scholarly journals Selenium status highly regulates selenoprotein mRNA levels for only a subset of the selenoproteins in the selenoproteome

2009 ◽  
Vol 29 (5) ◽  
pp. 329-338 ◽  
Author(s):  
Roger A. Sunde ◽  
Anna M. Raines ◽  
Kimberly M. Barnes ◽  
Jacqueline K. Evenson
Keyword(s):  
Thioredoxin Reductase ◽  
Selenium Deficiency ◽  
Underlying Mechanism ◽  
Pcr Analysis ◽  
Mrna Levels ◽  
Nonsense Mediated Decay ◽  
Liver And Kidney ◽  
Se Deficiency ◽  
Selenoprotein Mrnas ◽  
Se Status

Gpx (glutathione peroxidase)-1 enzyme activity and mRNA levels decrease dramatically in Se (selenium) deficiency, whereas other selenoproteins are less affected by Se deficiency. This hierarchy of Se regulation is not understood, but the position of the UGA selenocysteine codon is thought to play a major role in making selenoprotein mRNAs susceptible to nonsense-mediated decay. Thus in the present paper we studied the complete selenoproteome in the mouse to uncover additional selenoprotein mRNAs that are highly regulated by Se status. Mice were fed on Se-deficient, Se-marginal and Se-adequate diets (0, 0.05 and 0.2 μg of Se/g respectively) for 35 days, and selenoprotein mRNA levels in liver and kidney were determined using microarray analysis and quantitative real-time PCR analysis. Se-deficient mice had liver Se concentrations and liver Gpx1 and thioredoxin reductase activities that were 4, 3 and 3% respectively of the levels in Se-adequate mice, indicating that the mice were Se deficient. mRNAs for Selh (selenoprotein H) and Sepw1 (selenoprotein W) as well as Gpx1 were decreased by Se deficiency to <40% of Se-adequate levels. Five and two additional mRNAs were moderately down-regulated in Sedeficient liver and kidney respectively. Importantly, nine selenoprotein mRNAs in liver and fifteen selenoprotein mRNAs in the kidney were not significantly regulated by Se deficiency, clearly demonstrating that Se regulation of selenoprotein mRNAs is not a general phenomenon. The similarity of the response to Se deficiency suggests that there is one underlying mechanism responsible. Importantly, the position of the UGA codon did not predict susceptibility to Se regulation, clearly indicating that additional features are involved in causing selenoprotein mRNAs to be sensitive to Se status.

scholarly journals Selenium-Related Transcriptional Regulation of Gene Expression

2018 ◽  
Author(s):  
Mikko J. Lammi ◽  
Chengjuan Qu
Keyword(s):  
Stop Codon ◽  
Regulation Of Gene Expression ◽  
Selenium Deficiency ◽  
Mrna Levels ◽  
Translation Elongation ◽  
Nonsense Mediated Decay ◽  
Specific Complex ◽  
System Functioning ◽  
The One ◽  
Selenoprotein Mrnas

Selenium is a trace metal essential to human health, and its deficiency has been related to, for instance, cardiovascular and myodegenerative diseases, infertility and osteochondropathy Kashin-Beck disease. It is incorporated as selenocysteine to selenoproteins, which protect against reactive oxygen and nitrogen species. They also participate in the activation of thyroid hormone, and play a role in immune system functioning. The synthesis and incorporation of selenocysteine occurs via a special mechanism, which differs from the one used for standard amino acids. The codon for selenocysteine is the regular in-frame stop codon, which can be passed by specific complex machinery participating in translation elongation and termination. This includes the presence of selenocysteine insertion sequence (SECIS) in the 3&rsquo;-untranslated part of the selenoprotein mRNAs. Selenium deficiency is known to control both selenoprotein and non-selenoprotein transcriptomes. Nonsense-mediated decay is involved in the regulation of selenoprotein mRNA levels, both other mechanisms are also possible.

scholarly journals Effects of Dietary Selenium Deficiency or Excess on Selenoprotein Gene Expression in the Spleen Tissue of Pigs

Animals ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 1122 ◽  
Author(s):  
Zhuang Lu ◽  
Pengzu Wang ◽  
Teng Teng ◽  
Baoming Shi ◽  
Anshan Shan ◽  
...  
Keyword(s):  
Glutathione Peroxidase ◽  
Thioredoxin Reductase ◽  
Selenium Deficiency ◽  
Type I ◽  
Mrna Levels ◽  
Spleen Tissue ◽  
Selenoprotein K ◽  
Selenoprotein Genes ◽  
Se Deficiency ◽  
Selenoprotein M

