The application of organic selenium (SeMet) improve the photosynthetic characteristics, yield and quality of hybrid rice.

Rice is an important food in the world, and selenium (Se) is a necessary trace element for the human. So the effects of selenomethionine (SeMet) on photosynthetic capacity, yield and quality of rice at different stages were studied. The results show that SeMet can increase the Ppotosynthetic capacity of rice leaves during each growth stage, the effect of 5 mg/L SeMet treatment was the most significant. At the mature stage of rice, SeMet significantly increased rice yield and total plant biomass, 7.5and 5 mg/L SeMet treatments had the most significant effects, respectively. In addition, SeMet significantly improved the content of Se and processing quality of rice, decreased chalkiness, inhibited amylose synthesis, and optimized flavor. The above indices showed the best results after treatment with 5 mg/L SeMet. It is hoped that this study will provide a theoretical basis for the application of organic selenium in rice production.

Effects of various selenium-enriched yeasts, selenomethionine, and nanoselenium on production performance, quality, and antioxidant capacity in laying hens.

This study aimed to compare the effects of various selenium (Se) sources (2 mg/kg) on the performance, quality, and antioxidant capacity of laying hens as well as the Se content in their eggs and blood. We selected 720 34-wk-old Lohmann pink-shell laying hens were randomly assigned into 6 groups and fed a basal diet (control) or a basal diet supplemented with various Se sources (Se-enriched yeast, SY-A, SY-C, SY-N; selenomethionine SM, nano-Se SN) for 16 wk. There were 10 replicates of 120 hens per group. Dietary Se supplementation increased the egg production rate of all laying hens. Egg and serum Se deposition was highest in the SM group. Yolk color scores of SY-A and SY-N groups were significantly lower than those of other groups (P < 0.01). The protein height and Haugh unit were significantly lower in the SN group than in the other groups (P < 0.05). The yolk height was significantly higher in the SN and SY-N groups than in the SY-A group (P < 0.05). Dietary supplementation of selenium can improve the antioxidant capacity of laying hens. The SOD content of SM group was significantly lower than that of SY-A and SN group (P < 0.05). The malondialdehyde (MDA) content was significantly higher in the SM group than in the SY-A group (P < 0.05). The present work empirically demonstrated that the production performance of laying hens supplemented with 2 mg/kg Se was superior to that of the hens receiving only a basal diet. The SY-C group exhibited the best production performance, the SY-A group had the highest antioxidant capacity, and the SM group produced eggs with the highest level of Se enrichment.

Selenomethionine modulates the JAK2 / STAT3 / A20 pathway through oxidative stress to alleviate LPS-induced pyroptosis and inflammation in chicken hearts.

Selenium (Se) is involved in many physiopathologic processes in humans and animals and is strongly associated with the development of heart disease. Lipopolysaccharides (LPS) are cell wall components of gram-negative bacteria that are present in large quantities during environmental pollution. To investigate the mechanism of LPS-induced cardiac injury and the efficacy of the therapeutic effect of SeMet on LPS, a chicken model supplemented with selenomethionine (SeMet) and/or LPS treatment, as well as a primary chicken embryo cardiomyocyte model with the combined effect of SeMet / JAK2 inhibitor (INCB018424) and/or LPS were established in this experiment. CCK8 kit, Trypan blue staining, DCFH-DA staining, oxidative stress kits, immunofluorescence staining, LDH kit, real-time fluorescence quantitative PCR, and western blot were used. The results proved that LPS exposure led to ROS explosion, hindered the antioxidant system, promoted the expression of the JAK2 pathway, and increased the expression of genes involved in the pyroptosis pathway, inflammatory factors, and heat shock proteins (HSPs). Upon co-treatment with SeMet and LPS, SeMet reduced LPS-induced pyroptosis and inflammation and restored the expression of HSPs by inhibiting the ROS burst and modulating the antioxidant capacity. Co-treatment with INCB018424 and LPS resulted in inhibited of the JAK2 pathway, attenuating pyroptosis, inflammation, and high expression of HSPs. Thus, LPS induced pyroptosis, inflammation, and changes in HSPs activity by activating of the JAK2 / STAT3 / A20 signaling axis in chicken hearts. Moreover, SeMet has a positive effect on LPS-induced injury. This work further provides a theoretical basis for treating cardiac injury by SeMet.

Dietary selenomethionine reduced oxidative stress by resisting METTL3-mediated m6A methylation level of Nrf2 to ameliorate LPS-induced liver necroptosis in laying hens.

