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

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)

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

Journal of the South African Veterinary Association ◽

10.4102/jsava.v70i3.768 ◽

1999 ◽

Vol 70 (3) ◽

Cited By ~ 2

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).

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

Bioscience Reports ◽

10.1042/bsr20080146 ◽

2009 ◽

Vol 29 (5) ◽

pp. 329-338 ◽

Cited By ~ 137

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.

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Dietary Selenium Regulates microRNAs in Metabolic Disease: Recent Progress

Nutrients ◽

10.3390/nu13051527 ◽

2021 ◽

Vol 13 (5) ◽

pp. 1527

Author(s):

Xin Huang ◽

Yu-Lan Dong ◽

Tong Li ◽

Wei Xiong ◽

Xu Zhang ◽

...

Keyword(s):

Physiological State ◽

Essential Element ◽

Dietary Factors ◽

Regulatory Mechanisms ◽

Metabolic Risk ◽

Messenger Rnas ◽

Immune Disorders ◽

Se Deficiency ◽

Safety Range ◽

Se Status

Selenium (Se) is an essential element for the maintenance of a healthy physiological state. However, due to environmental and dietary factors and the narrow safety range of Se, diseases caused by Se deficiency or excess have gained considerable traction in recent years. In particular, links have been identified between low Se status, cognitive decline, immune disorders, and increased mortality, whereas excess Se increases metabolic risk. Considerable evidence has suggested microRNAs (miRNAs) regulate interactions between the environment (including the diet) and genes, and play important roles in several diseases, including cancer. MiRNAs target messenger RNAs to induce changes in proteins including selenoprotein expression, ultimately generating disease. While a plethora of data exists on the epigenetic regulation of other dietary factors, nutrient Se epigenetics and especially miRNA regulated mechanisms remain unclear. Thus, this review mainly focuses on Se metabolism, pathogenic mechanisms, and miRNAs as key regulatory factors in Se-related diseases. Finally, we attempt to clarify the regulatory mechanisms underpinning Se, miRNAs, selenoproteins, and Se-related diseases.

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Selenium in Pediatric Nutrition

PEDIATRICS ◽

10.1542/peds.87.3.339 ◽

1991 ◽

Vol 87 (3) ◽

pp. 339-351

Author(s):

Richard E. Litov ◽

Gerald F. Combs

Keyword(s):

Age Groups ◽

Signs And Symptoms ◽

Infants And Children ◽

Keshan Disease ◽

National Academy Of Sciences ◽

Maple Syrup ◽

Clinical Impairment ◽

Se Deficiency ◽

Se Status

Se is an essential nutrient that provides antioxidant protection in concert with vitamin E. Several selenoproteins have been identified, but only one, SeGSHpx, has a known function, that of neutralizing toxic hydroperoxides. Plasma Se concentration, being responsive to changes in Se intake, is the most practical and widely used measure of nutritional Se status. The plasma Se concentrations of the majority of healthy infants and children fall within the range of 50 to 150 µg/L. Although SeGSHpx activity measures the metabolically functional form of Se, the lack of a standardized analytical method has limited its usefulness as an index of nutritional Se status. Se deficiency was first observed in animals, but it is now recognized to occur in humans. Two human diseases associated with severe nutritional Se deficiency have been reported from China: a juvenile cardiomyopathy named Keshan disease and a chondrodystrophy named Kaschin-Beck disease. Long-term TPN, which provides negligible amounts of intrinsic Se, has been demonstrated in some cases to result in biochemical and clinical impairment. Although there are no consistent signs and symptoms characteristic of TPN-associated Se deficiency, in addition to the low blood selenium levels, some patients will experience leg muscle pain and altered serum transaminase and creatine kinase activities. These manifestations of Se deficiency usually take years to develop. Recent information about the amount of dietary Se needed to maximize plasma SeGSHpx activity in adult men has allowed for better estimates of the Se requirement for humans. Recommended daily dietary allowances published recently by the National Academy of Sciences have been revised for infants and children in this paper by making appropriate adjustments for the protein requirements of these age-groups. These recommended intakes for Se can generally be met by consuming adequate amounts of cereals, meat, eggs, dairy products, human milk, and infant formula, which are good sources of highly available Se and are of low risk of providing excess amounts of Se. Suboptimal Se intakes by pregnant women may predispose their infants to low Se status at birth, which in turn may affect the infants' ability to maintain adequate Se status during the first few months of life. In those situations where protein intake is restricted, such as in phenylketonuria and maple syrup urine disease, Se-supplemented formulas should be used. The most critical situation for Se supplementation is in pediatric patients receiving long-term TPN therapy. When supplementing with Se, consideration must be given to the amount and form of Se to be used; with long-term TPN therapy, plasma Se levels should be monitored.

