Topic
Selenium
About: Selenium is a research topic. Over the lifetime, 21192 publications have been published within this topic receiving 429715 citations. The topic is also known as: Se & selen.
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TL;DR: Measurement of the GSH-Px:Se ratio indicated that Se supplied as selenite or selenocystine was a better source of Se for plasma G SHPx than was Se from selenomethionine or fishmeal.
110 citations
01 Jun 1979
TL;DR: Suppression was shown to be associated with serum factors coating lymphocytes from dogs deficient in vitamin E and selenium, and was most marked in dogs fed diets highest in polyunsaturated fatty acid (PUFA) content, providing conditions most conductive to lipid peroxidation in vivo.
Abstract: Vitamin E and selenium have both been shown to have immunostimulatory effects in a variety of species when administered in quantities in excess of established deitary requirements. Responses to each nutrient appeared to be independent of the nutrition of the other. Deficiencies of vitamin E and selenium conversely caused suppression of the immune response system, particularly, cell mediated mechanisms. Suppression was shown to be associated with serum factors coating lymphocytes from dogs deficient in vitamin E and selenium. Oral supplementation with vitamin E transformed or removed the suppressive factors, dietary selenium had no effect. In vitro peripheral lymphocyte blast transformation tests corroborated observations of in vivo studies. Reducing agents and synthetic anti-oxidants eliminated suppressive effects in vitro. Suppression was most marked in dogs fed diets highest in polyunsaturated fatty acid (PUFA) content, providing conditions most conductive to lipid peroxidation in vivo. The essential fatty acids linoleic and arachidonic have been shown to similarly influence immunoregulatory mechanisms in vivo. The effect may be a direct one since plasma membrane fluidity of lymphoid cells increases the probability of modification of cell--antigen interactions by PUFA. However, their effect may also be an indirect one. PUFA are known precursor substances of E anf F type prostaglandins which have been shown to affect immediate and delayed hypersensitivity by stimulating synthesis of cyclic AMP. More definitive studies are needed to resolve this question.
110 citations
TL;DR: It is suggested that dietary selenium supplementation decreases DNA damage and increases epithelial cell apoptosis within the aging canine prostate.
Abstract: The trace mineral selenium inhibits cancer development in a variety of experimental animal models. We used an in vivo canine model to evaluate the effects of dietary selenium supplementation on DNA damage in prostate tissue and on apoptosis in prostate epithelial cells. Sexually intact elderly male beagle dogs were randomly assigned to receive an unsupplemented diet (control group) or diets that were supplemented with selenium (treatment group), either as selenomethionine or as high-selenium yeast at 3 micro g/kg or 6 micro g/kg body weight per day for 7 months. The extent of DNA damage in prostate cells and in peripheral blood lymphocytes, as determined by the alkaline comet assay, was lower among the selenium-supplemented dogs than among the control dogs (prostate P<.001; peripheral blood lymphocytes P =.003; analysis of variance) but was not associated with the activity of the antioxidant enzyme glutathione peroxidase in plasma. The median number of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling-positive (i.e., apoptotic) prostate epithelial cells was 3.7 (interquartile range = 1.1-7.6) for the selenium-supplemented dogs and 1.7 (interquartile range = 0.2-2.8) for the control dogs ( P =.04, Mann-Whitney U test). These data suggest that dietary selenium supplementation decreases DNA damage and increases epithelial cell apoptosis within the aging canine prostate.
110 citations
110 citations
TL;DR: In this paper, the authors explored the reactions between selenium compounds and the glutaredoxin system and found that selenite and GS-Se-SG were reduced by Grx1 and Grx2 in a non-stoichiometric manner due to redox cycling with oxygen, which in turn generated reactive oxygen species.
Abstract: The Grx (glutaredoxin) proteins are oxidoreductases with a central function in maintaining the redox balance within the cell. In the present study, we have explored the reactions between selenium compounds and the glutaredoxin system. Selenite, GS-Se-SG (selenodiglutathione) and selenocystine were all shown to be substrates of human Grx1, implying a novel role for the glutaredoxins in selenium metabolism. During the past few years, selenium has further evolved as a potential therapeutic agent in cancer treatment, and a leading mechanism of cytotoxicity is the generation of ROS (reactive oxygen species). Both selenite and GS-Se-SG were reduced by Grx1 and Grx2 in a non-stoichiometric manner due to redox cycling with oxygen, which in turn generated ROS. The role of Grx in selenium toxicity was therefore explored. Cells were treated with the selenium compounds in combination with transient overexpression of, or small interfering RNA against, Grx1. The results demonstrated an increased viability of the cells during silencing of Grx1, indicating that Grx1 is contributing to selenium toxicity. This is in contrast with TrxR (thioredoxin reductase), which previously was shown to protect cells from selenium cytotoxicity, verifying a diverse role between Grx and TrxR in selenium-mediated cytotoxicity. Furthermore, selenium treatment led to a marked increase in protein glutathionylation and cysteinylation that potentially can influence the activity and function of several proteins within the cell.
110 citations