To evaluate the effects of dietary Se deficiency and excess on the mRNA levels of selenoproteins in pig spleen tissues, 20 healthy uncastrated boars (Duroc × Landrace × Yorkshire, 10 ± 0.72 kg) were randomly divided into four groups (5 pigs per group). The pigs were fed a Se deficient corn-soybean basal feed (Se content <0.03 mg/kg) or basal feed with added sodium selenite at 0.3, 1.0, or 3.0 mg Se/kg diet, respectively. The experiment lasted 16 weeks. The spleen tissue was collected to examine the mRNA expression levels of 24 selenoprotein genes at the end of the study. Compared with pigs in other groups, those fed with the 1.0 mg Se/kg diet had higher mRNA levels of glutathione peroxidase 1 (Gpx1), glutathione peroxidase 2 (Gpx2), deiodinase type II (Dio2), thioredoxin reductase 3 (Txnrd3), selenoprotein H (Selh), selenoprotein N, 1 (Sepn1), selenoprotein P1 (Sepp1), and selenoprotein V (Selv) in the spleen (p < 0.05). Dietary Se deficiency resulted in lower mRNA levels of Gpx1, Gpx2, glutathione peroxidase 3 (Gpx3), Dio2, thioredoxin reductase 2 (Txnrd2), Txnrd3, Selh, selenoprotein I (Seli), selenoprotein K (Selk), selenoprotein M (Selm), Sepn1, Sepp1, and Selv in the spleen than the other three groups. Dietary Se levels did not affect the mRNA levels of glutathione peroxidase 4 (Gpx4), deiodinase type I (Dio1), deiodinase type III (Dio3), selenophosphate synthetase 2 (Sephs2), thioredoxin reductase 1 (Txnrd1), selenoprotein O (Selo), selenoprotein S (Sels), selenoprotein W (Selw), selenoprotein X (Selx), and selenoprotein 15 (Sel15) in the spleen (p > 0.05). Dietary Se levels can affect the transcription levels of 14 selenoprotein genes in the spleen of pigs.

Selenium regulation of transcript abundance and translational efficiency of glutathione peroxidase-1 and −4 in rat liver

2001 ◽  
Vol 357 (3) ◽  
pp. 851-858 ◽  
Author(s):  
Sherri WEISS SACHDEV ◽  
Roger A. SUNDE
Keyword(s):  
Glutathione Peroxidase ◽  
Rat Liver ◽  
Transcript Abundance ◽  
Translational Efficiency ◽  
Mrna Levels ◽  
Glutathione Peroxidase 1 ◽  
Relative Contribution ◽  
Se Deficiency ◽  
Selenoprotein Mrnas ◽  
Se Status

Glutathione peroxidase (GPX)1 mRNA in rat liver falls dramatically during Se deficiency to levels that are approx. 10% of Se-adequate levels. This regulation is mediated by mRNA stability, and is hypothesized to involve nonsense-mediated mRNA decay. mRNA levels for GPX4 and other selenoproteins are much less regulated by Se status. To evaluate the relative contribution of mRNA abundance versus translational efficiency to overall regulation of GPX1 expression, we quantified GPX1, GPX4 and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) transcripts per cell in rat liver. Surprisingly, we found that GPX1 transcripts in Se deficiency are moderately abundant and similar in abundance to GAPDH and other selenoprotein mRNAs; Se supplementation increases GPX1 mRNA so that it is 30-fold higher than GAPDH mRNA. Translational efficiency of GPX1 mRNA is half of that of GPX4. Translational efficiency of GPX1 mRNA increases approx. 20-fold with Se supplementation and appears to switch GPX1 mRNA from nonsense-mediated degradation to translation. This regulatory switch can explain why GPX1 expression is an excellent parameter for assessment of Se status.

scholarly journals Selenium Requirements Are Higher for Glutathione Peroxidase-1 mRNA than Gpx1 Activity in Rat Testis

2009 ◽  
Vol 234 (5) ◽  
pp. 513-521 ◽  
Author(s):  
Sonja C. Schriever ◽  
Kimberly M. Barnes ◽  
Jacqueline K. Evenson ◽  
Anna M. Raines ◽  
Roger A. Sunde
Keyword(s):  
Glutathione Peroxidase ◽  
Critical Role ◽  
Cell Types ◽  
Pcr Analysis ◽  
Testis Weight ◽  
Mrna Levels ◽  
Response Curves ◽  
Lower Priority ◽  
Selenoprotein Mrnas ◽  
Se Status

