Role Of Selenium Supplementation Research Articles

Selenoprotein-P1 (SEPP1) Expression in Human Proximal Tubule Cells after Ischemia-Reperfusion Injury: An In Vitro Model.

Background and Objectives: Selenium deficiency represents a risk factor for the occurrence of severe diseases, such as acute kidney injury (AKI). Recently, selenoprotein-p1 (SEPP1), a selenium transporter, mainly released by the liver, has emerged as a promising plasmatic biomarker of AKI as a consequence of cardio-surgery operations. The aim of the present study was to investigate, on an in vitro model of hypoxia induced in renal tubular cells, HK-2, the effects of sodium selenite (Na2SeO3) and to evaluate the expression of SEPP1 as a marker of injury. Materials and Methods: HK-2 cells were pre-incubated with 100 nM Na2SeO3 for 24 h, and then, treated for 24 h with CoCl2 (500 µM), a chemical hypoxia inducer. The results were derived from an ROS assay, MTT, and Western blot analysis. Results: The pre-treatment determined an increase in cells' viability and a reduction in reactive oxygen species (ROS), as shown by MTT and the ROS assay. Moreover, by Western blot an increase in SEPP1 expression was observed after hypoxic injury as after adding sodium selenite. Conclusions: Our preliminary results shed light on the possible role of selenium supplementation as a means to prevent oxidative damage and to increase SEPP1 after acute kidney injury. In our in vitro model, SEPP1 emerges as a promising biomarker of kidney injury, although further studies in vivo are necessary to validate our findings.

Selenium, Stroke, and Infection: A Threefold Relationship; Where Do We Stand and Where Do We Go?

Stroke is currently the second most common cause of death worldwide and a major cause of serious long-term morbidity. Selenium is a trace element with pleotropic effects on human health. Selenium deficiency has been associated with a prothrombotic state and poor immune response, particularly during infection. Our aim was to synthesize current evidence on the tripartite interrelationship between selenium levels, stroke, and infection. Although evidence is contradictory, most studies support the association between lower serum selenium levels and stroke risk and outcomes. Conversely, limited evidence on the role of selenium supplementation in stroke indicates a potentially beneficial effect of selenium. Notably, the relationship between stroke risk and selenium levels is bimodal rather than linear, with higher levels of serum selenium linked to disturbances of glucose metabolism and high blood pressure, morbidities which are, in turn, substrates for stroke. Another such substrate is an infection, albeit forming a bidirectional relationship with both stroke and the consequences of impaired selenium metabolism. Perturbed selenium homeostasis leads to impaired immune fitness and antioxidant capacity, which both favor infection and inflammation; specific pathogens may also contend with the host for transcriptional control of the selenoproteome, adding a feed-forward loop to this described process. Broader consequences of infection such as endothelial dysfunction, hypercoagulation, and emergent cardiac dysfunction both provide stroke substrates and further feed-forward feedback to the consequences of deficient selenium metabolism. In this review, we provide a synthesis and interpretation of these outlined complex interrelationships that link selenium, stroke, and infection and attempt to decipher their potential impact on human health and disease. Selenium and the unique properties of its proteome could provide both biomarkers and treatment options in patients with stroke, infection, or both.

Rethinking treatment of mercury poisoning: the roles of selenium, acetylcysteine, and thiol chelators in the treatment of mercury poisoning: a narrative review

We reevaluate the treatment of mercury poisoning, incorporating recent advances in understanding of mercury toxicity and the mercury:selenium interaction. This review focuses on: 1) the role, limitations and benefits of chelation (Unithiol, succimer and N-Acetylcysteine); 2) the role of selenium supplementation; and 3) how the different forms of mercury are impacted by use of chelation and selenium. Unithiol and succimer produce increases in urinary excretion of mercury and to a lesser degree blood and total body mercury. The primary role of N-acetylcysteine is increasing renal mercury excretion, similar to the thiol-chelators. Additional unique features of acetylcysteine include increased efflux of methylmercury from the brain, and reduced oxidative stress via increased glutathione production. The role of selenium includes: 1) restoration of selenoprotein activity, 2) protection against mitochondrial injury and DNA damage, 3) demethylation of methylmercury, 4) sequestering of mercury via Hg:Se complexes, and 5) redistribution of Hg inside organisms. Selenium may increase blood Hg, via a “sink” effect, causing a redistribution of mercury away from the brain. A combined approach for mercury poisoning treatment was developed focusing on restoration of selenoprotein function, reduction of oxidative stress and increased mercury elimination.

