Protecting spring wheat plants using selenium and pesticides.

The research was carried out in order to find ways to optimize the system of protection of spring wheat crops. In the conducted studies, the effect of combinations of sodium selenite and various pesticides, differing in the specifics of action and biological activity, on the yield and quality of spring wheat of the Yubileinaya 80 variety was studied. Currently, there is a need to achieve a sufficient effect of the action of chemical plant protection products and to obtain a minimum impact on human health and the environment. The purpose of the research is to study the influence of various combinations of chemical plant protection products and methods of using sodium selenite on the yield and grain quality indicators of spring wheat variety Yubileinaya 80. The studies were carried out under the conditions of a vegetative experiment with spring wheat variety Yubileinaya 80. Two methods of using sodium selenite and chemical plant protection agents of different specifics of action were studied: fungicide, herbicide, and insecticide, which were applied in different combinations and at different times. As a result of the studies, the phytotoxicity of the studied preparations of chemical plant protection was revealed, which apparently manifests itself as a result of inhibition of the morphometric indicators of the growth of the root system and vegetative organs of wheat plants, resulting in a violation of the processes of accumulation of assimilates and their outflow to the reproductive organs. Optimal combinations of pesticides and sodium selenite have been established, allowing to obtain reliable changes in yield and quality indicators of wheat grain. It was revealed that the use of selenium treatment before sowing seeds contributed to a decrease in the phytotoxicity of the studied pesticides, as a result of stimulating the processes of absorption by plants and the redistribution of nitrogen to the reproductive organs of wheat, which had a positive effect not only on the yield and quality of spring wheat of the Yubileynaya 80 variety, but also on the external surface microstructure of the fruit shell of the grain. The noted features of the surface of the fruit shell of the grain will reduce losses during grain processing and obtain processed products from such grain of higher quality.

A study on the effectiveness of sodium selenite in treating cadmium and perfluoro octane sulfonic (PFOS) poisoned zebrafish (Danio rerio).

Perfluoro octane sulfonate (PFOS) and cadmium (Cd) are toxic elements in the environment. As a micronutrient trace element, selenium (Se) can mitigate the adverse effects induced by PFOS and Cd. However, few studies have examined the correlation between Se, PFOS and Cd in fish. The present study focused on the antagonistic effects of Se on PFOS+Cd-induced accumulation in the liver of zebrafish. The fish was exposed to PFOS (0.08mg/L), Cd (1mg/L), PFOS+ Cd (0.08 mg/L PFOS+1 mg/L Cd), L-Se (0.07mg/L Sodium selenite +0.08mg/L PFOS+1mg/L Cd), M-Se (0.35mg/L Sodium selenite + 0.08mg/L PFOS+ 1 mg/L Cd), H-Se (1.75 mg/L Sodium selenite + 0.08 mg/L PFOS+ 1mg/L Cd) for 14d. The addition of selenium to fish exposed to PFOS and Cd has been found to have significant positive effects. Specifically, selenium treatments can alleviate the adverse effects of PFOS and Cd on fish growth, with a 23.10% improvement observed with the addition of T6 compared to T4. In addition, selenium can alleviate the negative effects of PFOS and Cd on antioxidant enzymes in zebrafish liver, thus reducing the liver toxicity caused by PFOS and Cd. Overall, the supplementation of selenium can reduce the health risks to fish and mitigate the injuries caused by PFOS and Cd in zebrafish.

Comparison of Sodium Selenite and Selenium-Enriched Spirulina Supplementation Effects After Selenium Deficiency on Growth, Tissue Selenium Concentrations, Antioxidant Activities, and Selenoprotein Expression in Rats.