Selenium (Se) plays a critical role in testis, sperm, and reproduction, and testis Se levels are remarkably maintained in Se deficiency. In most other tissues, Se levels decrease dramatically as do levels of most selenoproteins and levels of a subset of Se-regulated selenoprotein mRNAs. Because of the recent identification of key molecules in the targeted trafficking of Se to the testis, we examined the hierarchy of Se regulation in testis by determining the dietary Se regulation of the full testis selenoproteome in rats fed graded levels of Se (0 to 0.8 μg Se/g) as Na2SeO3 for 28 d. Se status did not significantly affect testis weight or glutathione peroxidase 4 (Gpx4) activity ( P > 0.05). qRT-PCR analysis of selenoprotein mRNA expression revealed that 21 of the 24 selenoprotein mRNAs and ApoER2 mRNA (the selenoprotein P [Sepp1] receptor) were also not regulated significantly by dietary Se status. In contrast, Gpx1 activity decreased to 28% of Se-adequate levels, and mRNA levels for Gpx1, Sepp1, and Sepw1 (selenoprotein W) decreased significantly in Se-deficient rats to 45, 46, and 55%, respectively, of Se-adequate plateau levels. Overlap of hyperbolic Gpx4 activity and Sepw1 mRNA response curves with testis Se concentration, all with minimum dietary Se requirements <0.016 μg Se/g, showed the priority for synthesis of Gpx4. Higher minimum dietary Se requirements of 0.04 μg Se/g for Gpx1 activity and Sepp1 mRNA, and the even higher minimum dietary Se requirement of 0.08 μg Se/g for Gpx1 mRNA, suggest that the hierarchy of these biomarkers reflects distinct, lower priority pools, cell types, and roles for Se within the testis.

scholarly journals PSIII-24 Selenium requirement of turkeys based on tissue selenium concentration and selenoprotein activity and transcript expression

2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 177-178
Author(s):  
Rachel M Taylor ◽  
Roger A Sunde
Keyword(s):  
Selenium Concentration ◽  
Transcript Expression ◽  
Life Stages ◽  
Growth Data ◽  
Turkey Poults ◽  
Liver And Kidney ◽  
Tissue Selenium ◽  
Se Deficiency ◽  
Commercial Turkey ◽  
Se Status

Abstract Selenium (Se) is an essential and toxic trace mineral in animal diets. The current NRC turkey Se requirement is 0.2 µg Se/g diet for all life stages, higher than the published rat and mouse requirements. The studies that form the basis for the turkey requirement were performed over 50 years ago and based on prevention of Se-deficiency disease. With the genetic improvement of commercial turkey flocks and emerging new Se status biomarkers, we fed day-old male poults a Se-deficient (0.005 µg/g), vitamin E-adequate torula-based diet supplemented with graded levels of Se, from 0 to 5 µg/g, for 28 days. Poults supplemented with <0.05 µg/g had reduced growth, but there was no effect of high Se on growth. Se biomarkers responded hyperbolically to increasing dietary Se and reached plateaus at or before 0.4 µg/g. In deficiency, liver and kidney Se fell to <10% of Se-adequate levels. Activities of plasma GPX3; liver, kidney, pancreas and muscle GPX1; and liver, kidney, muscle and gizzard GPX4 all decreased to <10% in Se deficiency and reached plateau levels by 0.4 µg/g. In the same tissues, ≤6 out of 24 selenoprotein transcripts were downregulated to 2X Se-adequate levels in poults fed up to 5 µg/g diet. Liver Se increased to 5.6X Se-adequate levels with 5 µg/g diet. We conclude that the dietary Se level to maximize Se status biomarkers in growing turkey poults is 0.4 µg Se/g diet, double the current NRC requirement. Transcript expression is maximized at lower dietary Se levels than enzyme activities of the corresponding selenoproteins. Lastly, based on growth data, the turkey appears resistant to excess dietary Se, suggesting FDA Se supplementation limits can be safely raised. (Funded by USDA Hatch 1013496)

scholarly journals Selenium Deficiency Aggravates Aflatoxin B1–Induced Immunotoxicity in Chick Spleen by Regulating 6 Selenoprotein Genes and Redox/Inflammation/Apoptotic Signaling

2019 ◽  
Vol 149 (6) ◽  
pp. 894-901 ◽  
Author(s):  
Ling Zhao ◽  
Yue Feng ◽  
Jiang Deng ◽  
Ni-Ya Zhang ◽  
Wan-Po Zhang ◽  
...  
Keyword(s):  
Aflatoxin B1 ◽  
Body Weight Gain ◽  
Selenium Deficiency ◽  
B Cell Lymphoma ◽  
Underlying Mechanism ◽  
Protective Role ◽  
White Pulp ◽  
Feed Conversion ◽  
Apoptotic Signaling ◽  
Se Deficiency