Case Report on Importance of Role of Selenium Supplementation in Autoimmune Thyroiditis: 8 Months Follow-Up with Variable Doses

Introduction: India in present situation has passed through the Iodine deficient to Iodine sufficient country due to higher access of iodised salt to people consuming higher iodine intake. Higher iodine intake increases the risk of lymphocytic infiltration of thyroid gland by 3 folds, and this has increased the prevalence of thyroid autoantibody positivity by almost 40-50%. Background: Selenium as know n has an antioxidant and anti-inflammatory property, and has the highest concentration in the thyroid gland. Several studies have shown that or studied that selenium has a close relationship with Hashimotos Thyroiditis characterized by presence of antithyroid peroxidase auto antibody. Aims and Objective: To study the effect of selenium supplementation in autoimmune thyroid disease. Two patients A and B with hypothyroidism both females with mean age 40+2 years were taken for this study, euthyroidism was achieved with substitutional therapy of levothyroxine of 100mcg dose. Both were then supplemented with selenium therapy. Results: Female patient A whose (mean TPOAb was 815) received 200 mg L-selenomethionine per day, orally for 4 months, and other female patient B whose (mean TPOAb was 790 IU/ml) also received 200mg of L-selenomethionine per day for duration of 4 months. The profile was assessed with the compared value of Anti TPO Ab and found decrease in the level of TPO antibodies by around 10-12 % after 8 weeks of therapy as assessed by the lab values, patient A values were 716 IU/ml and patient B values were 695 IU/ml, and 18-20 % at the end of 16 weeks i.e. 4 months, patient A values were 669 IU/ml and patient B values were 631 IU/ml. After 1st phase the thyroid profile of both the patients were stable on 100mcg. After duration of 6 months Female A was continued on L-selenomethionine 200 mg/day, while other female B the dose was reduced to 100 mg/day. Serum titers of TPOAb was assessed in both the female patients after 4 months. TPOAb titers increased significantly in female patient B with values of 820IU/ml around 30% as compared to female patient A with further decrease in titre values of 600 IU/ml.

Oxidative stress in hypothyroid patients and the role of antioxidant supplementation.

Context:The available data concerning oxidant stress and antioxidant capacity in hypothyroidism are scanty and inconclusive. While some authors suggest that tissues may be protected from oxidant damage because of a hypometabolic state in hypothyroidism, others report increased oxidative stress in hypothyroidism. Selenium acts as a cofactor for the thyroid hormone (TH) deiodinases that activate and then deactivate various THs and their metabolites. Selenium may inhibit thyroid autoimmunity.Aims:The study was designed, first, to study the impact of oxidative stress in patients of primary hypothyroidism due to autoimmune thyroiditis, by estimation of serum malondialdehyde (MDA) as a biomarker of oxidative stress. Second, to study the change in MDA level pre- and post-L-thyroxine treatment. Finally, to look into the possible role of selenium supplementation on oxidative stress in autoimmune hypothyroidism.Subjects and Methods:Patients attending endocrine outpatient department (OPD) services of IPGMER and SSKM hospital were considered for the study. Sixty treatment-naive adult patients (age > 18 years) with hypothyroidism were included in the study. The patients were divided into two groups, each comprised thirty patients. One group was treated with L-thyroxine and placebo (Group A). The other group received L-thyroxine replacement along with selenium (100 mcg twice a day) as antioxidant supplementation (Group B). The patients were blinded about selenium and placebo. The study duration for both groups was 6 months. The starting dose of L-thyroxine was 1.6 mcg/kg body weight free thyroxine (FT4), and thyroid-stimulating hormone (TSH) was repeated after 12 weeks. L-thyroxine dose adjustments were done if needed. MDA was assessed at the beginning and at the end of the study, i.e., after 6 months of treatment. The control cohort was composed of thirty healthy adults. Only overt hypothyroidism (OH) cases were included in the study.Statistical Analysis Used:Normality of data was determined using Anderson–Darling test, Shapiro–Wilk test, and QQ plot. P values were calculated using ANOVA and post hoc Bonferroni tests for normally distributed data. Correlation analysis was carried out using Pearson correlation test. P < 0.05 considered to be statistically significant.Results:After treatment in Group A patients, FT4 showed a significant increment while TSH value decreased. MDA level reduced after treatment, (P < 0.001). After treatment in Group B patients, FT4 showed increment while TSH value decreased (P < 0.05). After treatment, there was a drop in estimated MDA level (P < 0.001). MDA level shows a significant drop in both groups after treatment. In Group B, there is more decline in the MDA percentage but did not reach statistical significance. By performing repeated measure MANOVA, no significant difference was found in the MDA levels between the two groups. MDA reduction when expressed as percentage showed reduction of 39.5% in patients of Group A. Similarly, Group B patients showed a percentage reduction of 45.4%.Conclusions:Oxidative stress compounds hypothyroidism. Hypothyroidism is a state of increased oxidative stress. In this study, biomarker, MDA level is high in treatment-naive primary hypothyroid patients. After treatment with L-thyroxine, the stress marker is reduced to a significant extent. MDA can be used as a useful biomarker to measure and monitor oxidative stress. The role of the addition of antioxidant in the form of selenium remained inconclusive.

