Effects Of Sodium Selenite Supplementation Research Articles

Selenium inhibits ferroptosis in ulcerative colitis through the induction of Nrf2/Gpx4

Background and aimSelenium, an essential micronutrient for human and has been reported to have a protective effect in ulcerative colitis (UC). However, the role of selenium in UC is unclear. Our aim was to investigate the mechanism of action of selenium in UC. MethodsSerum selenium levels were measured in UC patients and healthy controls. In addition, the effect of sodium selenite supplementation on experimental colitis in mice treated with dextran sulfate sodium (DSS) was investigated. The effect of sodium selenite on IECs ferroptosis was evaluated by observing the cell mortality, intracellular ferrous content, lipid reactive oxygen species and mitochondrial membrane damage in DSS-treated Caco2 cells. In addition, glutathione peroxidase 4 (Gpx4) and nuclear factor erythroid 2-like 2 (Nrf2) were detected in Caco2 cells and mouse intestines to explore their mechanisms. ResultsThe serum selenium content of UC patients was lower than that of healthy subjects. In addition, serum selenium levels were negatively correlated with disease activity. The in vivo results showed that selenium treatment could improve colitis induced by DSS and inhibit IECs ferroptosis. The in vitro results further showed that selenium inhibited the ferroptosis of Caco-2 cells induced by DSS. Nrf2/Gpx4 was up-regulated after selenium supplementation in vivo and in vitro. ConclusionsSerum selenium level is associated with IECs ferroptosis in UC patients. Selenium can relieve DSS-induced colitis and inhibit IECs ferroptosis by up-regulating the expression of Nrf2/Gpx4.

Selenium alleviates dextran sulfate sodium-induced colitis and inhibits ferroptosis of intestinal epithelial cells via upregulating glutathione peroxidase 4.

Selenium, an essential micronutrient for humans, has been shown to be protective against ulcerative colitis (UC), but the exact mechanism remains unclear. The role of selenium, protecting against ferroptosis of intestinal epithelial cells (IECs) in colitis, was investigated in this current study. Serum selenium level and ferroptosis-related gene expression in the colonic mucosa were measured in UC patients and healthy controls. The effects of sodium selenite supplementation on experimental colitis were investigated in dextran sulfate sodium (DSS)-treated mice. The influence of sodium selenite on IEC ferroptosis was evaluated through assessing cell death rate, intracellular ferrous iron content, lipid reactive oxygen species level, and mitochondrial membrane damage of DSS-treated Caco-2 cells. Moreover, glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long-chain family member 4, ferroptosis-related genes, were detected in Caco-2 cells and mouse intestines. Serum selenium was decreased in UC patients in comparison with healthy individuals. Additionally, serum selenium level was negatively correlated with disease activity and was associated with clinical inflammation and nutrition indicators. The expression of GPX4 in the mucosa of UC was positively correlated with serum selenium level. The in vivo experiments showed that selenium treatment ameliorated DSS-induced colitis and inhibited ferroptosis in IECs. The in vitro results suggested that selenium supplementation inhibited DSS-induced ferroptosis in Caco-2 cells. GPX4 was upregulated after selenium supplementation both in vivo and in vitro. Serum selenium level was associated with IEC ferroptosis in UC patients. Selenium supplementation alleviates DSS-induced colitis and inhibits ferroptosis in IECs by upregulating the expression of GPX4.

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

BackgroundThe 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.MethodsMTT 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.ResultsMedia 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.ConclusionsWe showed that sodium selenite could help protect MSCs during in-vitro manipulations, probably via the Nrf2 pathway.

Effects of selenium supplementation on glycaemic control markers in healthy rodents: a systematic review and meta-analysis.

Overexposure to Se is detrimental to glucose metabolism, mainly because of its pro-oxidant effects and the overexpression of selenoproteins. This systematic review evaluated the effects of Se supplementation on glycaemic control in healthy rodents. The methodology followed the PRISMA. We searched the databases for articles published up to May 2022. The risk of bias and the methodological quality were assessed using the SYRCLE and CAMARADES. The results are presented as meta-analytic estimates of the overall standardised mean difference (SMD) and 95 % CI. Of the 2359 records retrieved, thirteen studies were included, of which eleven used sodium selenite and two used zero-valent Se nanoparticles as supplement. Nine studies were included in the meta-analysis. Generally, the risk of bias was high, and 23·1 % of the studies were of high quality. Supplementation with sodium selenite significantly increased fasting blood glucose (SMD = 2·57 (95 % CI (1·07, 4·07)), I2 = 93·5 % (P = 0·001). Subgroup analyses showed effect size was larger for interventions lasting between 21 and 28 d (SMD = 25·74 (95 % CI (2·29, 9·18)), I2 = 96·1 % (P = 0·001)) and for a dose of 864·7 μg/kg/d of sodium selenite (SMD = 10·26 (95 % CI (2·42, 18·11), I2 = 97·1 % (P = 0·010)). However, it did not affect glutathione peroxidase activity (SMD = 0·60 (95 % CI (-0·71, 1·91)), I2 = 83·2 % (P = 0·37)). The current analysis demonstrated the adverse effects of sodium selenite supplementation on glycaemic control in healthy rodents.