Selenium contributes to physiological functions through its incorporation into selenoproteins. It is involved in oxidative stress defense. A selenium deficiency results in the onset or aggravation of pathologies. Following a deficiency, the repletion of selenium leads to a selenoprotein expression hierarchy misunderstood. Moreover, spirulina, a microalga, exhibits antioxidant properties and can be enriched in selenium.. Our objective was to determine the effects of a sodium selenite or selenium-enriched spirulina supplementation. Thirty-two female Wistar rats were fed for 12 weeks with a selenium-deficient diet. After 8 weeks, rats were divided into 4 groups and were fed with water, sodium selenite (20 µg Se/kg body weight), spirulina (3 g/kg bw), or selenium-enriched spirulina (20 µg Se/kg bw + 3 g spirulina/kg bw). Another group of 8 rats was fed with normal diet during 12 weeks. Selenium concentration and antioxidant enzyme activities were measured in plasma, urine, liver, brain, kidney, heart, and soleus. Expression of GPx (1, 3), Sel (P, S, T, W), SEPHS2, TrxR1, ApoER2, and megalin were quantified in liver, kidney, brain, and heart. We showed that a selenium deficiency leads to a growth delay, reversed by selenium supplementation despite a minor loss of weight in week 12 for SS rats. All tissues displayed a decrease in selenium concentration following deficiency. The brain seemed protected. We demonstrated a hierarchy in selenium distribution and selenoprotein expression. A supplementation of sodium selenite improved GPx activities and selenoprotein expression while a selenium-enriched spirulina was more effective to restore selenium concentration especially in the liver, kidney, and soleus.

Transcriptomic characterization of interactions between sodium selenite and coenzyme Q10 on preventing cadmium-induced testicular defects.

The effect of heavy metal cadmium (Cd) on testicular function is recognized. However, the mechanism involved is not well-established. In the present study, we analyzed the testicular transcriptomic changes induced by acute Cd exposure of adult rats with and without supplementation of antioxidants selenium (Se) and/or coenzyme Q10 (CoQ). Cd significantly decreased serum testosterone and two steroidogenic proteins SCARB1 and STAR. RNA-Seq analyses of testicular RNAs revealed specific activation of oxidative stress-, inflammation-, MAPK- and NF-κB-related signaling molecules. In addition, Cd treatment down-regulated gene for I, III and IV complexes of mitochondrial electron transport chain and up-regulated genes for NADPH-oxidase, major cascade in ROS production. The decrease in steroidogenesis and increase in inflammation may result from oxidative stress since supplementation of Se and CoQ, but not with either alone, almost completely prevented these changes, including overall alterations in transcriptome. Cd exposure induced total of 1192 differentially expressed genes (DEGs), which was reduced to 29 without considering confounding factors associated with Se/CoQ, a 97.6% protection rate. In conclusion, Cd exposure inhibited Leydig cell steroidogenesis by down-regulating SCARB1 and STAR through increasing oxidative stress and inflammation, but Se plus CoQ synergistically prevented all the changes induced by the Cd exposure.

Sodium selenite (Na2SeO3) attenuates T-2 toxin-induced iron death in LMH cells through the ROS/PI3K/AKT/Nrf2 pathway.

T-2 toxin, is a monotrichous mycotoxin commonly found in animal feed and agricultural products that can damage tissues and organs through oxidative stress. Selenium is a trace element with favorable antioxidant effects. However, it is unclear whether T-2 toxin-induces ferroptosis in LMH cells and whether Na2SeO3 has a protective role in this process. To investigate the process of hepatic injury by T-2 toxin and its antagonistic effect by Na2SeO3, we used 20 ng/mL T-2 toxin as well as 160 nmol/L Na2SeO3 to treat the LMH cells. The results demonstrated that exposure to the T-2 toxin induced iron death by increasing the quantity of ROS, leading to oxidative damage, decreasing the quantities of SOD, GPx, and T-AOC, and increasing the accumulation of MDA and H2O2, which resulted in the accumulation of Fe2+ and the down-regulation of the manifestation of linked genes and proteins including FTH1, Gpx4, NQO-1, and HO-1. After the addition of Na2SeO3, the PI3K/AKT/Nrf2 pathway is activated by regulating the selenoproteins gene level, and the above abnormal changes are reversed. In summary, Na2SeO3 alleviated T-2 toxin-induced iron death via the PI3K/AKT/Nrf2 pathway. These study not only broaden the cytotoxic knowledge regarding T-2 toxin, but also serve as a foundation for the use of Na2SeO3 in daily life.

