive substances declined in supplemented women but showed a curvilinear response in unsupplemented women, suggesting peroxidative stress in these women. GPX, selenium, and peroxidative responses in plasma and milk following parturition is advocated as a new method to assess selenium status of lactating women.

Journal Article↗

Selenium from selenium-rich Spirulina is less bioavailable than selenium from sodium selenite and selenomethionine in selenium-deficient rats.

The bioavailabilty of selenium (Se) from selenium-rich Spirulina (SeSp) was assessed in Se-deficient rats by measuring tissue Se accumulation and glutathione peroxidase (GSH-Px) activity. For 42 d, rats were subjected to dietary Se depletion by consumption of a Torula yeast (TY)-based diet with no Se; controls were fed the same diet supplemented with 75 microg Se/kg diet as sodium selenite. Se-deficient rats were then repleted with Se (75 microg/kg) by the addition of sodium selenite, selenomethionine (SeMet) or SeSp to the TY basal diet. Selenium speciation in SeSp emphasized the quasi-absence of selenite (2% of total Se); organic Se comprised SeMet (approximately 18%), with the majority present in the form of two selenoproteins (20-30 kDa and 80 kDa). Gross absorption of Se from SeSp was significantly lower than from free SeMet and sodium selenite. SeMet was less effective than sodium selenite in restoring Se concentration in the liver but not in kidney. SeSp was always much less effective. Similarly, Se from SeSp was less effective than the other forms of Se in restoring GSH-Px activity, except in plasma and red blood cells where no differences were noted among the three sources. This was confirmed by measuring the bioavailability of Se by slope-ratio analysis using selenite as the reference form of Se. Although Se from SeSp did not replenish Se concentration and GSH-Px activity in most tissues to the same degree as the other forms of Se, we conclude that it is biologically useful and differently metabolized due to its chemical form.

Animals↗

Influence of dietary selenium on performance, tissue selenium content, and plasma concentrations of selenium-dependent glutathione peroxidase, vitamin E, and ascorbic acid in ducklings.

Low-selenium corn-soya diets (.04 ppm Se) supplemented with 0, .1, or .2 ppm was selenium (as Na2SeO3), in the presence or absence of 10 IU of supplemental vitamin E per kilogram, were fed to progeny of selenium-depleted breeder ducks. Ducklings from nondepleted breeders received selenium-adequate diets supplemented with 0, .1, or 1.0 ppm selenium from Na2SeO3. High mortalityyy, extensive muscle necrosis, and depressed early weight gain occurred in ducklings fed the low-selenium diets without added selenium. These effects were not prevented by supplemental vitamin E. None of the above manifestations of selenium deficiency were observed in ducklings fed the low-selenium diets supplemented with .1 or .2 ppm selenium. The addition of up to 1.0 ppm selenium to the adequate-selenium diet had no significant effect on mortality or weight gain. The selenium content of kidney, liver, and muscle increased with the addition of .1 ppm selenium to the low-selenium diet. Relatively small increases in tissue selenium concentrations resulted from the addition, to either diet, or levels of selenium in excess of the nutritional requirement. Glutathione peroxidase in plasma varied directly with selenium additions to the low-selenium diets. Plasma vitamin E increased as dietary vitamin E and selenium were increased. Dietary treatment had no significant effect on the concentration of ascorbic acid in plasma.

Animals↗

Kinetic changes of oxidative stress and selenium status in plasma and tissues following burn injury in selenium-deficient and selenium-supplemented rats.

BACKGROUND: This study investigates the relationship between the burn-induced oxidative stress and the selenium status. METHODS: The rats were fed with a selenium-adequate diet or a selenium-depleted diet for 5 weeks, before a third-degree thermal injury was applied to the animals. One group of selenium-depleted animals received injections of sodium selenite after the injury. The selenium status and the oxidative stress parameters were measured for 5 days. RESULTS: The selenium-deficient diet leads to oxidative stress with a high stimulation of the superoxide dismutase activity. After the burn injury, the oxidative stress appears important because the initial selenium status is already impaired and, in all animals, the selenium levels and the antioxidant seleno-dependent glutathione peroxidase (GPx) activity decrease in the plasma and the tissues. A treatment with daily selenium injections is efficient in normalizing selenium levels and restores the GPx activity, but fails to counteract the initial oxidative damages induced by the selenium-deficient diet. CONCLUSIONS: The selenium status before the burn injury is a modulating factor of the burn-induced oxidative stress. A single selenium supplement is not sufficient to counteract these oxidative damages and henceforth combined antioxidant supplementations should be investigated to improve the early treatment of the burn patients.