Selenomethionine (SeMet) as the main form of daily dietary selenium, occupies essential roles in providing antioxidant and anti-inflammatory properties, which alleviates inflammatory liver damage. N6-methyladenosine (m6A) is one of the most prevalent and abundant internal transcriptional modifications that regulate gene expression. To investigate the protective mechanism of SeMet on liver injury and the regulatory effect of m6A methylation modification, we established the model by supplementing dietary SeMet, and LPS as stimulus in laying hens. LMH cells were intervened with SeMet (0.075 µM) and/or LPS (60 µg/mL). Subsequently, histopathology and ultrastructure of liver were observed. Western Blot, qRT-PCR, colorimetry, MeRIP-qPCR, fluorescent probe staining and AO/EB were used to detect total m6A methylation level, m6A methylation level of Nrf2, ROS, inflammatory and necroptosis factors. Studies showed that SeMet suppressed LPS-induced upregulation of total m6A methylation levels and METTL3 expression. Interestingly, SeMet reduced the m6A methylation level of Nrf2, activated antioxidant pathways and alleviated oxidative stress. LMH cells were transfected with 50 µm siMETTL3. SeMet/SiMETTL3 reversed the LPS-induced reduction in Nrf2 mRNA stability, slowed down its degradation rate. Moreover, LPS induced oxidative stress, led to necroptosis and activated NF-κB to promote the expression of inflammatory factors. SeMet/SiMETTL3 alleviated LPS-induced necroptosis and inflammation. Altogether, SeMet enhanced antioxidant and anti-inflammatory capacity by reducing METTL3-mediated m6A methylation levels of Nrf2, ultimately alleviating liver damage. Our findings provided new insights and therapeutic target for the practical application of dietary SeMet in the treatment and prevention of liver inflammation, and supplied a reference for comparative medicine.

Selenomethionine Inhibits NF-κB-mediated Inflammatory Responses of Bovine Mammary Epithelial Cells Caused by Klebsiella pneumoniae by Increasing Autophagic Flux.

Klebsiella pneumoniae (K. pneumoniae) is one of the major pathogens causing bovine clinical mastitis. Autophagy maintains cellular homeostasis and resists excessive inflammation in eukaryotic organisms. Selenomethionine (Se-Met) is commonly used as a source of selenium supplementation for dairy cows. This study aimed to investigate the effects of Se-Met on inflammatory responses mediated by nuclear factor-kappa B (NF-κB) through autophagy. We infected bovine mammary epithelial cell line (MAC-T) with K. pneumoniae and examined the expression of autophagy-related proteins and changes in autophagic vesicles, LC3 puncta, and autophagic flux at various intervals. The results showed that K. pneumoniae activated the early-stage autophagy of MAC-T cells. The levels of LC3-II, Beclin1, and ATG5, as well as the number of LC3 puncta and autophagic vesicles, increased after 2 h post-treatment. However, the late-stage autophagic flux was blocked. Furthermore, the effect of autophagy on NF-κB-mediated inflammation was investigated with different autophagy levels. The findings showed that enhanced autophagy inhibited the K. pneumoniae-induced inflammatory responses of MAC-T cells. The opposite results were found with the inhibition of autophagy. Finally, we examined the effect of Se-Met on NF-κB-mediated inflammation based on autophagy. The results indicated that Se-Met alleviated K. pneumoniae-induced autophagic flux blockage, inhibited NF-κB-mediated inflammation, and decreased the adhesion of K. pneumoniae to MAC-T cells. The inhibitory effect of Se-Met on NF-κB-mediated inflammation could be partially blocked by the autophagy inhibitor chloroquine (CQ). Overall, Se-Met attenuated K. pneumoniae-induced NF-κB-mediated inflammatory responses by enhancing autophagic flux.

SeMet alleviates LPS-induced eggshell gland necroptosis mediated inflammation by regulating the Keap1/Nrf2/HO-1 pathway.