In vitro EFFECTS OF SODIUM SELENITE SUPPLEMENTATION ON CELL VIABILITY OF DIFFERENT FORMS OF Trypanosoma cruzi

Selenium is an essential trace element which, at adequate levels, presents different beneficial biological effects, such as cancer regression, tissue development and protection against oxidative damage. The positive effects of this element are related to the expression of selenoproteins and their ability to modulate the immune system and the oxidative stress response. In Chagas disease and sleeping sickness, selenium supplementation has shown blood parasitism reduction and the alleviation of specific aspects of the diseases, such as diminishing anemia in sleeping sickness or minimization of myocardial and right ventricular chamber damage in Chagasdisease. Although the influence of selenium in trypanosomiasis has been investigated, the direct effects of sodium selenite supplementation on trypanosome cells are poorly understood. Treatment of Trypanosoma cruzi cultures with low selenium doses demonstrated different results, according to the parasite evolutive form analyzed. Epimastigote cultures supplemented with 100 nM of sodium selenite presented cell growth increment, which varies from 10 to 40% according to the parasite strain assayed. Selenium concentration around 600nM leads to a 30% increase in the amastigote form number, whereas, at the same dose, the mammal host cell presented no cellular growth alteration. For the bloodstream form, the results agree with theliterature, and all sodium selenite concentrations tested, demonstrated a reduction in parasite viability. The data suggest that selenium supplementation, under specific conditions, could increase T. cruzi viability, demonstrating that a strategy for using selenium as an adjuvant in Chagas disease treatment requires additional experimentation. KEY WORDS: Selenium; trypanosomiasis; Chagas disease; Trypanosoma cruzi.

Protective effects of sodium selenite supplementation against irradiation-induced damage in non-cancerous human esophageal cells.

The administration of radioprotective compounds is one approach to preventing radiation damage in non-cancerous tissues. Therefore, radioprotective compounds are crucial in clinical radiotherapy. Selenium is a radioprotective compound that has been used in previous clinical studies of radiotherapy. However, evidence regarding the effectiveness of selenium in radiotherapy and the mechanisms underlying the selenium-induced reduction of the side effects of radiotherapy remains insufficient. To further investigate the effectiveness of selenium in radiotherapy, the present study examined the protective effects of sodium selenite supplementation administered prior to X-ray radiation treatment in CHEK-1 non-cancerous human esophageal cells. Sodium selenite supplementation increased glutathione peroxidase 1 (GPx-1) activity in a dose- and time-dependent manner. The sodium selenite dose that induced the highest GPx-1 activity was determined to be 50 nM for 72 h prior to radiotherapy. The half-maximal inhibitory concentration of sodium selenite in CHEK-1 cells was 3.6 µM. Sodium selenite supplementation increased the survival rate of the cells in a dose-dependent manner and enhanced the degree of cell viability at 72 h post-irradiation (P<0.05). Combined treatment with 50 nM sodium selenite and 2 gray (Gy) X-ray irradiation decreased the number of sub-G1 cells from 5.9 to 4.2% (P<0.05) and increased the proportion of G1 cells from 58.8 to 62.1%, compared with 2 Gy X-ray irradiation alone; however, this difference was not statistically significant (P=1.00). Western blot analysis revealed that treatment with 2 Gy X-ray irradiation significantly increased the expression levels of cleaved poly (ADP-ribose) polymerase (PARP; P<0.05). In addition, combined treatment with 50 nM sodium selenite and 2 Gy X-ray irradiation reduced the expression levels of cleaved PARP protein, compared with 2 Gy X-ray irradiation alone; however, this reduction was not statistically significant (P=0.423). These results suggest that 50 nM sodium selenite supplementation administered for 72 h prior to irradiation may protect CHEK-1 cells from irradiation-induced damage by inhibiting irradiation-induced apoptosis. Therefore, sodium selenite is a potential radioprotective compound for non-cancerous cells in clinical radiotherapy.