Animals↗

Selenoprotein P concentration in plasma is an index of selenium status in selenium-deficient and selenium-supplemented Chinese subjects.

Selenoprotein P, a selenium-rich plasma protein, is an index of selenium status in rats. Antibodies against human selenoprotein P were raised to study the protein and to develop a radioimmunoassay for it. A single collection of plasma from a healthy person in the United States contained 1.84 mumol selenium/L and was defined as containing 1 Unit (U) selenoprotein P/L. Removal of selenoprotein P from the reference plasma by an antibody column indicated that 0.81 mumol selenium/L, or 44% of the plasma selenium, was present as selenoprotein P. Work by others had determined that glutathione peroxidase accounted for 12% of plasma selenium. Stored plasma samples from selenium-deficient (Dechang County) and selenium-supplemented (Mianning County) populations in China were assayed for selenoprotein P. Boys aged 8-12 y had selenoprotein P concentrations of 0.10 +/- 0.04 U/L (n = 22) in Dechang and 0.39 +/- 0.17 U/L (n = 17) in Mianning. Supplementation with 100 micrograms selenium as selenate per day for 14 d raised those levels to 0.51 +/- 0.13 U/L in Dechang and to 0.76 +/- 0.27 U/L in Mianning. Similar results were obtained in men, and plasma selenium concentrations correlated with selenoprotein P concentrations. A study comparing indices of selenium status was conducted in the two counties. Selenoprotein P concentration in Dechang subjects (n = 79) was 36% of that in Mianning subjects (n = 117). For plasma glutathione peroxidase activity the value was 54%; for plasma selenium, 47%; and for whole blood selenium, 64%. We conclude that selenoprotein P is the major selenoprotein in human plasma and that its concentration is an index of selenium nutritional status that appears to be as sensitive as other indices in common use.

Adolescent↗

An essential role of s-adenosyl-L-methionine:L-methionine s-methyltransferase in selenium volatilization by plants. Methylation of selenomethionine to selenium-methyl-L-selenium- methionine, the precursor of volatile selenium.

Selenium (Se) phytovolatilization, the process by which plants metabolize various inorganic or organic species of Se (e.g. selenate, selenite, and Se-methionine [Met]) into gaseous Se forms (e.g. dimethylselenide), is a potentially important means of removing Se from contaminated environments. Before attempting to genetically enhance the efficiency of Se phytovolatilization, it is essential to elucidate the enzymatic pathway involved and to identify its rate-limiting steps. The present research tested the hypothesis that S-adenosyl-L-Met:L-Met S-methyltransferase (MMT) is the enzyme responsible for the methylation of Se-Met to Se-methyl Se-Met (SeMM). To this end, we identified and characterized an Arabidopsis T-DNA mutant knockout for MMT. The lack of MMT in the Arabidopsis T-DNA mutant plant resulted in an almost complete loss in its capacity for Se volatilization. Using chemical complementation with SeMM, the presumed enzymatic product of MMT, we restored the capacity of the MMT mutant to produce volatile Se. Overexpressing MMT from Arabidopsis in Escherichia coli, which is not known to have MMT activity, produced up to 10 times more volatile Se than the untransformed strain when both were supplied with Se-Met. Thus, our results provide in vivo evidence that MMT is the key enzyme catalyzing the methylation of Se-Met to SeMM.

Adaptation, Physiological↗

Toenail selenium as an indicator of selenium intake among middle-aged men in an area with low soil selenium.

Toenail selenium concentration has been proposed as a long-term (6-12 mo) indicator of human selenium status. This study investigated the association between toenail selenium concentration and selenium intake and other dietary factors among 166 urban men aged 55-69 y. The dietary information was collected by food records covering a 6-mo period. Toenail clippings were collected by mail 9-10 mo after food recording. The mean selenium intake from food was 42.5 micrograms/d and the dietary intake was equal to that of users and nonusers of selenium supplements. The mean toenail selenium concentration was 0.47 mg/kg. The mean selenium intake from supplements was 29.7 micrograms/d among supplement users. In the analysis of covariance the best predictors of toenail selenium concentration were selenium intake from supplements and food, and among supplement users dietary beta-carotene also.

Aged↗

The influence of dietary selenium as selenium yeast or sodium selenite on the concentration of selenium in the milk of Suckler cows and on the selenium status of their calves.