Exposure to lipopolysaccharide (LPS) can lead to inflammation in a variety of tissues and organs. Selenium (Se) plays a crucial role in mitigating inflammatory damage. Compared with inorganic selenium, organic selenium, such as selenomethionine (SeMet), has the advantages of a higher absorption rate and lower toxicity in animals. This study examined the protective effects of SeMet on eggshell gland tissue damage caused by LPS. Hy-Line Brown laying hens were chosen as the experimental animals and were randomly assigned to four groups: control group (C), lipopolysaccharide group (LPS), SeMet group (Se), and SeMet + lipopolysaccharide group (Se + LPS). H&E staining and transmission electron microscope were performed to observe the pathological changes of eggshell glands, oxidative stress related indicators were measured using relevant kits, qRT‒PCR and western blotting were used to evaluate the mRNA and protein levels of the Nrf2 pathway, necroptosis, and inflammation related indicators. The results showed that LPS treatment increased the content of malondialdehyde (MDA), decreased the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX), and decreased the content of glutathione (GSH). LPS increased the levels of Keap1, RIPK1, RIPK3, MLKL, TNF-α, COX-2, and NF-κB, while decreasing the levels of HO-1, NQO1, Nrf2, and Caspase-8. However, SeMet treatment effectively reversed the changes of the above indicators, indicating that SeMet alleviates eggshell gland cell necroptosis-mediated inflammation induced by LPS via regulating the Keap1/Nrf2/HO-1 pathway. This study elucidated the mechanism by which SeMet alleviates LPS-induced eggshell gland tissue damage in Hy-Line Brown laying hens and provided a new direction for expanding the application of SeMet in the feeding and production of laying hens.

Selenomethionine alleviates environmental heat stress induced hepatic lipid accumulation and glycogen infiltration of broilers via maintaining mitochondrial and endoplasmic reticulum homeostasis.

With the increasing of global mean surface air temperature, heat stress (HS) induced by extreme high temperature has become a key factor restricting the poultry industry. Liver is the main metabolic organ of broilers, HS induces liver damage and metabolic disorders, which impairs the health of broilers and affects food safety. As an essential trace element for animals, selenium (Se) involves in the formation of antioxidant system, and its biological functions are generally mediated by selenoproteins. However, the mechanism of Se against HS induced liver damage and metabolic disorders in broilers is inadequate. Therefore, we developed the chronic heat stress (CHS) broiler model and investigated the potential protection mechanism of organic Se (selenomethionine, SeMet) on CHS induced liver damage and metabolic disorders. In present study, CHS caused liver oxidative damage, and induced hepatic lipid accumulation and glycogen infiltration of broilers, which are accompanied by mitochondrial dysfunction, abnormal mitochondrial tricarboxylic acid (TCA) cycle and endoplasmic reticulum (ER) stress. Dietary SeMet supplementation increased the hepatic Se concentration and exhibited protective effects via promoting the expression of selenotranscriptome and several key selenoproteins (GPX4, TXNRD2, SELENOK, SELENOM, SELENOS, SELENOT, GPX1, DIO1, SELENOH, SELENOU and SELENOW). These key selenoproteins synergistically improved the antioxidant capacity, and mitigated the mitochondrial dysfunction, abnormal mitochondrial TCA cycle and ER stress, thus recovered the hepatic triglyceride and glycogen concentration. What's more, SeMet supplementation suppressed lipid and glycogen biosynthesis and promoted lipid and glycogen breakdown in liver of broilers exposed to CHS though regulating the AMPK signals. Overall, our present study reveals a potential mechanism that Se alleviates environment HS induced liver damage and glycogen and lipid metabolism disorders in broilers, which provides a preventive and/or treatment measure for environment HS-dependent hepatic metabolic disorders in poultry industry.

Transcriptome-based exploration of potential molecular targets and mechanisms of selenomethionine in alleviating renal ischemia-reperfusion injury.

Renal ischemia-reperfusion injuries (IRIs) are one of the leading causes of acute kidney injuries (AKIs). Selenium, as an essential trace element, is able to antioxidant stress and reduces inflammatory responses. The regulation mechanism of selenomethionine, one of the major forms of selenium intake by humans, is not yet clear in renal IRIs. Therefore, we aimed to explore the key targets and related mechanisms of selenomethionine regulation in renal IRIs and provide new ideas for the treatment of selenomethionine with renal IRIs. We used transcriptome sequencing data from public databases as well as animal experiments to explore the key target genes and related mechanisms regulated by selenomethionine in renal IRI. We found that selenomethionine can effectively alleviate renal IRI by a mechanism that may be achieved by inhibiting the MAPK signaling pathway. Meanwhile, we also found that the key target of selenomethionine regulation in renal IRI might be selenoprotein GPX3 based on the PPI protein interaction network and machine learning. Through a comprehensive analysis of bioinformatic techniques and animal experiments, we found that Gpx3 might serve as a key gene for the regulation of selenomethionine in renal IRIs. Selenomethionine may exert a protective effect against renal IRI by up-regulating GPX3, inhibiting the MAPK signaling pathway, increased production of antioxidants, decreasing inflammation levels, mitigation of apoptosis in renal tubular epithelial cells, this reduces renal histopathological damage and protects renal function. Providing a theoretical basis for the mechanism of selenomethionine actions in renal IRIs.

