Abstract

Dietary organic selenium (Se) is commonly utilized to increase formation of selenoproteins, including the major antioxidant protein, glutathione peroxidase (GPx). Inorganic Se salts, such as sodium selenite, are also incorporated into selenoproteins, and there is evidence that nanoelemental Se added to the diet may also be effective. We conducted two trials, the first investigated inorganic Se (selenite), organic Se (L-selenomethionine) and nanoelemental Se, in conventional mice. Their bioavailability and effectiveness to increase GPx activity were examined. The second trial focused on determining the mechanism by which dietary Se is incorporated into tissue, utilising both conventional and germ-free (GF) mice. Mice were fed a diet with minimal Se, 0.018 parts per million (ppm), and diets with Se supplementation, to achieve 0.07, 0.15, 0.3 and 1.7 ppm Se, for 5 weeks (first trial). Mass spectrometry, Western blotting and enzymatic assays were used to investigate bioavailability, protein levels and GPx activity in fresh frozen tissue (liver, ileum, plasma, muscle and feces) from the Se fed animals. Inorganic, organic and nanoelemental Se were all effectively incorporated into tissues. The high Se diet (1.7 ppm) resulted in the highest Se levels in all tissues and plasma, independent of the Se source. Interestingly, despite being ~11 to ~25 times less concentrated than the high Se, the lower Se diets (0.07; 0.15) resulted in comparably high Se levels in liver, ileum and plasma for all Se sources. GPx protein levels and enzyme activity were significantly increased by each diet, relative to control. We hypothesised that bacteria may be a vector for the conversion of nanoelemental Se, perhaps in exchange for S in sulphate metabolising bacteria. We therefore investigated Se incorporation from low sulphate diets and in GF mice. All forms of selenium were bioavailable and similarly significantly increased the antioxidant capability of GPx in the intestine and liver of GF mice and mice with sulphate free diets. Se from nanoelemental Se resulted in similar tissue levels to inorganic and organic sources in germ free mice. Thus, endogenous mechanisms, not dependent on bacteria, reduce nanoelemental Se to the metabolite selenide that is then converted to selenophosphate, synthesised to selenocysteine, and incorporated into selenoproteins. In particular, the similar efficacy of nanoelemental Se in comparison to organic Se in both trials is important in the view of the currently limited cheap sources of Se.

Highlights

  • Oxidative stress, which is a common occurrence in livestock that can be caused by a wide range of factors, compromises gut health and reduces the efficiency with which the intestine absorbs nutrients [1,2]

  • Nanoelemental Se was produced in the laboratory by reducing selenite (Se+IV ) with reduced glutathione (GSH) in the presence of bovine serum albumin (BSA)

  • Levels of selenium as measured by mass spectrometry were significantly increased in the liver, ileum, muscle, plasma and feces of mice after 5 weeks on Se enriched diets

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Summary

Introduction

Oxidative stress, which is a common occurrence in livestock that can be caused by a wide range of factors, compromises gut health and reduces the efficiency with which the intestine absorbs nutrients [1,2]. This intestinal dysfunction can be ameliorated by increasing antioxidant activity, for example through administration of selenium (Se) or vitamin E [2,3]. The bioavailability of Se regulates GPx activity, supplemental Se generally increasing its total catalytic activity For this reason, Se is added to animal food to reduce oxidative stress [5]. SeMet can substitute for methionine it has been reported to have adverse effects at high doses [7,8,9]

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