The aim of this trial was to determine whether the selenium status of suckling calves could be improved by supplementing their dams' diet with organic Se instead of sodium selenite. A herd of 103 Hereford cows, which were on grass paddocks all year round, was divided into two groups. Both groups had free access to a mineral supplement that contained 30 mg of Se/kg; for one group the source of the Se was a Se yeast product, and for the other group the source was sodium selenite. The basal feed contained .02 mg of Se/kg DM. During the trial, the mean daily consumption of the mineral supplement was approximately 110 g/cow. The calving season started in the middle of March and ended in the middle of May. Blood samples were taken from 11 cows and their calves in the yeast group and from nine in the selenite group at the end of April and again at the beginning of June, and milk samples were taken at the same times. At both samplings, the concentration of Se in whole blood and the activity of glutathione peroxidase (GSH-Px) in the erythrocytes of the cows and calves in the yeast group were higher than in the samples from the animals in the selenite group. The same pattern was seen for plasma, except for the cows at the first sampling. The mean concentrations of Se in whole blood from calves in the yeast and selenite groups were 130 and 84 microg/L, respectively, and plasma concentrations were 48 and 34 microg/ L, respectively. Mean Se concentration in the milk from the yeast group (17.3 microg/L) was higher than that in milk from the selenite group (12.7 microg/L). There were significant correlations (r = .59 to .68) between the concentrations of Se in the cow's milk or cow's whole blood compared with Se concentrations in the calves whole blood and plasma or with the erythrocyte GSH-Px activity of the calves. The Se status of the calves in the selenite group was considered to be marginal, but the status of the calves in the yeast group was considered to be adequate. Supplementation of the suckler cows' diet with organic Se in the form of Se yeast rather than sodium selenite improved the Se status of their calves when the Se was mixed into a mineral supplement containing 30 mg of Se/kg. In practice, such supplementation would probably eliminate the risk of nutritional muscular degeneration in suckling calves.

Animal Feed↗

Identification of selenium species in selenium-enriched Lens esculenta plants by using two-dimensional liquid chromatography-inductively coupled plasma mass spectrometry and [77Se]selenomethionine selenium oxide spikes.

Selenium speciation in Se-enriched Lens esculenta grown in hydroponic culture containing inorganic selenium as Na(2)SeO(3) and Na(2)SeO(4) was performed. After 16 days of growth, the plants were collected and divided in two parts, roots and stems and then analysed to identify and quantify selenium species. Speciation studies of the enzymatic extracts were carried out by using anion-exchange (PRP-X100) and size-exclusion/ion-exchange (Shodex Asahipak) columns coupled to inductively coupled plasma mass spectrometry (ICP-MS). The need of using two independent chromatographic mechanisms for unambiguous species identification is demonstrated. Moreover, the use of a [(77)Se]selenomethionine selenium oxide spike turned out to be critical to discriminate between selenium selenomethioine selenium oxide and selenocysteine.

Chromatography, Liquid↗

Effects of cadmium treatment on selenium-dependent and selenium-independent glutathione peroxidase activities and lipid peroxidation in the kidney and liver of rats maintained on various levels of dietary selenium.

Rats fed a basal, low-selenium diet, or this diet supplemented with 0.1 ppm and 1.0 ppm selenium and treated with cadmium, showed significant reductions in the activity of the selenoenzyme glutathione peroxidase in kidney and liver. Cadmium treatment resulted in a significant increase in the activity of selenium-independent glutathione peroxidase activity in the liver of selenium-supplemented rats. Selenium-independent glutathione peroxidase activity was significantly reduced in the kidney of rats fed the basal low-selenium diet. There was no significant increase in lipid peroxidation in any of the groups studied. Cadmium concentrations in the kidney and liver of these animals ranged from about 250 to 700 micrograms Cd/g tissue, dry weight.

Animals↗

Effect of selenium on rat thioredoxin reductase activity: increase by supranutritional selenium and decrease by selenium deficiency.