Selenomethionine Antagonized microRNAs Involved in Apoptosis of Rat Articular Cartilage Induced by T-2 Toxin.

T-2 toxin and selenium deficiency are considered important etiologies of Kashin-Beck disease (KBD), although the exact mechanism is still unclear. To identify differentially expressed microRNAs (DE-miRNAs) in the articular cartilage of rats exposed to T-2 toxin and selenomethionine (SeMet) supplementation, thirty-six 4-week-old Sprague Dawley rats were divided into a control group (gavaged with 4% anhydrous ethanol), a T-2 group (gavaged with 100 ng/g·bw/day T-2 toxin), and a T-2 + SeMet group (gavaged with 100 ng/g·bw/day T-2 toxin and 0.5 mg/kg·bw/day SeMet), respectively. Toluidine blue staining was performed to detect the pathological changes of articular cartilage. Three rats per group were randomly selected for high-throughput sequencing of articular cartilage. Target genes of DE-miRNAs were predicted using miRanda and RNAhybrid databases, and the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway were enriched. The network map of miRNA-target genes was constructed using Cytoscape software. The expression profiles of miRNAs associated with KBD were obtained from the Gene Expression Omnibus database. Additionally, the DE-miRNAs were selected for real-time quantitative PCR (RT-qPCR) verification. Toluidine blue staining demonstrated that T-2 toxin damaged articular cartilage and SeMet effectively alleviated articular cartilage lesions. A total of 50 DE-miRNAs (28 upregulated and 22 downregulated) in the T-2 group vs. the control group, 18 DE-miRNAs (6 upregulated and 12 downregulated) in the T-2 + SeMet group vs. the control group, and 25 DE-miRNAs (5 upregulated and 20 downregulated) in the T-2 + SeMet group vs. the T-2 group were identified. Enrichment analysis showed the target genes of DE-miRNAs were associated with apoptosis, and in the MAPK and TGF-ß signaling pathways in the T-2 group vs. the control group. However, the pathway of apoptosis was not significant in the T-2 + SeMet group vs. the control group. These results indicated that T-2 toxin induced apoptosis, whereas SeMet supplementation antagonized apoptosis. Apoptosis and autophagy occurred simultaneously in the T-2 + SeMet group vs. T-2 group, and autophagy may inhibit apoptosis to protect cartilage. Compared with the GSE186593 dataset, the evidence of miR-133a-3p involved in apoptosis was more abundant. The results of RT-qPCR validation were consistent with RNA sequencing results. Our findings suggested that apoptosis was involved in articular cartilage lesions induced by T-2 toxin, whereas SeMet supplementation antagonized apoptosis, and that miR-133a-3p most probably played a central role in the apoptosis process.

Effect of Organic Selenium on the Homeostasis of Trace Elements, Lipid Peroxidation, and mRNA Expression of Antioxidant Proteins in Mouse Organs.

(1) In this study we determined the effect of long-term selenomethionine administration on the oxidative stress level and changes in antioxidant protein/enzyme activity; mRNA expression; and the levels of iron, zinc, and copper. (2) Experiments were performed on 4-6-week-old BALB/c mice, which were given selenomethionine (0.4 mg Se/kg b.w.) solution for 8 weeks. The element concentration was determined via inductively coupled plasma mass spectrometry. mRNA expression of SelenoP, Cat, and Sod1 was quantified using real-time quantitative reverse transcription. Malondialdehyde content and catalase activity were determined spectrophotometrically. (3) After long-term SeMet administration, the amount of Se increased by 12-fold in mouse blood, 15-fold in the liver, and 42-fold in the brain, as compared to that in the control. Exposure to SeMet decreased amounts of Fe and Cu in blood, but increased Fe and Zn levels in the liver and increased the levels of all examined elements in the brain. Se increased malondialdehyde content in the blood and brain but decreased it in liver. SeMet administration increased the mRNA expression of selenoprotein P, dismutase, and catalase, but decreased catalase activity in brain and liver. (4) Eight-week-long selenomethionine consumption elevated Se levels in the blood, liver, and especially in the brain and disturbed the homeostasis of Fe, Zn, and Cu. Moreover, Se induced lipid peroxidation in the blood and brain, but not in the liver. In response to SeMet exposure, significant up-regulation of the mRNA expression of catalase, superoxide dismutase 1, and selenoprotein P in the brain, and especially in the liver, was determined.