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Turkey Origin Reovirus-Induced Immune Dysfunction in Specific Pathogen Free and Commercial Turkey Poults

Avian Diseases ◽

10.1637/8190-120607-reg ◽

2008 ◽

Vol 52 (3) ◽

pp. 387-391 ◽

Cited By ~ 7

Author(s):

J Michael Day ◽

Erica Spackman ◽

Mary J. Pantin-Jackwood

Keyword(s):

Immune Dysfunction ◽

Specific Pathogen Free ◽

Turkey Poults ◽

Specific Pathogen ◽

Commercial Turkey

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Effects of Time and Dietary Selenium Concentration as Sodium Selenite on Tissue Selenium Uptake by Sheep

Journal of Animal Science ◽

10.2527/jas1988.6692299x ◽

1988 ◽

Vol 66 (9) ◽

pp. 2299 ◽

Cited By ~ 17

Author(s):

M. G. Echevarria ◽

P. R. Henry ◽

C. B. Ammerman ◽

P. V. Rao

Keyword(s):

Sodium Selenite ◽

Selenium Concentration ◽

Dietary Selenium ◽

Selenium Uptake ◽

Tissue Selenium

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Selenium Deficiency Is Widespread and Spatially Dependent in Ethiopia

Nutrients ◽

10.3390/nu12061565 ◽

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.

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Serum Selenium Status and Its Interrelationship with Serum Biomarkers of Thyroid Function and Antioxidant Defense in Hashimoto’s Thyroiditis

Antioxidants ◽

10.3390/antiox9111070 ◽

2020 ◽

Vol 9 (11) ◽

pp. 1070

Author(s):

Rahim Rostami ◽

Sarmad Nourooz-Zadeh ◽

Afshin Mohammadi ◽

Hamid Reza Khalkhali ◽

Gordon Ferns ◽

...

Keyword(s):

Thyroid Function ◽

Hashimoto’S Thyroiditis ◽

Antioxidant Defense ◽

Thyroid Volume ◽

Hashimoto's Thyroiditis ◽

Thyroid Peroxidase ◽

Urinary Iodine Concentration ◽

Serum Selenium ◽

Se Deficiency ◽

Se Status

Selenium (Se) deficiency has been implicated in the pathogenesis of Hashimoto’s thyroiditis (HT), although the available evidence is limited. The present study aimed to explore the interrelationships between serum Se status with measures of thyroid function and antioxidant defense in new cases of HT patients with hypoechogenic thyroid. HT patients (n = 49) and matched controls (n = 50) were recruited. Selenium, thyroid hormone panel, thyroid volume (TVol), glutathione (GSH), glutathione peroxidase3 (GPx3) activity, urinary iodine concentration (UIC), and urinary creatinine (Cr) were assessed. HT patients exhibited lower Se levels compared to controls (p < 0.001) with the rates of Se-deficient (<0.85 µmol/L) participants being 58.8% and 34%, respectively. Se-deficient patients exhibited higher thyroid stimulating hormone (TSH), Thyroid volume (TVol), thyroglobulin, antibody-titers, GPx3 activity and UIC/Cr compared to Se-sufficient patients (all p < 0.001). In the Se-deficient patients, inverse correlations were seen between Se-levels with TSH, TVol, and Thyroid peroxidase antibody (TPO-Ab) (all p < 0.001). This study is the first to uncover that coexisting Se-deficiency and elevated iodine in HT may enhance autoimmune reactions and accelerate the deterioration of thyroid function through oxidative stress. Our study also highlights the importance of optimal Se status in this disease, thus providing a rationale for the execution of intervention trials for the evaluation of the clinical benefits of antioxidant-status improvement in HT.

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