The present experiment aimed to compare toxic effects of dietary organic or inorganic selenium (Se) and to predict of Se intake and tissue Se concentrations in broiler chickens based on feather Se concentrations. A total of four hundred twenty 7-day-old Ross 308 male broiler chicks were allotted to 1 of 7 dietary treatments in a completely randomized design. Each treatment had 6 replicates with 10 birds per replicate. Organic Se (selenium yeast) or inorganic Se (sodium selenite) was added to the basal diet at the levels of 5, 10, or 15 mg/kg Se. All experimental diets were fed to birds on an ad libitum basis for 28 d. Results indicated that a significant interaction (P < 0.01) was observed between Se sources and inclusion levels for the BW gain and feed intake of broiler chickens with inorganic Se at 15 mg/kg in diets showing a greatest negative effect. Increasing inclusion levels of Se in diets increased (linear, P < 0.01) plasma concentrations of uric acid. Increasing inclusion levels of Se in diets increased (linear, P < 0.01) relative liver weight. No significant interactions were observed between Se sources and inclusion levels in diets on hepatic antioxidant capacity. Increasing inclusion levels of Se in diets increased (linear, P < 0.01) Se concentrations in the liver, breast, and feather. The concentrations of Se in the breast, liver, and feather were greater (P < 0.05) for organic Se than for inorganic Se in diets. The toxic levels of organic or inorganic Se in broiler diets were near 7 or 9 mg/kg based on the BW gain, respectively. The prediction equations indicate that feather Se concentrations in broiler chickens can be used to predict both daily Se intake and Se concentrations in the liver and breast.

Selenoprotein P (SEPP1) distributes selenium (Se) throughout the body via the circulatory system. For vertebrates, the Se content of SEPP1 varies from 7 to 18 Se atoms depending on the species, but the reason for this variation remains unclear. Herein we provide evidence that vertebrate SEPP1 Sec content correlates positively with Se requirements. As the Se content of full length SEPP1 is genetically determined, this presents a unique case where a nutrient requirement can be predicted based on genomic sequence information.

In intensive care units, sepsis is the first cause of death. In this pathology, inflammation and oxidative status play a crucial role in patient outcomes. Interestingly, 92% of septic patients exhibit low selenium plasma concentrations (a component of antioxidant enzymes). Moreover, Spirulina platensis, a blue-green algae, demonstrated anti-inflammatory effects. In this context, the main purpose of our study was to analyze the effect of a selenium-enriched spirulina after a selenium deficiency on sepsis outcome in rats. Sixty-four rats were fed 12 weeks with a selenium-deficient food. After 8 weeks, rats were supplemented (via drinking water) for 4 weeks with sodium selenite (Se), spirulina (Spi), or selenium-enriched spirulina (SeSp). Sepsis was then induced by cecal ligature and puncture, and survival duration was observed. The plasma selenium concentration was measured by ICPMS. Expression of GPx1 and GPx3 mRNA was measured by RT-PCR. Blood parameters (lactates and HCO3- concentrations, pH, PO2 , and PCO2 ) were analyzed at 0, 1, and 2 h as well as inflammatory cytokines (IL-6, TNF-α, IL-10). Sodium selenite and SeSP supplementations restored plasma selenium concentration prior to sepsis. The survival duration of SeSP septic rats was significantly lower than that of selenium-supplemented ones. Gpx1 mRNA was increased after a selenium-enriched spirulina supplementation while Gpx3 mRNA levels remained unchanged. Furthermore, sodium selenite prevented sepsis-induced acidosis. Our results show that on a basis of a Se deficiency, selenium-enriched spirulina supplementations significantly worsen sepsis outcome when compared to Se supplementation. Furthermore, Se supplementation but not selenium-enriched spirulina supplementation decreased inflammation and restored acid-base equilibrium after a sepsis induction.