Evaluation of Selenomethionine Entrapped in Nanoparticles for Oral Supplementation Using In Vitro, Ex Vivo and In Vivo Models.

Selenium methionine (SeMet) is an essential micronutrient required for normal body function and is associated with additional health benefits. However, oral administration of SeMet can be challenging due to its purported narrow therapeutic index, low oral bioavailability, and high susceptibility to oxidation. To address these issues, SeMet was entrapped in zein-coated nanoparticles made from chitosan using an ionic gelation formulation. The high stability of both the SeMet and selenomethionine nanoparticles (SeMet-NPs) was established using cultured human intestinal and liver epithelial cells, rat liver homogenates, and rat intestinal homogenates and lumen washes. Minimal cytotoxicity to Caco-2 and HepG2 cells was observed for SeMet and SeMet-NPs. Antioxidant properties of SeMet were revealed using a Reactive Oxygen Species (ROS) assay, based on the observation of a concentration-dependent reduction in the build-up of peroxides, hydroxides and hydroxyl radicals in Caco-2 cells exposed to SeMet (6.25-100 µM). The basal apparent permeability coefficient (Papp) of SeMet across isolated rat jejunal mucosae mounted in Ussing chambers was low, but the Papp was increased when presented in NP. SeMet had minimal effects on the electrogenic ion secretion of rat jejunal and colonic mucosae in Ussing chambers. Intra-jejunal injections of SeMet-NPs to rats yielded increased plasma levels of SeMet after 3 h for the SeMet-NPs compared to free SeMet. Overall, there is potential to further develop SeMet-NPs for oral supplementation due to the increased intestinal permeability, versus free SeMet, and the low potential for toxicity.

Hydroxy-Selenomethionine Mitigated Chronic Heat Stress-Induced Porcine Splenic Damage via Activation of Nrf2/Keap1 Signal and Suppression of NFκb and STAT Signal.

Chronic heat stress (CHS) compromised the immunity and spleen immunological function of pigs, which may associate with antioxidant suppression and splenocyte apoptosis and splenic inflammation. Selenium (Se) exhibited antioxidant function and immunomodulatory through selenoprotein. Thus, this study aimed to investigate the protective effect of dietary hydroxy-selenomethionine (Selisso®, SeO) on chronic heat stress (CHS)-induced porcine splenic oxidative stress, apoptosis and inflammation. Growing pigs were raised in the thermoneutral environment (22 ± 2 °C) with the basal diet (BD), or raised in hyperthermal conditions (33 ± 2 °C) with BD supplied with 0.0, 0.2, 0.4 and 0.6 mg Se/kg SeO for 28 d, respectively. The results showed that dietary SeO supplementation recovered the spleen mass and enhanced the splenic antioxidant capacity of CHS growing pigs. Meanwhile, SeO activated the Nrf2/Keap1 signal, downregulated p38, caspase 3 and Bax, inhibited the activation of NFκb and STAT3, and enhanced the protein expression level of GPX1, GPX3, GPX4, SELENOS and SELENOF. In summary, SeO supplementation mitigates the CHS-induced splenic oxidative damages, apoptosis and inflammation in pigs, and the processes are associated with the activation of Nrf2/Keap1 signal and the suppression of NFκb, p38(MAPK) and STAT signal. It seems that the antioxidant-related selenoproteins (GPXs) and functional selenoproteins (SELENOS and SELENOF) play important roles in the alleviation processes.

Efficacy of feeding hydroxy-selenomethionine on plasma and milk selenium in mid-lactation dairy cows.