Thioredoxin reductase is a newly identified selenocysteine-containing enzyme that catalyzes the NADPH-dependent reduction of the redox protein thioredoxin. Thioredoxin stimulates cell growth, is found in dividing normal cells, and is over-expressed in a number of human cancers. Redox activity is essential for the growth effects of thioredoxin; thus, thioredoxin reductase could be involved in regulating cell growth through its reduction of thioredoxin. In rats fed a selenium-deficient diet (<0.01 ppm) for up to 98 days, thioredoxin reductase activity was decreased, compared with that of rats fed a normal selenium diet (0.1 ppm), in lung, liver, and kidney, while thioredoxin reductase activity in the spleen and prostate was unaltered. Rats fed a high selenium diet (1.0 ppm) exhibited a 1.5-fold increase in kidney and a 2.0-fold increase in lung thioredoxin reductase activity that began to return to control values after 20 and 69 days, respectively. Liver showed a 2.1-fold increase in thioredoxin reductase activity at 20 days only. Thioredoxin reductase protein levels measured by western blotting using an antibody to human thioredoxin reductase were decreased in rats fed the selenium-deficient diet and did not increase in rats fed the high selenium diet. Rat thioredoxin reductase was shown to incorporate 75Selenium. Thus, in some tissues at least, the increase in thioredoxin reductase activity of rats fed a high selenium diet appears to be due to an increase in the specific activity of the enzyme, possibly caused by increased selenocysteine incorporation without an increase in thioredoxin reductase protein synthesis.

Animals↗

Availability of selenium in fish meal in comparison with soybean meal, corn gluten meal and selenomethionine relative to selenium in sodiumselenite for restoring glutathione peroxidase activity in selenium-depleted chicks.

We assayed the availability of selenium in feeds and selenomethionine relative to selenium in sodium selenite for restoring blood serum glutathione peroxidase activity in selenium-depleted chicks. The contents of total selenium (determined by neutron activation analyses) were for eight samples of capelin fish meal, 1.34, two samples of mackerel fish meal, 6.17, one sample of solvent-extracted soybean meal, 0.42, and one sample of corn gluten meal, 0.54 ppm in dry matter. The availability of the selenium (relative to selenium in selenite=100%) in capelin fish meal was 48.0 (38.5--60.0), mackerel fish meal, 34.1 (32.3--35.8), soybean meal, 17.5, corn gluten meal, 25.7, and in selenomethionine, 78.3%.

Animal Feed↗

Effect of selenium supplementation in hypothyroid subjects of an iodine and selenium deficient area: the possible danger of indiscriminate supplementation of iodine-deficient subjects with selenium.

Selenium and seleno dependent glutathione peroxidase (GPX) deficiency has been described in endemias of myxedematous cretinism. In northern Zaire, a selenium supplementation trial has been conducted. Beside correcting the GPX activity, two months of selenium supplementation was shown to modify the serum thyroid hormones parameters in clinically euthyroid subjects and to induce a dramatic fall of the already impaired thyroid function in clinically hypothyroid subjects. These results further support a role of selenium in thyroid hormone metabolism. In an iodine deficient area, this selenium deficiency could lead to opposite clinical consequences: protect the general population and the fetus against iodine deficiency and brain damage; and in turn, favour the degenerative process of the thyroid gland leading to myxoedematous cretinism.

Child↗

Selenium and human lactation in Australia: milk and blood selenium levels in lactating women, and selenium intakes of their breast-fed infants.

A series of 20 mother-infant pairs were studied in Brisbane, Australia, at 6-12 weeks postpartum. The mean selenium concentration in maternal blood was 101 (SD +/- 19) ng/g and in maternal serum 81(+/- 15) ng/g; serum values appeared low in comparison with those reported for lactating women from Japan and the USA, but similar to those from Finland and from a previous Australian study. Breast milk selenium concentrations (11.9 +/- 3.5 ng/g) were also low by international standards, but not as low as in New Zealand or Scandinavia. There was no correlation between selenium concentrations in milk and blood (or serum). The infants' 24-h breast-milk intakes were 856 +/- 172 g, and their 24-h selenium intakes 10.7 +/- 4.1 micrograms (compared to the Australian RDI of 10 micrograms).

Adolescent↗

The selenium state of healthy children. I. Serum selenium concentration at different ages; activity of glutathione peroxidase of erythrocytes at different ages; selenium content of food of infants.

The selenium concentration of serum is age-dependent. The median value at birth (chi=50 X 10(-9)g/ml) amounts to half of the median value of adults (chi=102 X 10(-9)g/ml). After a decrease in early infancy to chi=34 X 10(-9)g/ml it steadily increases to chi=58 X 10(-9)g/ml in the second half of the first year, to chi=82 X 10(-9)g/ml in 1--5 year old children, and to chi=92 X 10(-9)g/ml in school children. The activities of the selenium containing enzyme glutathione peroxidase of erythrocytes are also reduced in early infancy (chi=7.2 +/- 0.36 U37/g Hb), whereas the enzyme activities of cord blood erythrocytes (chi=8.72 +/- 0.76 U37/g Hb) are in the same range as those of older children or adults. The selenium content of some commercially available milk formulas for infants are lower than those of human and cow's milk.