Sodium selenite preserves rBM-MSCs' stemness, differentiation potential, and immunophenotype and protects them against oxidative stress via activation of the Nrf2 signaling pathway.

BACKGROUND: The physiological level of reactive oxygen species (ROS) is necessary for many cellular functions. However, during the in-vitro manipulations, cells face a high level of ROS, leading to reduced cell quality. Preventing this abnormal ROS level is a challenging task. Hence, here we evaluated the effect of sodium selenite supplementation on the antioxidant potential, stemness capacity, and differentiation of rat-derived Bone Marrow MSCs (rBM-MSCs) and planned to check our hypothesis on the molecular pathways and networks linked to sodium selenite's antioxidant properties. METHODS: MTT assay was used to assess the rBM-MSCs cells' viability following sodium selenite supplementation (concentrations of: 0.001, 0.01, 0.1, 1, 10 µM). The expression level of OCT-4, NANOG, and SIRT1 was explored using qPCR. The adipocyte differentiation capacity of MSCs was checked after Sodium Selenite treatment. The DCFH-DA assay was used to determine intracellular ROS levels. Sodium selenite-related expression of HIF-1α, GPX, SOD, TrxR, p-AKT, Nrf2, and p38 markers was determined using western blot. Significant findings were investigated by the String tool to picture the probable molecular network. RESULTS: Media supplemented with 0.1 µM sodium selenite helped to preserve rBM-MSCs multipotency and keep their surface markers presentation; this also reduced the ROS level and improved the rBM-MSCs' antioxidant and stemness capacity. We observed enhanced viability and reduced senescence for rBM-MSCs. Moreover, sodium selenite helped in rBM-MSCs cytoprotection by regulating the expression of HIF-1 of AKT, Nrf2, SOD, GPX, and TrxR markers. CONCLUSIONS: We showed that sodium selenite could help protect MSCs during in-vitro manipulations, probably via the Nrf2 pathway.

Transcriptome analysis reveals different mechanisms of selenite and selenate regulation of cadmium translocation in Brassica rapa.

Selenium (Se) inhibits cadmium (Cd) root-to-shoot translocation and accumulation in the shoots of pak choi; however, the mechanism by which Se regulates Cd retention in roots is still poorly understood. A time-dependent hydroponic experiment was conducted to compare the effects of selenite and selenate on Cd translocation and retention in the roots. The underlying mechanisms were investigated regarding Se biotransformation and metal transportation in roots using HPLC and transcriptome analyses. Selenite showed reducing effects on Cd translocation and accumulation in shoots earlier than selenate. Selenite is mainly biotransformed into selenomethionine (80% of total Se in roots) at 72 h, while SeO42- was the dominant species in the selenate treatments (68% in shoots). Selenite up-regulated genes involved in the biosynthesis of lignin, suberin, and phytochelatins and those involved in stress signaling, thereby helping to retain Cd in the roots, whereas essentially, selenate had opposite effects and impaired the symplastic and apoplastic retention of Cd. These results suggest that cell-wall reinforcement and Cd retention in roots may be the key processes by which Se regulates Cd accumulation, and faster biotransformation into organic seleno-compounds could lead to earlier effects.

Sodium Selenite Modulates Global Activation of Proinflammatory M1-like Macrophages, Necroinflammation and M1-like/M2-like Dichotomy at the Onset of Human Type 1 Diabetes.