In this study, we aimed to determine the amount of Se transferred to milk and blood of mid- to late-lactation dairy cows when supplemental Se from hydroxy-selenomethionine (OH-SeMet) was fed compared with an unsupplemented group and a group supplemented with a seleno-yeast (SY). Twenty-four lactating Holstein cows (178 ± 43 d in milk) were used in a complete randomized block design for 91 d (7-d covariate period and 84-d treatment period). Treatments were (1) basal diet with an analyzed Se background of 0.2 mg of Se per kg as-fed (control); (2) basal diet + 0.3 mg of Se/kg as-fed from SY (SY-0.3); (3) basal diet + 0.1 mg of Se/kg as-fed from OH-SeMet (OH-SeMet-0.1); and (4) basal diet + 0.3 mg of Se/kg as-fed from OH-SeMet (OH-SeMet-0.3). During the trial, plasma and milk were analyzed for total Se, and plasma was analyzed for glutathione peroxidase activity. The mean plasma and milk Se concentrations exhibited the same relationship, where OH-SeMet-0.3 resulted in the highest values (142 µg/L of plasma and 104 µg/kg of milk), followed by SY-0.3 (134 µg/L and 85 µg/kg), OH-SeMet-0.1 (122 µg/L and 67 µg/kg), and the control group had the lowest values (120 µg/L and 50 µg/kg). The increment of Se in milk induced by OH-SeMet-0.3 (+54 µg/kg) was 54% higher than that induced by SY-0.3 (+35 µg/kg). Additionally, dietary supplementation of 0.2 mg/kg Se from OH-SeMet in the total mixed ration was estimated to be similar to 0.3 mg/kg Se from SY in the total mixed ration when considering the level of Se in the milk. There was no difference in plasma glutathione peroxidase activity between groups; however, OH-SeMet-0.3 significantly decreased somatic cell count. The results confirmed that supplementation with organic Se increases milk and plasma Se concentrations. Moreover, when administered at the same level of supplementation, OH-SeMet was shown to be more efficient than SY in improving milk quality by increasing Se content and decreasing milk somatic cell count.

L-selenomethionine affects liver development and glucolipid metabolism by inhibiting autophagy in zebrafish embryos.

Selenium plays a vital role in cancer prevention, antioxidation, and the growth of humans and other vertebrates. Excessive selenium can cause liver injury and metabolic disorders, which can lead to hepatic disease, but few studies have shown the effects of excessive selenium on liver development and its mechanism in zebrafish embryos. In this study, liver development and glucolipid metabolism were investigated in selenium-stressed zebrafish embryos. Under selenium treatment, transgenic fabp10a-eGFP zebrafish embryos showed reduced liver size, and wild-type zebrafish embryos exhibited steatosis and altered lipid metabolism-related indexes and glucose metabolism-related enzyme activities. In addition, selenium-stressed embryos exhibited damaged mitochondria and inhibited autophagy in the liver. An autophagy inducer (rapamycin) alleviated selenium-induced liver injury and restored the expression of some genes related to liver development and glucolipid metabolism. In summary, our research evaluated liver developmental toxicity and metabolic disorders under selenium stress, and confirmed that autophagy and oxidative stress might involve in the selenium-induced hepatic defects.

Antitumor effect of selenium-rich Brazil nuts and selenomethionine dietary supplementation on pre-existing 4T1 mammary tumor growth in mice.

Selenium (Se) is an essential micronutrient known to play an important role in the antioxidant system that can potentially influence tumor growth. We aimed to investigate the effects of dietary Se supplementation after detection of 4T1 mammary tumor growth in BALB/c mice. Thirty female mice received subcutaneous inoculation of 4T1 cells. After five days, all animals presenting palpable tumors were randomly assigned to three groups: a control group (Se-control) receiving a diet with adequate Se (0.15 mg/kg) and two other groups that received Se-supplemented diets (1.4 mg/kg of total Se) with either Brazilian nuts (Se-Nuts) or selenomethionine (SeMet). Data were assessed by either One or Two-way ANOVA followed by Tukey's HSD or Bonferroni's post hoc tests, respectively. Both Se-supplemented diets reduced tumor volume from the thirteenth day of feeding compared with the Se-adequate (control) diet (p < 0.05). The SeMet group presented a higher Se blood concentration (p < 0.05) than the Se-control group, with the Se-Nuts group presenting intermediate values. Selenoprotein P gene expression in the liver was higher in the Se-Nuts group than in the Se-control group (p < 0.05), while the SeMet group presented intermediate expression. Dietary Se supplementation, starting after detection of 4T1 palpable lesions, reduced tumor volume in mice.

Dietary selenium supplementation alleviates low salinity stress in the Pacific white shrimp Litopenaeus vannamei: growth, antioxidative capacity and hepatopancreas transcriptomic responses.