Selenium (Se) is an element that in trace quantities is both essential in mammals but also toxic to bacteria, yeast, plants and animals, including C. elegans. Our previous studies showed that selenite was four times as toxic as selenate to C. elegans, but that deletion of thioredoxin reductase did not modulate Se toxicity. To characterize Se regulation of the full transcriptome, we conducted a microarray study in C. elegans cultured in axenic media supplemented with 0, 0.05, 0.1, 0.2, and 0.4 mM Se as selenite. C. elegans cultured in 0.2 and 0.4 mM Se displayed a significant delay in growth as compared to 0, 0.05, or 0.1 mM Se, indicating Se-induced toxicity, so worms were staged to mid-L4 larval stage for these studies. Relative to 0.1 mM Se treatment, culturing C. elegans at these Se concentrations resulted in 1.9, 9.7, 5.5, and 2.3%, respectively, of the transcriptome being altered by at least 2-fold. This toxicity altered the expression of 295 overlapping transcripts, which when filtered against gene sets for sulfur and cadmium toxicity, identified a dataset of 182 toxic-Se specific genes that were significantly enriched in functions related to oxidoreductase activity, and significantly depleted in genes related to structural components of collagen and the cuticle. Worms cultured in low Se (0 mM Se) exhibited no signs of deficiency, but low Se was accompanied by a transcriptional response of 59 genes changed ≥2-fold when compared to all other Se concentrations, perhaps due to decreases in Se-dependent TRXR-1 activity. Overall, these results suggest that Se toxicity in C. elegans causes an increase in ROS and stress responses, marked by increased expression of oxidoreductases and reduced expression of cuticle-associated genes, which together underlie the impaired growth observed in these studies.

Selenium is an essential trace element and micronutrient for human health. Application of organic selenium in plants and microorganisms as trace element supplement is attracting more and more attention. In this study, Bacillus cereus, an important probiotic, was used for selenium enrichment with sodium selenite as selenium source. The growth curve of B. cereus was investigated, and 150 μg/ml was selected as the concentration of selenium for B. cereus fermentation. With application of response surface methodology, the optimal fermentation conditions were obtained as follows: inoculation quantity of 7%, culture temperature of 33°C, and shaking speed of 170 rpm, leading to the maximal selenium conversion ratio of 94.3 ± 0.2%. Field emission scanning electron microscope and energy dispersive spectrometry evidenced that inorganic selenium had been successfully transformed. This study may contribute to get a strain with high Se conversion ratio, so as to extract organic selenium in the form of selenoprotein to be used for further application.

Selenium (Se) is an essential trace element in the human body. Se-enriched agricultural products, obtained by applying Se fertilizer, are important sources of Se supplement. However, Se fertilizer may cause a series of environmental problems. This study investigated the transformation of exogenous selenium nanoparticles (SeNPs) and selenite (SeO3 2-) in soil and explored their effects on soil microbial community and typical microorganisms. SeNPs exhibited a slow-release effect in soil, which promoted the growth of soil microorganisms and enriched soil probiotics. SeO3 2- was converted to a stable and low toxic state in soil, increasing persistent free radicals and decreasing microbial abundance and diversity. The influences of SeNPs and SeO3 2- on two typical soil microorganisms (Bacillus sp. and Escherichia coli) were also evaluated, and SeNPs were more difficult to enter into microorganisms directly, with lower toxicity and higher safety. These results indicated that SeNPs were a more environment-friendly Se additive for agriculture applications. This work provides useful information for better understanding the environmental fate and behavior of Se fertilizer in the soil.