ABSTRACTBackgroundSelenium (Se) plays a protective role in aflatoxin B1 (AFB1)–induced splenic immunotoxicity in chicks.ObjectiveThis study was designed to reveal the underlying mechanism of Se-mediated protection against AFB1-induced splenic injury in broilers.MethodsFour groups of 1-d-old Cobb male broilers (n = 5 cages/diet, 6 chicks/cage) were arranged in a 3-wk 2 × 2 factorial design trial whereby they were fed an Se-deficient, corn- and soy-based diet [base diet (BD), 36 μg Se/kg], BD plus 1.0 mg AFB1/kg, BD plus 0.3 mg Se/kg, or BD plus 1.0 mg AFB1/kg and 0.3 mg Se/kg (as 2-hydroxy-4-methylselenobutanoic acid). Serum and spleen were collected at week 3 to assay for cytokines, histology, redox status, selected inflammation- and apoptosis-related genes and proteins, and the selenogenome.ResultsDietary AFB1 induced growth retardation and spleen injury, decreasing (P < 0.05) body weight gain, feed intake, feed conversion efficiency, and serum interleukin-1β by 17.8–98.1% and increasing (P < 0.05) the spleen index and serum interleukin-6 by 37.6–113%. It also reduced the splenic lymphocyte number, the white pulp region, and histiocyte proliferation in Se-adequate groups. However, Se deficiency aggravated (P < 0.05) these AFB1-induced alterations by 16.2–103%. Moreover, Se deficiency decreased (P < 0.05) splenic glutathione peroxidase (GPX) activity and glutathione-S transferase and glutathione concentrations by 35.6–89.4% in AFB1-exposed groups. Furthermore, Se deficiency upregulated (P < 0.05) the apoptotic (Caspase 3 and Caspase 9) and antimicrobial (β defensin 1 and 2) genes, but downregulated (P < 0.05) antiapoptotic (B-cell lymphoma 2) and inflammatory (E3 ubiquitin-protein ligase CBL-B) genes at the mRNA and/or protein level in AFB1 supplementation groups. Additionally, Se deficiency downregulated (P < 0.05) GPX3, thioredoxin reductase 1 (TXNRD 1), GPX4, and selenoprotein (SELENO) S, and upregulated (P < 0.05) SELENOT and SELENOU in spleen in AFB1 administered groups.ConclusionsDietary Se deficiency exacerbated AFB1-induced spleen injury in chicks, partially through the regulation of oxidative stress, inflammatory and apoptotic signaling, and 6 selenoproteins.

scholarly journals Selenium Deficiency Is Widespread and Spatially Dependent in Ethiopia

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1565
Author(s):  
Adamu Belay ◽  
Edward J. M. Joy ◽  
Christopher Chagumaira ◽  
Dilnesaw Zerfu ◽  
E. Louise Ander ◽  
...  
Keyword(s):  
Essential Element ◽  
Selenium Deficiency ◽  
Sub Saharan Africa ◽  
Eastern Ethiopia ◽  
North West ◽  
Targeted Interventions ◽  
North East ◽  
Se Deficiency ◽  
Western Ethiopia ◽  
Se Status

Selenium (Se) is an essential element for human health and livestock productivity. Globally, human Se status is highly variable, mainly due to the influence of soil types on the Se content of crops, suggesting the need to identify areas of deficiency to design targeted interventions. In sub-Saharan Africa, including Ethiopia, data on population Se status are largely unavailable, although previous studies indicated the potential for widespread Se deficiency. Serum Se concentration of a nationally representative sample of the Ethiopian population was determined, and these observed values were combined with a spatial statistical model to predict and map the Se status of populations across the country. The study used archived serum samples (n = 3269) from the 2015 Ethiopian National Micronutrient Survey (ENMS). The ENMS was a cross-sectional survey of young and school-age children, women and men. Serum Se concentration was measured using inductively coupled plasma mass spectrometry (ICPMS). The national median (Q1, Q3) serum Se concentration was 87.7 (56.7, 123.0) μg L−1. Serum Se concentration differed between regions, ranging from a median (Q1, Q3) of 54.6 (43.1, 66.3) µg L−1 in the Benishangul-Gumuz Region to 122.0 (105, 141) µg L−1 in the Southern Nations, Nationalities, and Peoples’ Region and the Afar Region. Overall, 35.5% of the population were Se deficient, defined as serum Se < 70 µg L−1. A geostatistical analysis showed that there was marked spatial dependence in Se status, with serum concentrations greatest among those living in North-East and Eastern Ethiopia and along the Rift Valley, while serum Se concentrations were lower among those living in North-West and Western Ethiopia. Selenium deficiency in Ethiopia is widespread, but the risk of Se deficiency is highly spatially dependent. Policies to enhance Se nutrition should target populations in North-West and Western Ethiopia.