Se is an essential trace element associated with animal growth and antioxidant and metabolic processes. However, whether Se, especially organic Se with higher bioavailability, can alleviate the adverse effects of low salinity stress on marine economic crustacean species has not been investigated. Accordingly, juvenile Pacific white shrimp (Litopenaeus vannamei) were reared in two culture conditions (low and standard salinity) fed diets supplemented with increasing levels of l-selenomethionine (0·41, 0·84 and 1·14 mg/kg Se) for 56 d, resulting in four treatments: 0·41 mg/kg under standard seawater (salinity 31) and 0·41, 0·84 and 1·14 mg/kg Se under low salinity (salinity 3). The diet containing 0·84 mg/kg Se significantly improved the survival and weight gain of shrimp under low salinity stress and enhanced the antioxidant capacity of the hepatopancreas. The increased numbers of B and R cells may be a passive change in hepatopancreas histology in the 1·14 mg/kg Se group. Transcriptomic analysis found that l-selenomethionine was involved in the regulatory pathways of energy metabolism, retinol metabolism and steroid hormones. In conclusion, dietary supplementation with 0·84 mg/kg Se (twice the recommended level) effectively alleviated the effects of low salinity stress on L. vannamei by regulating antioxidant capacity, hormone regulation and energy metabolism.

Effect of Supranutritional Dosage Selenium in Neonatal Goat Kids on Productive Performance, Physicochemical Profiles in Meat, Selenium Levels in Tissues, and Histopathological Findings.

Selenium (Se) is an essential element and antioxidant that catalyzes the destruction of hydrogen peroxide formed during cellular oxidative metabolism. Doses of Se as selenomethionine (SeMe) by oral route are 0.1-0.3 mgSe/kg DM, while the dose by parenteral route with sodium selenite (Na2SeO3) is 0.1 mgSe/BW. The effects of supranutritional Se supplementation on normal kids have rarely been studied. The objective of the study was to evaluate both Se sources on growth performance, Se in tissues, histopathological findings, and meat characteristics. Forty-five kids of the Pastoreña breed with 25-day age were distributed (4.7 ± 1.13 kg) in three treatments: a) control group, C: consumption with goat milk (GM: containing 0.135 mgSe/g); b) NaSe: GM plus Na2SeO3 injectable, 0.25 mgSe/kg BW; c) SeMe: GM plus oral dosage, 0.3 mgSe as SeMe daily. Fifteen animals per treatment were slaughtered at 7, 14, and 21 days. Feed conversion improved (P < 0.05) with Se supplement (P < 0.05) at 7 and 14 days. SeMe had higher protein and fat meat content (P < 0.05). SeMe increased Se liver at 14 and 21 days. NaSe and SeMe had higher (P < 0.05) levels of Se kidney. SeMe-21d showed 42% mononuclear and periportal cell infiltration lesions. In conclusion, Se administered through milk in goat kids was insufficient to prevent nutritional muscular dystrophy. The supranutritional dose of 0.25 mg/kg as NaSe was sufficient to maintain the Se level in tissues. SeMe increased Se liver and kidney efficiently. Both Se sources improved the bioavailability of the mineral in kids.

Organic Selenium Alleviates Ammonia-Mediated Abnormal Autophagy by Regulating Inflammatory Pathways and the Keap1/Nrf2 Axis in the Hypothalamus of Finishing Pigs.

Ammonia is a significant pollutant in the livestock houses and the atmospheric environment, and excessive ammonia would harm the health of livestock and breeders. Previous studies have shown that ammonia exposure could damage the tissue structure of the nervous system, but the molecular mechanism of ammonia-induced hypothalamus damage was still unclear. The purpose of this study was to determine the role of excessive ammonia in abnormal autophagy of pig hypothalamus and whether selenomethionine would have a mitigating effect on ammonia toxicity. Twenty-four 18-week pigs were randomly divided into four groups: the control group (C group), the selenium group (Se group), the ammonia + selenium group (A + Se group), and the ammonia group (A group). In our study, the expression levels of NF-κB, IL-1ß, iNOS, TNF-α, IKK-α, p-IKK-α, Nrf2, ATG5, ATG 10, ATG 12, LC3 I/II, HSP60, HSP70, and HSP90 were increased after ammonia exposure; meanwhile, IFN-γ, IKB-α, p-IKB-α, Keap1, P62, mTOR, AKT, p-AKT, PI3K, SQSTM, and Beclin1 showed decreasing trends. The results indicated that excessive ammonia inhalation inhibited the AKT/mTOR pathway to acclerated autophagy through oxidative stress-mediated inflammation in the porcine hypothalamus. L-selenomethionine could alleviate hypothalamus injury induced by ammonia exposure.