No abstract available

Selenium (Se) is an important micronutrient that, as a component of selenoproteins, influences oxidative and inflammatory processes. Its' levels vary considerably, with different ethnic and geographic population groups showing varied conditions, ranging from frank Se deficiencies to toxic effects. An optimum Se level is essential for the maintenance of homeostasis, and this optimum may vary according to life stage, general state of health, and genotype. Nutrigenetic studies of different Se levels, in the presence of genetic variants in selenoproteins, suggest that an effective dietary Se intake for one individual may be very different from that for others. However, we are just starting to learn the significance of various genes in selenoprotein pathways, functional variants in these, and how to combine such data from genes into pathways, alongside dietary intake or serum levels of Se. Advances in systems biology, genetics, and genomics technologies, including genetic/genomic, epigenetic/epigenomic, transcriptomic, proteomic, and metabolomic information, start to make it feasible to assess a comprehensive spectrum of the biological activity of Se. Such nutrigenomic approaches may prove very sensitive biomarkers of optimal Se status at the individual or population level. The premature cessation of a major human Se intervention trial has led to considerable controversy as to the value of Se supplementation at the population level. New websites provide convenient links to current information on methodologies available for nutrigenetics and nutrigenomics. These new technologies will increasingly become an essential tool in optimizing the level of Se and other micronutrients for optimal health, in individuals and in population groups. However, definitive proof of such effects will require very large collaborative studies, international agreement on study design, and innovative approaches to data analysis.

The effects of selenium (Se) yeast supplementation on performance, blood biochemical and antioxidant parameters, and milk Se content and speciation were evaluated. Thirty-six mid-lactation Holstein dairy cows were randomly assigned to 1 of 3 treatments: 1) control (basal diet containing Se at 0.11 mg/kg DM), 2) basal diet + 0.5 mg supplemental Se/kg DM (SY-0.5), and 3) basal diet + 5 mg supplemental Se/kg DM (SY-5). Selenium was supplemented as Se yeast. The trial consisted of a 1-week pretrial period and an 8-week experimental period. Milk somatic cell score decreased with SY-5 supplementation (P < 0.05), but other performance parameters were not affected (P > 0.05). The serum Se concentration increased with the increasing levels of Se yeast supplementation (P < 0.05), however, blood biochemical parameters showed few treatment effects. The antioxidant capacity of dairy cows was improved with Se yeast supplementation reflected in increased serum glutathione peroxidase activity (P < 0.05) and total antioxidant capacity (P = 0.08), and decreased malondialdehyde concentration (P < 0.05). Milk total Se concentration increased with Se dose (P < 0.05). Also, the selenomethionine concentration increased with Se dose from 13.0 ± 0.7 μg/kg in control to 33.1 ± 2.1 μg/kg in SY-0.5 and 530.4 ± 17.5 μg/kg in SY-5 cows (P < 0.05). Similarly, selenocystine concentration increased from 15.6 ± 0.9 μg/kg in control and 18.9 ± 1.1 μg/kg in SY-0.5 to 22.2 ± 1.5 μg/kg in SY-5 cows (P < 0.05). In conclusion, Se yeast is a good organic Se source to produce Se-enriched cow milk with increased Se species including selenomethionine and selenocystine. The results can provide useful information on milk Se species when a high dose Se yeast was supplemented in the cow diet.

Selenium (Se) is an essential human micronutrient with critical roles in immune functioning and antioxidant defence. Estimates of dietary Se intakes and status are scarce for Africa although crop surveys indicate deficiency is probably widespread in Malawi. Here we show that Se deficiency is likely endemic in Malawi based on the Se status of adults consuming food from contrasting soil types. These data are consistent with food balance sheets and composition tables revealing that >80% of the Malawi population is at risk of dietary Se inadequacy. Risk of dietary Se inadequacy is >60% in seven other countries in Southern Africa, and 22% across Africa as a whole. Given that most Malawi soils cannot supply sufficient Se to crops for adequate human nutrition, the cost and benefits of interventions to alleviate Se deficiency should be determined; for example, Se-enriched nitrogen fertilisers could be adopted as in Finland.