AIM: The study aims to show that sodium selenite (Ss) would have an immunomodulatory effect on the functional activity of proinflammatory macrophages (Mφs) during their extended extracellular activation at the onset of human type 1 diabetes (T1D). BACKGROUND: Exacerbated activation of proinflammatory "M1" macrophages (Mφs) can promote chronic local pancreatic islet inflammation and T1D development. OBJECTIVE: We investigated the ex vivo effects of Ss on the immune modulation of global/extended activation of human proinflammatory M1-like Mφs. METHODS: Experiments were carried out on primary monocytes-derived Mφs (MDMs). RESULTS: The levels of IL-1ß, TNF-α, H2O2 and intracellular free calcium ions (ifCa2+), and the ratios of IL-1ß-to-IL-10 and TNF-α-to-IL-10 were markedly increased in T1D Mφs than in healthy control Mφs. Conversely, both IL-10 production and arginase 1 (ARG1) activity were downregulated in T1D Mφs. Additionally, Ss treatment induced a marked downregulation of respiratory burst, ifCa2+ levels, M1-like Mφ-associated inducible nitric oxide (NO) synthase (iNOS) activity, cell necrosis and related necroinflammation biomarkers, including IL-1ß and TNF-α, CD14 expression, and the ratios of iNOS-to-ARG1, IL-1ß-to-IL-10, and TNF-α-to-IL-10. Moreover, Ss upregulated anti-inflammatory "M2-like" Mφ activity as demonstrated by ARG1 activity and IL-10 production, as well as phagocytosis capacity. CONCLUSION: Ss exerts a potent immunomodulatory role on functional activities of human proinflammatory T1D M1-like Mφs subjected to extended activation, as well as on the M1-like/M2-like dichotomy. Additionally, the current study provides a novel therapeutic approach using Ss to promote the anti-inflammatory function of Mφs at the onset of T1D.

High-Dose Selenium Induces Ferroptotic Cell Death in Ovarian Cancer.

Selenium is a promising multi-target chemotherapeutic agent with controversial clinical results. Hence, reassessing the anticancer effects of Se is necessary to clearly understand the potential of high-dose selenium in cancer treatment. Here, we observed that high-dose sodium selenite (SS) significantly decreased the proliferation and increased the death of ovarian cancer cells, mediated by an increased generation of reactive oxygen species. Notably, high-dose SS decreased the levels of glutathione peroxidase (GPx), a selenoprotein with antioxidant properties, without altering other selenoproteins. Furthermore, high-dose SS triggered lipid peroxidation and ferroptosis, a type of iron-dependent cell death, due to dysregulated GPx4 pathways. We demonstrated that intravenous high-dose SS significantly reduced the tumor growth and weight in SKOV3-bearing mice. Consistent with our in vitro results, mice with SKOV3 cells treated with high-dose SS showed decreased GPx4 expression in tumors. Therefore, we highlight the significance of high-dose SS as a potential chemotherapeutic agent for ovarian cancer. High-dose SS-mediated ferroptotic therapy integrating glutathione depletion and ROS generation is a promising strategy for cancer therapy.

Antioxidants supplementation improves the quality of in vitro produced ovine embryos with amendments in key development gene expressions.

