Analysis of Bioavailability and Induction of Glutathione Peroxidase by Dietary Nanoelemental, Organic and Inorganic Selenium

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.

Effects of Selenium Nanoparticles-loaded Chitosan Microspheres on Meat Selenium Content and Oxidative Stability in Broiler Chickens

“…The size distribution analysis was conducted in the final colloid before lyophilization. The results showed an acceptable size (80.50 ± 20.0 nm) very close to that reported in previous studies using CS [1,7,22,25,[30][31][32] or other capping agents [33,34].…”

“…Selenium (Se) is an integral part of at least 25 selenoproteins, which exert multiple biological activities regarding animal growth performance, fertility and disease prevention. Some of these selenoproteins are actively involved in antioxidant defense and redox regulation of the animals by controlling the levels of free radicals that are produced during normal metabolic activity [1]. Due to its antioxidant potential, dietary Se supplementation has been extensively investigated, among other antioxidants, as a key trace mineral for enhancing oxidative stability and shelf life of poultry meat, which is quite sensitive to oxidation owing to its high content of polyunsaturated fatty acids (PUFA) [2,3].…”

“…The least expensive are inorganic Se salts, usually sodium selenite, but inorganic Se incorporation into tissues and antioxidant activity vary [6]. Organic Se, in the form of selenomethionine is more efficiently incorporated into tissues and it is more bioactive, but its production process makes it more expensive [1]. Both forms can be toxic when provided at excessive levels i.e.…”

“…On the other hand, it may retard the release of SeNP due to the deficiency of the enzymes to deal with CS in some species of animals and human beings [22]. Hence, it is not clear how effectively the CS-SeNP can be solubilized in the gastrointestinal tract of animals, and permit the release, absorption, and incorporation of Se into tissues [1].…”

“…composition of the the starter (0-10 d), grower(11-24 d) and finisher(25-42 d) basal diets (g/kg as fed basis), and selenium (Se) level of the experimental diets 1. Premix supplied per kg of diet: 10,000 IU vitamin A (retinyl acetate), 5,000 IU vitamin D 3 (cholecalciferol), 75 mg vitamin E (DL-α-tocopheryl acetate), 6.25 mg vitamin K 3 (menadione),3.25 …”