Selenium-enriched rapeseed (SER) is an emerging oil seed. Roasting is beneficial in improving oil yield and promoting the release of micronutrients into SER oil, but high temperatures and dry air lead to selenium loss and fatty acid degradation in SER. To minimize the selenium loss and improve the SER oil quality, this study investigated the effects of vacuum (VC) roasting (90-170 °C for 30 min) on the SER selenium content, Maillard reaction products, oxidative stability, and physicochemical properties of SER oil, with conventional dry air (DA) roasting as the control. The results showed that the selenium loss in VC-roasted SER meals increased from 7.17 to 19.76% (90-170 °C for 30 min), which was 47.13 to 80.48% of that in DA-roasted SER meals, while no selenium was detected in the SER oils. Compared to DA roasting, VC roasting (90-170 °C for 30 min) reduced lipid oxidation products (LOPs), Maillard reaction products (MRPs), and benzo[a]pyrene contents, and increased carotenoids, unsaturated fatty acid contents, reaching a maximum oil yield of 35.58% at a lower temperature (130 °C for 30 min). Selenium contents exhibited a highly significant negative correlation with MRPs and LOPs (p ≤ 0.005). The VC roasting retarded selenium loss and improved SER oil quality compared to conventional DA roasting.

Selenium (Se) has been recognized as an essential micronutrient for nearly all forms of life. In recent decades, broiler responses to dietary Se supplemental levels and sources have received considerable attention. On environmental grounds, organic trace mineral utilization in practical broiler feeds has been defended due to its higher bioavailability. In such feeds, trace minerals are provided simultaneously in the same supplement as inorganic salts or organic chelates, a fact commonly ignored in assays conducted to validate organic trace mineral sources. The current assay aimed to investigate growth and biochemical responses, as well as Se retention of growing chicks fed diets supplemented with organic and inorganic Se levels and where the trace minerals (zinc, copper, manganese, and iron) were provided as organic chelates or inorganic salts according to Se source assessed. In so doing, a 2 × 5 factorial arrangement was used to investigate the effects of sodium selenite (SS) and selenium-yeast (SY) supplemented in feeds to provide the levels of 0, 0.08, 0.16, 0.24, and 0.32 mg Se/kg.

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.

The nutritional value of gluten-free products is the subject of interest for food technologists and nutritionists, as the only effective treatment for celiac disease is a lifelong gluten-free diet. As selenium deficiencies in celiac disease are observed, the aim of the study was to determine the selenium content in 27 grain gluten-free products available on the European Union (EU) market. Moreover, selenium content in products based on popular gluten-free cereals like corn, rice, and buckwheat and in relatively new or less popular products based on oat, amaranth, teff, and quinoa was compared. Selenium content in the tested products ranged from 0.9 to 24.5 μg/100 g. The average content of selenium in products based on popular gluten-free cereals was 2.8 μg/100 g and in products based on oat, amaranth, teff, and quinoa was 10.8 μg/100 g. It indicates that products based on less popular grains, especially on oat, should be more frequently chosen as a source of selenium by people on gluten-free diet than traditionally consumed gluten-free grains.

The essential trace element selenium is used in a wide variety of biological processes. Selenocysteine (Sec), the 21st amino acid, is co-translationally incorporated into a restricted set of proteins. It is encoded by an UGA codon with the help of tRNASec (SelC), Sec-specific elongation factor (SelB) and a cis-acting mRNA structure (SECIS element). In addition, Sec synthase (SelA) and selenophosphate synthetase (SelD) are involved in the biosynthesis of Sec on the tRNASec. Selenium is also found in the form of 2-selenouridine, a modified base present in the wobble position of certain tRNAs, whose synthesis is catalyzed by YbbB using selenophosphate as a precursor.