Adolescent↗

Effect of dietary organic versus inorganic selenium in laying hens on the productivity, selenium distribution in egg and selenium content in blood, liver and kidney.

We investigated the effect of organic versus inorganic dietary selenium in laying hens on the productivity, selenium distribution in egg and selenium content in blood, liver and kidney. Sixty Leghorn laying hens were fed a basic diet containing 0.23mg Se/kg DM (dry matter) for 2 weeks and then were allocated randomly into three groups. Thereafter, the hens were given the same basic diet without supplementation, or with 0.51 mg Se/kg DM as sodium selenite (SS) or Se-malt (SM). During the experiment, egg rate and dietary intake were recorded, blood was sampled on days 10 and 20, and six eggs were sampled on days 8, 16 and 24 from each treatment group for Se content determination. At the end of the experiment, 10 hens from each treatment were slaughtered, and liver and kidney were sampled for the determination of Se content. The result showed that with the increase of dietary Se level, the Se content in egg, blood, liver and kidney was elevated (P < 0.05), but the hens' productivity was not affected. SS increased liver Se content more than SM (P < 0.05), while the Se content both in blood and kidney did not differ significantly between the SS and SM treatments. Se from SM and SS mainly deposited in the egg yolk. This suggests that the metabolic route of Se from SM is similar to that of Se from SS in laying hens.

Animal Feed↗

Selenium-dependent and selenium-independent formate dehydrogenases of Methanococcus vannielii. Separation of the two forms and characterization of the purified selenium-independent form.

Anaerobic oxidation of formate by Methanococcus vannielii is catalyzed by two readily separable formate dehydrogenases. One of these is a 105,000-dalton protein that contains molybdenum, iron, and acid-labile sulfide, but not selenium. The other is a high molecular weight complex composed of selenoporotein and molybdo-iron sulfur protein subunits. Selenium occurs in this selenoenzyme in the chemical form of selenocysteine residues. M. vannielii cells from selenium-deficient media contain the 105,000-dalton formate dehydrogenase. Marked stimulation of growth by selenite supplementation is correlated with the simultaneous appearance in the cells of the high molecular weight selenoprotein . enzyme complex. The latter is the predominant form in cells from media additionally supplemented with tungstate. Under these conditions partial replacement of molybdenum with tungsten appears to occur. Both formate dehydrogenases are maximally active at pH 8.5 to 9.2 and at 60 degrees C and are extremely oxygen-sensitive. They utilize as electron acceptors 8-hydroxy-5-deazaflavin, FMN, FAD, and viologen and tetrazolium dyes.

Aldehyde Oxidoreductases↗

Selenium supplementation of children in a selenium-deficient area in China: blood selenium levels and glutathione peroxidase activities.

Keshan disease is a cardiomyopathy restricted to the endemic areas of China and seen in residents having an extremely low selenium (Se) status. Prophylactic administration of sodium selenite has been shown to decrease significantly the incidence of acute and subacute cases. The aim offthe study was to assess the relative bioavailability of selenite versus organic Se-yeast in a Se-deficient area in China with a randomized double-blind double-dummy design. Healthy children (n=30) between 14 and 16 yr of age were randomized into three equal groups receiving either 200 microg/d selenite Se or 200 microg/d Se-yeast or placebo for 12 wk. Blood was drawn at baseline, 4, 8, and 12 wk and 4 wk postsupplementation. The plasma Se concentration (mean +/- SD) was 0.16+/-0.03 micromol/L at baseline. Selenite and Se-yeast supplementation increased plasma Se to plateau values, 1.0+/-0.2 and 1.3+/-0.2 micromol/L, respectively. In red cells, Se-yeast increased the selenium level sixfold and selenite threefold compared to placebo. The relative bioavailability of Se-yeast versus selenite measured as glutathione peroxidase (GSHPx) activity was similar in plasma, red blood cells, and platelets. GSHPx activity reached maximal levels in plasma and platelets of 300% and 200%, respectively, after 8 wk compared to the placebo group, but continued to increase in red cells for 16 wk. Our study showed that although both forms of Se were equally effective in raising GSHPx activity, Se-yeast provided a longer lasting body pool of Se. Se-yeast may be a better alternative to selenite in the prophylaxis of Keshan disease with respect to building up of body stores.

Adolescent↗