Effects of Selenium Auricularia cornea Culture Supplementation on Growth Performance, Antioxidant Status, Tissue Selenium Concentration and Meat Quality in Growing-Finishing Pigs

Selenium Auricularia cornea culture (SAC) is a new source of organic selenium. Two experiments were conducted to determine the available energy of SAC fed to pigs and to evaluate the effects of dietary SAC supplementation on growth performance, serum biochemical profiles, fecal short chain fatty acids (SCFA), meat quality, tissue selenium concentration, and oxidative stability of fresh meat in growing-finishing pigs. In Experiment (Exp.) 1, 12 barrows with average body weight (BW) of 42.40 ± 5.30 kg were randomly allotted to two groups and fed the basal diet and SAC-supplemented diet, individually. In Exp. 2, 96 growing-finishing pigs (BW: 91.96 ± 7.55 kg) were grouped into four dietary treatments; each treatment contained six replicates with four pigs per replicate. The four treatments fed a control diet and three experimental diets supplemented with 0.6%, 1.2%, and 2.4% SAC, respectively. The trial lasted for 45 days. The results revealed that digestible energy (DE) of SAC was 11.21 MJ/kg. The average daily gain (ADG) was improved in pigs fed 1.2% and 2.4% SAC during day 24 to 45 and the overall period. Dietary 1.2% and 2.4% SAC supplementation had a lower F/G (p < 0.05) than the control diet during different stages. Dietary SAC supplementation increased fecal butyrate contents (p < 0.05), and pigs fed 1.2% and 2.4% SAC diets had a higher MCT1 mRNA expression (p = 0.04) in the colon. Pigs fed 2.4% SAC had higher GSH-Px contents (p < 0.05) in serum, liver, and longissimus dorsi muscle (LDM) than those in the control group. The 2.4% SAC-supplemented group revealed a higher Se content (p < 0.05) in LDM and a lower MDA concentration (p < 0.05) in fresh meat during the simulated retail display on day six. In conclusion, this study suggested that SAC was more effective in improving growth, enhancing the antioxidant status, depositing Se in muscle, and increasing meat oxidative stability of pigs.

Knockout of Selenoprotein V Affects Regulation of Selenoprotein Expression by Dietary Selenium and Fat Intakes in Mice

ABSTRACT Background The metabolic function of selenoprotein V (SELENOV) remains unknown. Objectives Two experiments were conducted to determine effects of the Selenov knockout (KO) on selenium concentration and mRNA, protein, and/or activity of 4 major selenoproteins [glutathione peroxidase (GPX) 1, GPX4, thioredoxin reductase-1 (TXNRD1), and selenoprotein P (SELENOP)] in the serum, liver, testis, and/or white adipose tissue (WAT) of mice fed different dietary selenium and fat concentrations. Methods In Experiment (Expt) 1, 40 KO and 40 wild-type (WT) mice (males, 8 wk old) were fed (n = 10/genotype) a casein-sucrose basal diet plus 0, 0.3, 1, or 3 mg Se/kg (as sodium selenite) for 32 wk . In Expt 2, 20 KO and 20 WT mice (males, 8 wk old) were fed (n = 10/genotype) a normal-fat diet (NF; 10% calories from fat) or a high-fat diet (HF; 60% calories from fat) for 19 wk. Results In Expt 1, the KO caused consistent or substantial decreases (P &lt; 0.05) of mRNA amounts of Gpx1, Txnrd1, and Selenop in the testis (≤52%), but selenium concentrations (19–29%) and GPX activities (≤ 50%) were decreased in the liver across different dietary selenium concentrations . Hepatic and testis GPX1 protein was elevated (≤31%) and decreased (≤45%) by the KO, respectively. In Expt 2, the genotype and dietary fat intake exerted interaction effects ( P &lt; 0.05) on Gpx1 mRNA amounts in the WAT; Gpx1, Txnrd1, and Selenop mRNA amounts and TXNRD activities in the testis; and selenium concentrations in the serum and liver. However, these 2 treatments produced largely independent or additive effects (P &lt; 0.05) on the GPX1 and SELENOP protein amounts in the liver and testis (up to ± 50% changes). Conclusions The KO-mediated changes in the tissue selenium concentrations and functional expression of 3 major selenoproteins implied potential for SELENOV in regulating body selenium metabolism in the mouse.