The present study assessed the effects of supplementation of different antioxidants on oocyte maturation, embryo production, reactive oxygen species (ROS) production and expression of key developmental genes. In this study, using ovine as an animal model, we tested the hypothesis that antioxidant supplementation enhanced the developmental competence of oocytes. Ovine oocytes aspirated from local abattoir-derived ovaries were subjected to IVM with different concentrations of antioxidants [(Melatonin, Ascorbic acid (Vit C), alpha-tocopherol (Vit E), Sodium selenite (SS)]. Oocytes matured without any antioxidant supplementation were used as controls. The oocytes were assessed for maturation rates and ROS levels. Further, embryo production rates in terms of cleavage, blastocysts and total cell numbers were evaluated after performing in vitro fertilization. Real-Time PCR analysis was used to evaluate the expression of stress related gene (SOD-1), growth related (GDF-9, BMP-15), and apoptosis-related genes (BCL-2 and BAX). We observed that maturation rates were significantly higher in alpha-tocopherol (100 µM; 92.4%) groups followed by melatonin (30 µM; 89.1%) group. However, blastocyst rates in ascorbic acid (100 µM; 19.5%), melatonin (30 µM; 18.4%), alpha-tocopherol (100 µM; 18.2%), and sodium selenite (20 µM; 16.9%) groups were significantly higher (P 0.05) than that observed in the control groups. Total cell numbers in blastocysts in the melatonin, ascorbic acid and alpha-tocopherol groups were significantly higher than those observed in sodium selenite and control groups. ROS production was reduced in groups treated with melatonin (30 µM), vitamin C (100 µM), sodium selenite (20 µM) and α-tocopherol (200 µM) compared with that observed in the control group. Supplementation of antioxidants caused the alterations in mRNA expression of growth, stress, and apoptosis related gene expression in matured oocytes. The results recommend that antioxidants alpha-tocopherol (200 µM), sodium selenite (40 µM), melatonin (30 µM) and ascorbic acid (100 µM) during IVM reduced the oxidative stress by decreasing ROS levels in oocytes, thus improving embryo quantity and quality.

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.

Sodium selenite inhibits cervical cancer growth via ROS mediated AMPK/FOXO3a /GADD45a axis.

Selenium is a trace element that has been shown to inhibit the growth of various cancer cell types. However, its role in cervical cancer and its underlying mechanisms remains largely unknown. Herein, we explored the anti-cervical cancer effect of selenium and its potential mechanisms through xenograft and in vitro experiments. HeLa cell xenografts in female nude mice showed tumor growth retardation, with no obvious liver and kidney toxicity, after being intraperitoneally injected with 3 mg/kg sodium selenite (SS) for 14 days. Compared to the control group, selenium levels in the tumor tissue increased significantly after SS treatment. In vitro experiments, SS inhibited the viability of HeLa and SiHa cells, blocked the cell cycle at the S phase, and enhanced apoptosis. RNA-sequencing, Kyoto encyclopedia of genes and genomes pathway analysis showed that forkhead box protein O (FOXO) was a key regulatory signaling pathway for SS to exhibit anticancer effects. Gene Ontology analysis filtered multiple terms associated with apoptosis, anti-proliferation, and cell cycle arrest. Further research revealed that SS increased intracellular reactive oxygen species (ROS) and impaired mitochondrial function, which activated adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) via phosphorylation at Thr172, resulting in activation of FOXO3a and its downstream growth arrest and DNA damage-inducible alpha (GADD45a). In summary, SS exhibited anti-cervical cancer effects, and their mechanisms may be that SS is involved in inducing cell cycle arrest and potentiating cell apoptosis caused by ROS-dependent activation of the AMPK/FOXO3a/GADD45a axis.

Biochemical and molecular assessment of selenium forms for the alleviation of oxidative stress in senescent human fibroblasts.

Selenium enhances the cellular antioxidant capacity and alleviates oxidative stress. We investigated the transcriptional and enzymatic activities of selenium-dependent glutathione peroxidase 1 and thioredoxin reductase 1 (TrxR1), and levels of glutathione, hydrogen peroxide, lipid peroxides, and protein carbonyls in primary passage 5 (P5) and senescent passage 25 (P25) and 30 (P30) fibroblasts. Cells were incubated in either standard Dulbecco growth medium (CM1) containing normal plasma selenium levels (0.8 µmol/l), or in CM2, CM3, and CM4 containing 3 µmol/l (5 µmol/l for TrxR1) sodium selenite, L-hydroxyselenomethionine, or Se-methylselenocysteine, respectively. Gene transcripts and activities of both investigated enzymes as well as the levels of reduced glutathione were significantly increased in CM2-, CM3-, and CM4-incubated senescent P25 and P35 cells compared against those incubated in CM1. In congruence, although all oxidative stress parameters including oxidized glutathione were significantly lower in CM2-, CM3-, and CM4-incubated senescent cells compared against those incubated in CM1, such reductions were of significantly higher magnitude in CM3 and CM4 cells compared against those in CM2. In conclusion, organic L-hydroxyselenomethionine and Se-methylselenocysteine are equally more potent at alleviating oxidative stress in senescent cells than inorganic sodium selenite, and thus could be beneficial for use in elderly subjects and those with oxidative stress-associated disease.

