MiR-196-5p involvement in selenium deficiency-induced immune damage via targeting of NFκBIA in the chicken trachea

Metallomics ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 1679-1692 ◽  
Author(s):  
Linqian Qin ◽  
Yiming Zhang ◽  
Chunyan Wan ◽  
Zhu Wang ◽  
Yimei Cong ◽  
...  
Keyword(s):  
Selenium Deficiency ◽  
Dietary Selenium ◽  
Immune Injury ◽  
Se Deficiency

Dietary selenium (Se) deficiency can induce multifarious immune injury in tissues, accompanied by inflammation and a decreased expression of selenoproteins.

scholarly journals Inhibition of hepatic deiodination of thyroxine is caused by selenium deficiency in rats

1987 ◽  
Vol 248 (2) ◽  
pp. 443-447 ◽  
Author(s):  
G J Beckett ◽  
S E Beddows ◽  
P C Morrice ◽  
F Nicol ◽  
J R Arthur
Keyword(s):  
Thyroid Hormones ◽  
Production Rate ◽  
Selenium Deficiency ◽  
Enzyme Complex ◽  
Measurable Effect ◽  
Direct Role ◽  
Mechanism Of Inhibition ◽  
Se Deficiency

Selenium (Se) deficiency produced up to a 14-fold decrease in hepatic tri-iodothyronine (T3) production from thyroxine (T4) in vitro. The T3 production rate could not be restored by the addition of a variety of cofactors, nor by the addition of control homogenate. The impairment in hepatic T3 production observed in Se deficiency was reflected in the concentrations of thyroid hormones circulating in plasma, T4 being increased approx. 40% and T3 being decreased by 30%. However, the fall in plasma T3 concentrations was smaller than might be expected in view of the marked decreased in T3 production. Se deficiency had no measurable effect on plasma reverse-tri-iodothyronine concentrations. The data suggest that Se deficiency produces an inhibition of both 5- and 5′-deiodination, consistent with the widely held view that these reactions are catalysed by the same enzyme complex. The mechanism of inhibition appears not be mediated by changes in thiol levels, but a direct role of Se in the activity of the deiodinase complex cannot be excluded.

scholarly journals Dietary Selenium Deficiency Exacerbates DSS-Induced Epithelial Injury and AOM/DSS-Induced Tumorigenesis

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e67845 ◽  
Author(s):  
Caitlyn W. Barrett ◽  
Kshipra Singh ◽  
Amy K. Motley ◽  
Mary K. Lintel ◽  
Elena Matafonova ◽  
...  
Keyword(s):  
Selenium Deficiency ◽  
Epithelial Injury ◽  
Dietary Selenium

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.

Effect of Dietary Selenium Deficiency on the Cell Apoptosis and the Level of Thyroid Hormones in Chicken

2015 ◽  
Vol 171 (2) ◽  
pp. 445-452 ◽  
Author(s):  
Yunmao Huang ◽  
Wanyan Li ◽  
Danning Xu ◽  
Bingxin Li ◽  
Yunbo Tian ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Cell Apoptosis ◽  
Selenium Deficiency ◽  
Dietary Selenium

Dietary Selenium Deficiency Exacerbates Lipopolysaccharide-Induced Inflammatory Response in Mouse Mastitis Models

Inflammation ◽  
2014 ◽  
Vol 37 (6) ◽  
pp. 1925-1931 ◽  
Author(s):  
Zhengkai Wei ◽  
Minjun Yao ◽  
Yimeng Li ◽  
Xuexiu He ◽  
Zhengtao Yang
Keyword(s):  
Inflammatory Response ◽  
Selenium Deficiency ◽  
Dietary Selenium

scholarly journals T-2 Toxin Induces Epiphyseal Plate Lesions via Decreased SECISBP2-Mediated Selenoprotein Expression in DA Rats, Exacerbated by Selenium Deficiency

Cartilage ◽  
2018 ◽  
Vol 12 (1) ◽  
pp. 121-131 ◽  
Author(s):  
Jian Sun ◽  
Zixin Min ◽  
Wenxiang Zhao ◽  
Safdar Hussain ◽  
Yitong Zhao ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Selenium Deficiency ◽  
Cartilage Degradation ◽  
Epiphyseal Plate ◽  
Dark Agouti ◽  
Deficient Diet ◽  
Metabolic Imbalance ◽  
Se Deficiency ◽  
Matrix Metabolism ◽  
T2 Toxin

Objective Both selenium (Se) deficiency and mycotoxin T2 lead to epiphyseal plate lesions, similar to Kashin-Beck disease (KBD). However, regulation of selenoproteins synthesis mediated by SECISBP2, in response to these 2 environmental factors, remained unclear. The present study proposed to explore the mechanism behind the cartilage degradation resulting from Se deficiency and mycotoxin T2 exposure. Design Deep chondrocyte necrosis and epiphyseal plate lesions were replicated in Dark Agouti (DA) rats by feeding them T2 toxin/Se deficiency artificial synthetic diet for 2 months. Results Se deficiency led to decreased expression of COL2α1, while T2 treatment reduced the heparan sulfate 6-O-sulfotransferase 2 (HS6ST2) expression, both of which affected the cartilage extracellular matrix metabolism in the rat models. The expression of Col2α1, Acan, Hs6st2, Secisbp2, Gpx1, and Gpx4 were all significantly decreased in cartilage tissues from DA rats, fed a Se-deficient diet or exposed to T2 toxin, contrary to Adamts4, whose expression was increased in both conditions. In addition, T2 treatment led to the decreased expression of SBP2, GPX1, GPX4, and total GPXs activity in C28/I2 cells. Conclusion DA rats exposed to T2 toxin and/or Se-deficient conditions serve as the perfect model of KBD. The 2 environmental risk factors of KBD, which serve as a “double whammy,” can intensify the extracellular matrix metabolic imbalance and the antioxidant activity of chondrocytes, leading to articular cartilage degradation and epiphyseal plate abnormalities similar to those observed in KBD.

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