Effect of sodium selenite supplementation in goats

An experiment was conducted on 12 male Black Bengal kids (2–3 months of age) to elucidate the effect of supplementation of sodium selenite on their growth and blood chemistry. Kids were randomly divided into two equal groups and fed a basal diet consisting of concentrate mixture and paddy straw. Gr-I served as control (without any supplementation), whereas animals in Gr-II were supplemented with 0.3 mg selenium/kg dry matter as sodium selenite. Experimental feeding continued for a period of 90 days, during which fortnightly body weights were recorded to assess their growth rate. Blood samples were collected on day 0 and 90 days of the experimental feeding to study the haematology and blood chemistry of goats. Results revealed significant (P<0.05) increase in average daily gain in selenium supplemented group than the control. Hemoglobin content, packed cell volume, glucose, total protein, albumin, globulin, A: G ratio and urea were similar between the two groups. Activities of serum aspirate amino transferase (AST), serum alanine amino transferase (ALT) and alkaline phosphatase (ALP) did not differ between the groups. It may be concluded that supplementation of 0.3 ppm selenium as sodium selenite enhanced the growth without affecting blood biochemistry of goats.

Effect of Sodium Selenite Supplementation on Glucose Intolerance and Pancreatic Oxidative Stress in Type 2 Diabetic Mice under Different Selenium Status

The objective of this study was to investigate the effect of various selenium (Se) status on glucose intolerance and pancreatic oxidative stress or the defense systems in Nagoya-Shibata-Yasuda (NSY) mice as the animal model for type 2 diabetes mellitus. To let the mice become Se-insufficient to Se-sufficient conditions, the NSY mice were given normal or Se-deficient diet with 0–7.0 mg/l Na2SeO3-containing drinking water for 6, 8 or 12 weeks. In NSY mice ingested normal diet, levels of blood glucose and plasma insulin after intraperitoneal glucose tolerance test (IPGTT) were not significantly affected by Na2SeO3-supplementation. In Se-deficient diet-treatment groups, however, the supplementation resulted in the decrease of blood glucose and the increase of plasma insulin after IPGTT. Although glutathione peroxidase (GPX) 1 activity in pancreas of the NSY mice ingested Se-deficient diet was augmente db y Na 2SeO3-supplementation, pancreatic glutathione was depressed by the supplementation, accompanying by the increase of 2-thiobarbituric acid-reactiv es ubstances. These results indicated that although the supplemented Na2SeO3 may not protect against oxidative stress in the pancreas of NSY mice under Se-insufficient condition, the Se compound improved glucose intolerance of the mice.

Effect of sodium selenite supplementation on the levels of Prostacyclin I 2 and Thromboxane A 2 in human

Selenium is an essential trace element in human health [1,2], an important part of the antioxidant enzymes that protect cells against the effects of free radicals that are produced during the normal oxygen metabolism. The body has developed defenses, such as antioxidants, to control the levels of free radicals, which can damage cells and contribute to the development of some chronic diseases. Several epidemiological studies have shown that serum selenium levels were associated

Sodium selenite, dietary micronutrient, prevents the lymphocyte DNA damage induced by N-nitrosodiethylamine and phenobarbital promoted experimental hepatocarcinogenesis.

Selenium (Se), a micronutrient, has a long history in chemoprevention of mammary and colon cancers in rodent models. Se is a current clinical trial, having shown promise in prevention of prostate and other human cancers. The mechanisms involved in the in vivo anti-carcinogenic activity of Se remain to be elucidated. In the present study, we examined the effect of sodium selenite supplementation in lymphocytes, obtained from hepatoma bearing rats on DNA damage in correlation with oxidative stress. In addition, this study examined the supplementation of Se at 4-ppm levels in the form of sodium selenite either before initiation or during initiation and/or promotion phase's increases lymphocyte Se concentrations. This in turn improves lymphocyte resistance to oxidative stress and protection against the lymphocytes DNA damage. Supplementation of Se increased lymphocyte Se concentration and reduced lymphocytes DNA damage as determined by single cell gel electrophoresis. The enzymatic antioxidants such as superoxide dismutase, glutathione peroxidase, and catalase were found to be decreased while the thiobarbituric acid reactive substances level was increased in the lymphocytes of hepatoma bearing rats. Furthermore, the reactive oxygen species such as superoxide radicals and hydroxyl radicals were also found to be high in lymphocytes. Our present results explain the understanding of unique association between anti-peroxidative effect of Se and ultimately the capability of Se to prevent cancer.