Sodium selenite inhibits proliferation and metastasis through ROS-mediated NF-κB signaling in renal cell carcinoma.

BACKGROUND: Sodium selenite (SSE) has been reported to exert anti-tumor effects in several cancer cells. However, the underlying mechanisms in renal cancer are yet to be elucidated. The effects of SSE on the proliferation, metastasis, and apoptosis of renal cancer cells, as well as its mechanism, were investigated in this study. METHODS: ACHN and 786-O renal cancer cells were treated with different concentrations of SSE, MTT, and colony formation assays were used to detect the proliferation ability of cells. The migration of cells was detected using scratch-wound-healing and transwell-migration assays. The effect of SSE on apoptosis was assessed by AnnexinV-FITC/PI double staining. Besides, Western blotting was employed to detect the protein-expression level and elucidate the underlying pathways. We also made subcutaneous xenografts in athymic mice to verify the effect of SSE on tumor growth in vivo. RESULTS: Our results demonstrated that treatment with SSE resulted in significant inhibition of cell proliferation and migration. Flow cytometry and Western blot confirmed that SSE induced apoptosis via the endogenous apoptotic pathway. We also confirmed that SSE treatment causes an increase in intracellular reactive oxygen species (ROS) levels, resulting in the inhibition of nuclear transcription factor-κB (NF-κB) signaling. Modulation of the ROS level by the chemical inhibitor N-acetyl-cysteine reversed the effect of SSE on cells. Similarly, subcutaneous xenografts in athymic mice models showed that SSE inhibits tumor growth in vivo. CONCLUSION: These results indicate that SSE inhibits proliferation and migration and induces apoptosis via ROS mediated inhibition of NF-κB signaling in renal cancer cells.

Preparation, characteristic and anti-inflammatory effect of selenium nanoparticle-enriched probiotic strain Enterococcus durans A8-1.

BACKGROUND: Elemental selenium, a new type of selenium supplement, can be biosynthesized via microorganisms. This study is to characterize a patent probiotic bacteria Enterococcus durans A8-1, capable of reducing selenite (Se6+ or Se4+) to elemental selenium (Se0) with the formation of Se nanoparticles (SeNPs). METHODS: The selenium nanoparticles synthesized from A8-1 were characterized using scanning electron microscopy (SEM), transmission electron microscopy (TEM), energy dispersive spectroscopy (EDS), and X-ray photoelectron energy (XPS). The Caco2 cells were used to investigate the effects of Se-enriched A8-1 on the viability, membrane integrity, and the regulation of cellular inflammation through MTT and ELISA assays. The selenium-enriched metabolic function of A8-1 was analyzed by transcriptome sequencing. RESULTS: E. durans A8-1 has the ability to synthesize intracellular SeNPs that are incubated with 60 mg/L sodium selenite for 18 h at 37 °C with 7 % inoculum under aerobic conditions. The selenium-enriched transformation rate increased to 43.46 %. After selenium enrichment, there were no significant morphological changes in E. durans A8-1 cells. The cells also exhibited no cytotoxicity when incubated with Caco-2 cells, and increased cellular proliferation. Furthermore, Se-enriched A8-1 cells antagonize the adhesion of S. typhimurium ATCC14028 onto the surface of Caco-2 cells protecting cell membrane integrity and was assessed by measuring LDH and AKP activities (P <0.001, P <0.001). Moreover, Se-enriched A8-1 could protect Caco-2 cells from inflammation induced by lipopolysaccharide and help the cells alleviate the inflammation through the reduced expression of cytokine IL-8 (P = 0.0012, P <0.001) and TNF-α (P <0.001, P <0.001). Based on transcriptome sequencing in Se-enriched E. durans A8-1 cells, there were 485 up-regulated genes and 322 down-regulated genes (Padj < 0.05). There were 19 predicted up-regulated genes that are highly related to the potential selenium metabolism pathway, which focuses on the transportation of Na2SeO3 by membrane proteins, and gradually reduces Na2SeO3 to elemental selenium aggregates that are deposited onto the membrane surface via the intracellular redox response. CONCLUSION: E. durans A8-1 could convert extracellular selenite into intracellular biological SeNPs via redox pathway with strong selenium-rich metabolism, and its biological SeNPs have anti-inflammatory properties, which have the potential for the development of composite selenium nanomaterials and can be further studied for the function of SeNPs with potential applications.