scholarly journals The application of a selenium fertiliser for the correction of marginal deficiencies in grazing sheep

1999 ◽  
Vol 70 (3) ◽  
Author(s):  
S.W.P. Cloete ◽  
F.E. Van Niekerk ◽  
M. Young ◽  
G.D. Van der Merwe ◽  
J. Clark
Keyword(s):  
Whole Blood ◽  
Sodium Selenite ◽  
Dry Matter ◽  
Liver And Kidney ◽  
Poorly Soluble ◽  
Se Deficiency ◽  
Ram Lambs ◽  
Grazing Sheep ◽  
Lamb Growth ◽  
Se Status

A commercial fertiliser, consisting of a poorly soluble barium selenate core with a coating of highly soluble sodium selenite, was evaluated in 2 trials for the provision of selenium (Se) to grazing sheep. The fertiliser was administered at a level of 1 kg per hectare to 3 of 6 kikuyu paddocks during 1995 and 1996 in Trial 1, while the other paddocks were left untreated. The Se status of SA mutton merino ram lambs, as reflected by whole blood, liver and kidney Se concentrations, was elevated (P<0.01) for at least 5 months after application of the fertiliser. Whole blood and liver Se concentrations of animals grazing unfertilised control paddocks were indicative of a subclinical Se deficiency at times (<100 ng Se/mℓ whole blood and <300 mg Se/kg liver dry matter). In Trial 2, 4 of 7 paddocks on which an oat fodder crop was established were treated with the Se fertiliser during 1995 and 1997. The remaining 3 paddocks were left unfertilised as controls. Groups of 10-15 pregnant SA mutton merino ewes were introduced to these paddocks within 2 weeks of parturition. These ewes and their progeny utilised these paddocks for a mean (+SD) period of 41+8 days after parturition. The whole blood Se concentrations of these ewes and their offspring were elevated (P < 0.01) relative to their contemporaries utilising control paddocks. No suggestion of a subclinical Se deficiency was discernible in animals grazing control paddocks, although whole blood Se levels approached 100 ng Se/mℓ during 1997. The application of Se fertiliser did not result in improvements in ewe reproduction or lamb growth. There was a suggestion of an improvement (P = 0.21) in mean (+SE) lamb survival on paddocks receiving Se fertiliser compared to control paddocks (71.5 + 4.6 % vs 62.2 + 5.3 % respectively).

scholarly journals Neonatal Selenoenzyme Expression Is Variably Susceptible to Duration of Maternal Selenium Deficiency

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 288
Author(s):  
Laura G. Sherlock ◽  
Durganili Balasubramaniyan ◽  
Lijun Zheng ◽  
Miguel Zarate ◽  
Thomas Sizemore ◽  
...  
Keyword(s):  
Thioredoxin Reductase ◽  
Selenium Deficiency ◽  
Deficient Diet ◽  
Hepatic Expression ◽  
Multiple Organs ◽  
Thioredoxin Reductase 1 ◽  
Neonatal Liver ◽  
Se Deficiency ◽  
The Impact ◽  
Gpx Activity

Maternal selenium (Se) deficiency is associated with decreased neonatal Se levels, which increases the risk for neonatal morbidities. There is a hierarchy to selenoprotein expression after Se deficiency in adult rodents, depending on the particular protein and organ evaluated. However, it is unknown how limited Se supply during pregnancy impacts neonatal selenoprotein expression. We used an Se-deficient diet to induce perinatal Se deficiency (SeD), initiated 2–4 weeks before onset of breeding and continuing through gestation. Neonatal plasma, liver, heart, kidney, and lung were collected on the day of birth and assessed for selenoproteins, factors required for Se processing, and non-Se containing antioxidant enzymes (AOE). Maternal SeD reduced neonatal circulating and hepatic glutathione peroxidase (GPx) activity, as well as hepatic expression of Gpx1 and selenophosphate synthetase 2 (Sps2). In contrast, the impact of maternal SeD on hepatic thioredoxin reductase 1, hepatic non-Se containing AOEs, as well as cardiac, renal, and pulmonary GPx activity, varied based on duration of maternal exposure to SeD diet. We conclude that the neonatal liver and circulation demonstrate earlier depletion in selenoenzyme activity after maternal SeD. Our data indicate that prolonged maternal SeD may escalate risk to the neonate by progressively diminishing Se-containing AOE across multiple organs.

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