The role of selenium supplementation in cardiovascular disease prevention: an in vitro study to identify the molecular mechanism(s)

The role of selenium supplementation in cardiovascular disease prevention: an <i>in vitro</i> study to identify the molecular mechanism(s)

Abstract A59: Selenoprotein gene variants and risk of esophageal and gastric cancer in a Chinese population

Abstract Objectives: Observational studies and intervention trials suggest that selenium has potential cancer prevention properties. We previously found that selenium supplementation reduces cancer mortality, particularly gastric cancer mortality, in a high-risk region in China, and that low serum selenium concentration is associated with increased risks of esophageal squamous cell carcinoma (ESCC) and gastric cardia adenocarcinoma (GCA). In humans, selenium may exert chemopreventive actions through the 25 known selenoproteins, which contain residues of selenocysteine, the 21st amino acid. Therefore, genetic variants in selenoprotein genes may influence susceptibility to ESCC and GCA, yet no previous studies have comprehensively investigated these potential associations. Thus, we examined the association between genetic variants in selenoprotein and selenium metabolism genes and risks of ESCC and GCA. Methods: We included 1027 ESCC and 753 GCA cases plus 1452 controls from two epidemiologic studies in the high-risk region in China. We genotyped 272 tag single nucleotide polymorphisms (SNPs) in all 25 known selenoprotein genes and 4 selenium metabolism genes. For each gene, we calculated a standardized summary p-value using the adaptive rank truncated product (ARTP) method. For SNPs, logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). Results: In gene-based tests, the selenoprotein gene SELS (selenoprotein S) was associated with ESCC risk (p=0.00070); TXNRD2 (thioredoxin reductase 2) showed borderline non-significant associations with both ESCC (p=0.063) and GCA (p=0.051). In SNP-based tests for these two genes, rs8029790 (tagged to SELS in the upstream noncoding region) was associated with a 1.30-fold increased risk of ESCC (CI=1.14, 1.47; p=0.000052), whereas rs2073750 (tagged to intron in TXNRD2) was associated with risks of both ESCC (OR=0.84, CI=0.74, 0.94; p=0.0029) and GCA (OR=0.82, CI=0.72, 0.93; p=0.0026). Conclusions: The potential anticarcinogenic properties of selenium may be due to its presence as the amino acid selenocysteine in human selenoproteins. The association of SNPs in selenoprotein genes SELS and TXNRD2 with ESCC and GCA risk suggests that selenium and these selenoproteins may play an important role in cancer development. Our findings warrant further research on elucidating the functional effects of these SNPs on selenoproteins in the context of upper gastrointestinal (UGI) carcinogenesis so that we can better understand the role of selenium supplementation in cancer prevention. Citation Information: Cancer Prev Res 2011;4(10 Suppl):A59.

Selenium Deficiency and HIV Infection

Selenium is a non-metallic chemical element of great important to human health. Low selenium levels in humans are associated with several pathological conditions and are a common finding in HIV infected individuals. We conducted a review of the literature to assess if selenium deficiency or selenium supplementation could play a role in modifying the clinical course of HIV disease.Several studies investigated the role of selenium in disease progression, morbidity and mortality in HIV infected individuals. Larger studies were conducted in countries with poor economic resources and limited access to HAART. According to the majority of published studies low selenium levels appear to have an association with mortality, and selenium supplementation appears to play a beneficial role on survival or on slowing disease progression among HIV infected individuals. The role of selenium supplementation on preventing hospital admission among HIV outpatients was also noticed. The literature suggests an association between selenium deficiency and development of HIV associated cardiomyopathy and furthermore, selenium supplementation appears to improve the cardiac function in HIV infected individuals with cardiomyopathy. However, there is conflicting evidence regarding the role selenium in modifying HIV viral load and immune status in HIV infection.

Effect of excessive iodine on immune function of lymphocytes and intervention with selenium

In order to study the effect of excessive iodine on immune function of lymphocytes and the role of selenium supplementation with excessive iodine intake, the changes of T lymphocyte number, ratio of subsets, activity of natural killer (NK) cells and lymphocytes proliferation response were investigated. 150 female BALB/C mice were randomly divided into 5 groups in terms of their body weight (n=30 in each group), and 10 of each group were taken as one batch for test. Mice in the 5 groups were orally administrated with iodine 0 (group I), 1500 (group II), 3000 (group III), 6000 microg/L (group IV), iodine 6000 microg/L plus selenium 0.3 mg/L (group V) respectively for 30 days Lymphocyte proliferation response, CD4(+)/CD8(+), Th1/Th2 and the activity of NK cells were measured. CD4(+)/CD8(+) was significantly lower, while lymphocyte proliferation response stronger, and Th1/Th2 and the activity of NK cells significantly higher in group IV than in group I (P<0.01). There was no significant difference in all indexes between group V and group I (P>0.05). It was suggested that excessive iodine as exogenous chemical materials can induce disorders of T lymphocyte immune function in mice. 0.3 mg/L selenium supplementation can protect mice against toxicity induced by 6000 microg/L iodine.

Role of Selenium Supplementation and Heat Stress on Trehalose and Glutathione Content in Saccharomyces cerevisiae

The role of selenium (Se) supplementation on glutathione, a potent intracellular redox buffer, and trehalose, a well-known stress protectant molecule, was studied. The amount of glutathione decreased significantly while that of trehalose showed a minor decrease in the cells grown in Se-supplemented medium. After heat shock, glutathione content diminished further, whereas that of trehalose increased significantly in control and Se-supplemented cells. These findings suggest the importance of trehalose as an antioxidant molecule.