Glutathione peroxidase (GPX) plays a pivotal role in the protection of cells against oxidative damage. The green alga Chlamydomonas reinhardtii expresses both selenocysteine-containing GPX and the non-selenium GPX homolog (GPXH). We previously reported that supplementation of selenium to algal culture induces GPXH to exhibit GPX activity. Here we investigated the incorporation of selenium into GPXH and its causal relationship with the upregulation of the enzymatic activity. GPXH was purified from algal cells grown with selenium and proteolytically digested into four fragments. Selenium content analysis for these proteolytic fragments confirmed that GPXH-incorporated selenium is predominantly enriched in a fragment that carries the putative catalytic residue Cys-38. We next constructed three kinds of engineered GPXH proteins by substituting Ser for one of three Cys residues in native GPXH, Cys-38, -66, and -84, using a bacterial overexpression system, resulting in Cys38Ser, Cys66Ser, and Cys84Ser derivatives, respectively. Of these, the Cys66Ser and Cys84Ser derivatives exhibited the same level of selenium-dependent GPX activity as the normal recombinant GPXH, whereas the Cys38Ser mutant GPXH not only lost its activity completely but also demonstrated severely impaired incorporation of selenium. These findings strongly suggest that selenium is post-translationally assimilated into the Cys-38 of the GPXH protein, thereby enhancing its enzymatic activity.

Low selenium status in pregnancy has been associated with a number of adverse conditions. In nonpregnant populations, the selenium status or response to supplementation has been associated with polymorphisms in dimethylglycine dehydrogenase (DMGDH), selenoprotein P (SEPP1) and the glutathione peroxidases [cytosolic glutathione peroxidase (GPx1) and phospholipid glutathione peroxidase (GPx4)].

Protein and mRNA levels for several selenoproteins, such as glutathione peroxidase-1 (Gpx1), are down-regulated dramatically by selenium (Se) deficiency. These levels in rats increase sigmoidally with increasing dietary Se and reach defined plateaus at the Se requirement, making them sensitive biomarkers for Se deficiency. These levels, however, do not further increase with super-nutritional or toxic Se status, making them ineffective for detection of high Se status. Biomarkers for high Se status are needed as super-nutritional Se intakes are associated with beneficial as well as adverse health outcomes. To characterize Se regulation of the transcriptome, we conducted 3 microarray experiments in weanling mice and rats fed Se-deficient diets supplemented with up to 5 μg Se/g diet.

Selenium (Se) is a trace element that occurs in proteins in the form of selenocysteine (Sec) and in tRNAs in the form of selenouridine (SeU). Selenophosphate synthetase (SelD) is required for both utilization traits. However, previous research also revealed SelDs in two organisms lacking Sec and SeU, suggesting a possible additional use of Se that is dependent on SelD.

Dietary selenium intake has been linked to reduced cancer risk, however the underlying mechanisms are yet unknown. We question the commonly used practice of applying selenium concentrations found in human blood to in vitro studies and evaluated the utility of biomarkers, e.g., glutathione peroxidase 1 (GPx1) and thioredoxin reductase 1 (TrxR1), to determine appropriate selenium levels for in vitro work. Furthermore, we investigated the effects of Se-methylselenocysteine (SeMSC) on prostate cancer cell migration and invasion. After excluding cytotoxicity, we demonstrated that prostate cancer cell lines respond differently to selenium treatment as observed through biomarker assessment. We found that the maximum levels of GPx1 activity and TrxR1 expression were reached at lower selenium concentrations in LNCaP compared to PC3 cells, and PC3 compared to DU145 cells. Therefore the use of selenium concentrations extrapolated from human studies for in vitro work may be applicable when further informed using a readout of selenium repletion including use of selenium responsive biomarkers. No effect on PC3 migration or invasion was observed after long term SeMSC treatment; however a slight increase was found when treatment was solely administered during the assay. The opposite could be observed when cells were cultured under low serum conditions, with a significant increase in migration upon long term but not upon acute SeMSC treatment. To conclude, these findings indicate that it is imperative to study the selenium sensitivity of an in vitro model preferably using biomarkers before investigating any effects on biological processes, or before comparing models.