The protective effect of pomegranate peel aqueous extract on selenite-induced cataract in rats.

The present study was performed to evaluate the preventive effect of pomegranate peel extract on sodium-induced cataract in rats. Sprague-Dawley suckling male rats were divided into four groups: group C: rats received no treatment, group P: rats received pomegranate peel aqueous extract (PPE) orally, group Se: rats received an injection of sodium selenite, group Se + P: rats received PPE and sodium selenite concomitantly. After 4 weeks, rats were sacrificed, and their lenses were homogenized and evaluated for biochemical parameters and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. In the Se group, developed cataract with significant lens opacity was observed. Other changes in enzymatic and non-enzymatic antioxidants, oxidative parameters, solubility of proteins, in NO and Ca levels and the electrophoresis pattern of proteins were observed in lenses of the Se group compared to control groups. After the preventive administration of PPE, most of these parameters were normalized due to antioxidant and anti-inflammatory activities of the extract. PRACTICAL APPLICATIONS: Cataract is one of the leading causes of vision impairment among the elderly, and surgery is the major therapeutic step taken to cure it. However, surgery has its limitations and complications. Therefore, prevention of cataract development, especially in high-risk individuals, can be better than cure. Pomegranate peel extract has a high potential to prevent cataract in these people.

Comparison of antagonistic effects of nanoparticle-selenium, selenium-enriched yeast and sodium selenite against cadmium-induced cardiotoxicity via AHR/CAR/PXR/Nrf2 pathways activation.

Selenium (Se), a nutritionally essential mineral for humans and animals, has a significant antagonistic effect on heavy metal cadmium (Cd) biotoxicity. Still, the impact of different Se sources on alleviating Cd toxicity has received only limited attention. Therefore, the purpose of the current study was to assess the mitigation level of Cd-induced cardiotoxicity by different sources such as nanoparticles of Se, Se-rich yeast, and sodium selenite (SS). The results evidenced that the presence of Cd led to a significant increase in biochemical parameters such as lactate dehydrogenase and creatine kinase, as well as histopathological lesions in the heart of chickens. Cd exposure also resulted in more extensive effects on phase I metabolism enzymes and transcript cytochrome P450 isoforms, elevated the levels of malondialdehyde (MDA), glutathione (GSH), and hydrogen peroxide (H2O2) and depressed total superoxide dismutase (T-SOD), copper-zinc SOD (Cu-Zn SOD), total antioxidant capacity (T-AOC) and catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione-S-transferase (GST) activities. The expression of nuclear receptors, aryl hydrocarbon receptor (AHR), constitutive androstane receptor (CAR), and pregnane X receptor (PXR) was declined, down-regulated nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream targets in the Cd-treat group. Notably, Se sources application alleviated Cd toxicity by triggering AHR/CAR/PXR/Nrf2 signaling pathway to promote restoring antioxidant defense system and phase I metabolism enzymes system. However, when compared to the effectiveness of antagonism, the nanoparticles of Se were superior in relieving Cd-induced cardiotoxicity via AHR/CAR/PXR/Nrf2 pathway activation than other Se-sources.