Selenium Mitigates Ammonia-Induced Neurotoxicity by Suppressing Apoptosis, Immune Imbalance, and Gut Microbiota-Driven Metabolic Disturbance in Fattening Pigs.

Ammonia could be regarded as one detrimental pollutant with an acrid smell in livestock sheds. So far, the pig breeding industry became the main source of atmospheric ammonia. Previous literature demonstrated that excessive ammonia inhalation might cause a series of physiological damage to multiple organs. Unfortunately, the toxicity mechanisms of gaseous ammonia to the porcine nervous system need further research to elucidate. Selenium (Se) involves in many essential physiological processes and has a mitigative effect on the exogenous toxicant. There were scant references that corroborated whether organic Se could intervene in the underlying toxicity of ammonia to the hypothalamus. In the present study, multi-omics tools, ethology, and molecular biological techniques were performed to clarify the detailed mechanisms of relaxation effects of L-selenomethionine on ammonia poisoning. Our results showed that ammonia inhalation caused the clinical symptoms and the increment of positive apoptosis rate in the hypothalamus with the dysfunction of mitochondrial dynamics factors, while obvious mitochondria structure defects were observed. In parallel, the inflammation medium levels and gut microbes-driven metabolism function were altered to mediate the neurotoxicity in fattening pigs through the initiation of inflammation development. Interestingly, L-selenomethionine could attenuate ammonia toxicity by activating the PI3K/Akt/PPAR-γ pathway to inhibit the mitochondria-mediated apoptosis process, blocking the abnormal immune response and the accumulation of reactive oxygen species in the nucleus. Meanwhile, Se could enhance the production performance of fattening sows. Taken together, our study verified the novel hypothesis for the toxicity identification of aerial ammonia and provided a therapeutic strategy for the treatment of occupational poisoning.

Selenium Speciation Analysis Reveals Improved Antioxidant Status in Finisher Pigs Fed L-Selenomethionine, Alone or Combined with Sodium Selenite, and Vitamin E.

Conditions associated with selenium (Se) and/or vitamin E (VitE) deficiency are still being reported in high-yielding pigs fed the recommended amounts. Here, the dietary effects of Se source (sodium selenite, NaSe, 0.40 or 0.65 mg Se/kg; L-selenomethionine, SeMet, 0.19 or 0.44 mg Se/kg; a NaSe-SeMet mixture, SeMix, 0.44-0.46 mg Se/kg) and VitE concentration (27, 50-53 or 101 mg/kg) on the antioxidant status of finisher pigs were compared with those in pigs fed non-Se-supplemented diets (0.08-0.09 mg Se/kg). Compared to NaSe-enriched diets, SeMet-supplemented diets resulted in significantly (p < 0.0018) higher plasma concentrations of total Se (14-27%) and selenospecies (GPx3, SelP, SeAlb; 7-83%), significantly increased the total Se accumulation in skeletal muscles, myocardium, liver and brain (10-650%), and enhanced the VitE levels in plasma (15-74%) and tissues (8-33%) by the end of the 80-day trial, proving better Se distribution and retention in pigs fed organic Se. Injecting lipopolysaccharide (LPS) intravenously half-way into the trial provoked a pyrogenic response in the pigs followed by a rapid increase of inorganic Se after 5-12 h, a drastic drop of SeMet levels between 12 and 24 h that recovered by 48 h, and a small increase of SeCys by 24-48 h, together with a gradual rise of GPx3, SelP and SeAlb in plasma up to 48 h. These changes in Se speciation in plasma were particularly significant (0.0024 > p > 0.00007) in pigs receiving SeMet- (0.44 mg Se/kg, above EU-legislated limits) or SeMix-supplemented (SeMet and NaSe both at 0.2 mg Se/kg, within EU-legislated limits) diets, which demonstrates Se metabolism upregulation to counteract the LPS-induced oxidative stress and a strengthened antioxidant capacity in these pigs. Overall, a Se source combination (without exceeding EU-legislated limits) and sufficient VitE supplementation (≥ 50 mg/kg) improved the pigs' antioxidant status, while doubling the allowed dietary organic Se increased the Se in tissues up to sixfold without compromising the animal's health due to toxicity. This study renders valuable results for revising the current dietary SeMet limits in swine rations.