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      The Relationship between Selenium and T3 in Selenium Supplemented and Nonsupplemented Ewes and Their Lambs

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          Abstract

          Twenty pregnant ewes were selected and classified into two groups. The first group received subcutaneous selenium supplementation (0.1 mg of sodium selenite/kg BW) at the 8th and 5th weeks before birth and 1st week after birth while the other was control group without selenium injection. Maternal plasma and serum samples were collected weekly from the 8th week before birth until the 8th week after birth and milk samples were taken from ewes weekly, while plasma and serum samples were collected at 48 hours, 1st, 2nd, 3rd, 5th, and 8th weeks after birth from the newborn lambs. Results demonstrated significant positive relationship between maternal plasma selenium and serum T3 in supplemented and control ewes ( r = 0.69 to 0.72, P < 0.05). There was significant ( P < 0.001) increase in T3 in supplemented ewes and their lambs until the 8th week after birth. There was positive relationship between milk, selenium concentration, and serum T3 in the newborn lambs of the supplemented group ( r = 0.84, P < 0.01), while the relationship was negative in the control one ( r = −0.89, P < 0.01). Muscular and thyroid pathological changes were independent of selenium supplementation. Selenium supplementation was important for maintaining T3 in ewes and newborn lambs until the 8th week after birth.

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          Most cited references41

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          Mechanism and regulation of selenoprotein synthesis.

          Selenium is an essential trace element that is incorporated into proteins as selenocysteine (Sec), the twenty-first amino acid. Sec is encoded by a UGA codon in the selenoprotein mRNA. The decoding of UGA as Sec requires the reprogramming of translation because UGA is normally read as a stop codon. The translation of selenoprotein mRNAs requires cis-acting sequences in the mRNA and novel trans-acting factors dedicated to Sec incorporation. Selenoprotein synthesis in vivo is highly selenium-dependent, and there is a hierarchy of selenoprotein expression in mammals when selenium is limiting. This review describes emerging themes from studies on the mechanism, kinetics, and efficiency of Sec insertion in prokaryotes. Recent developments that provide mechanistic insight into how the eukaryotic ribosome distinguishes between UGA/Sec and UGA/stop codons are discussed. The efficiency and regulation of mammalian selenoprotein synthesis are considered in the context of current models for Sec insertion.
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            Selenium, the thyroid, and the endocrine system.

            Recent identification of new selenocysteine-containing proteins has revealed relationships between the two trace elements selenium (Se) and iodine and the hormone network. Several selenoproteins participate in the protection of thyrocytes from damage by H(2)O(2) produced for thyroid hormone biosynthesis. Iodothyronine deiodinases are selenoproteins contributing to systemic or local thyroid hormone homeostasis. The Se content in endocrine tissues (thyroid, adrenals, pituitary, testes, ovary) is higher than in many other organs. Nutritional Se depletion results in retention, whereas Se repletion is followed by a rapid accumulation of Se in endocrine tissues, reproductive organs, and the brain. Selenoproteins such as thioredoxin reductases constitute the link between the Se metabolism and the regulation of transcription by redox sensitive ligand-modulated nuclear hormone receptors. Hormones and growth factors regulate the expression of selenoproteins and, conversely, Se supply modulates hormone actions. Selenoproteins are involved in bone metabolism as well as functions of the endocrine pancreas and adrenal glands. Furthermore, spermatogenesis depends on adequate Se supply, whereas Se excess may impair ovarian function. Comparative analysis of the genomes of several life forms reveals that higher mammals contain a limited number of identical genes encoding newly detected selenocysteine-containing proteins.
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              Energy metabolism in uncoupling protein 3 gene knockout mice.

              Uncoupling protein 3 (UCP3) is a member of the mitochondrial anion carrier superfamily. Based upon its high homology with UCP1 and its restricted tissue distribution to skeletal muscle and brown adipose tissue, UCP3 has been suggested to play important roles in regulating energy expenditure, body weight, and thermoregulation. Other postulated roles for UCP3 include regulation of fatty acid metabolism, adaptive responses to acute exercise and starvation, and prevention of reactive oxygen species (ROS) formation. To address these questions, we have generated mice lacking UCP3 (UCP3 knockout (KO) mice). Here, we provide evidence that skeletal muscle mitochondria lacking UCP3 are more coupled (i.e. increased state 3/state 4 ratio), indicating that UCP3 has uncoupling activity. In addition, production of ROS is increased in mitochondria lacking UCP3. This study demonstrates that UCP3 has uncoupling activity and that its absence may lead to increased production of ROS. Despite these effects on mitochondrial function, UCP3 does not seem to be required for body weight regulation, exercise tolerance, fatty acid oxidation, or cold-induced thermogenesis. The absence of such phenotypes in UCP3 KO mice could not be attributed to up-regulation of other UCP mRNAs. However, alternative compensatory mechanisms cannot be excluded. The consequence of increased mitochondrial coupling in UCP3 KO mice on metabolism and the possible role of yet unidentified compensatory mechanisms, remains to be determined.
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                Author and article information

                Journal
                Vet Med Int
                Vet Med Int
                VMI
                Veterinary Medicine International
                Hindawi Publishing Corporation
                2090-8113
                2042-0048
                2014
                10 February 2014
                : 2014
                : 105236
                Affiliations
                1Faculty of Veterinary Medicine, Benha University, Moshtohor 13736, Egypt
                2Instituto de Neurobiología, Universidad Nacional Autónoma de México, Mexico
                3Facultad de Estudios Superiores Cuautitlán, Universidad Nacional Autónoma de México, Km. 2.5 Carretera Cuautitlán-Teoloyucan, 54714 Cuautitlán Izcalli, MEX, Mexico
                Author notes
                *Abd Elghany Hefnawy: abdelghani72@ 123456yahoo.com

                Academic Editor: Philip H. Kass

                Article
                10.1155/2014/105236
                3934659
                10cb14b4-2c54-4a7e-813b-ca531030f696
                Copyright © 2014 Abd Elghany Hefnawy et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 19 September 2013
                : 1 January 2014
                : 2 January 2014
                Categories
                Research Article

                Veterinary medicine
                Veterinary medicine

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