Sodium Selenite Modulates IDO1/Kynurenine, TLR4, NF-κB and Bcl2/Bax Pathway and Mitigates Acetic Acid-Induced Colitis in Rat.

BACKGROUND/AIMS: Colitis is a main presentation of inflammatory bowel disease (IBD) and yet, has no definitive cure. Currently, corticosteroids, anti-tumor necrosis factor (anti-TNF) agents and 5-aminosalicylic acid derivatives are prescribed for management of colitis. Except their failure rate, they are not always tolerated because of their severe adverse effects. Additive formulas with fewer adverse effects may improve the treatment of colitis. METHODS: In this study, colitis was induced with intra-rectal injection of three concentrations of acetic acid (4, 6 and 8 v/v). Each group received sodium selenite (0.5 mg/kg) or saline, gavaged on days 0 and 1 for treatment. Two days after induction of colitis, rats were sacrificed and the end part of their colons were resected for macroscopic and microscopic evaluation and molecular measurement. RESULTS: Sodium selenite improved macroscopic and microscopic view of the colon, decreased cryptitis, crypt abscess and inflammatory cells infiltration and partly maintained mucosal structure. Sodium selenite markedly reduced tissue levels of malondialdehyde (MDA), TNF-α and interferon γ (INF-γ) and decreased myeloperoxidase (MPO) activity. Treatment with sodium selenite also significantly downregulated IL17, IL22, indoleamine 2,3-dioxygenase (IDO1), and kynurenine levels. Western blotting revealed that sodium selenite prevented apoptosis by increasing bcl2/Bax ratio. Furthermore, our findings showed that sodium selenite significantly downregulated the upstream inflammatory molecules such as nuclear factor kappa B (NF-κB) and toll-like receptor 4 (TLR4) in colitis. CONCLUSION: These findings show that sodium selenite alleviates inflammatory response and oxidative stress and protects against colitis.

Nano-selenium and Macleaya cordata Extracts Improved Immune Function and Reduced Oxidative Damage of Sows and IUGR Piglets After Heat Stress of Sows in Late Gestation.

To investigate the effects of nano-selenium (nano-Se) and Macleaya cordata extracts (MCE) on immune function and oxidative damage of sows and intrauterine growth retardation (IUGR) piglets exposed to heat stress (HS) in large-scale farms, a 2 × 2 factorial design was adopted in this test, and the two factors were nano-Se (0, 0.50 mg/kg) and MCE (0, 500 mg/kg). A total of 80 sows ([Landrace × Yorkshire] × Duroc, parity 2) were used in a 25-day trial from day 90 of gestation to delivery with 20 replications per group and 1 sow per replication. The dietary treatments of sows were as follows: (1) CON group, basic diet (0.30 mg/kg added Se, sodium selenite); (2) Nano-Se group, basic diet (0.00 mg/kg added Se) + 0.50 mg/kg added nano-Se; (3) MCE group, basic diet (0.00 mg/kg added Se) + 500 mg/kg added MCE; and (4) Combined group, basic diet (0.00 mg/kg added Se) + 0.50 mg/kg added nano-Se and 500 mg/kg added MCE. The activities of serum SOD, CAT, and GSH-Px of sows and IUGR piglets were significantly increased in MCE group and combined group, and the MDA content was extremely decreased. There were extreme differences in serum IgG level of sows and IUGR piglets, colostrum, and serum IgM level of IUGR piglets in MCE group and combined group compared with CON group. Maternal combined diets increased greatly the levels of serum IL-10 and IFN-γ of sows and IUGR piglets, and decreased extremely the contents of serum IL-1ß and TNF-α. MCE alone or combination with nano-Se in sow diets decreased greatly mRNA level of Hsp70 and increased mRNA level of Hsp27 in sows and IUGR piglets. In conclusion, nano-Se and/or MCE can be added to sow diets for the amelioration of HS-induced oxidative damage through improving immune function.