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.

Selenium supplementation for polycystic ovary syndrome: a meta-analysis of randomized controlled trials.

Introduction: The efficacy of selenium supplementation was elusive for polycystic ovary syndrome. This meta-analysis aimed to explore the efficacy of selenium supplementation for polycystic ovary syndrome. Methods: PubMed, EMbase, Web of science, EBSCO, Cochrane library database, CNKI, Chongqing VIP database and Wanfang databases have been searched through July 2022 and we included randomized controlled trials (RCTs) reporting the effect of selenium supplementation versus placebo in patients with polycystic ovary syndrome. Results: Five RCTs were included in the meta-analysis. Compared with placebo group for polycystic ovary syndrome, selenium supplementation was associated with significantly reduced total testosterone (SMD=-0.42; 95% CI=-0.78 to -0.06; p = 0.02) and cholesterol (SMD=-0.71; 95% CI=-1.41 to -0.02; p = 0.04), but revealed no remarkable influence on SHBG (SMD=-0.52; 95% CI=-1.29 to 0.25; p = 0.19), triglyceride (SMD=-1.45; 95% CI=-3.62 to 0.73; p = 0.19), LDL (SMD=-0.17; 95% CI=-0.72 to 0.37; p = 0.53), FPG (SMD=-0.95; 95% CI=-3.72 to 1.82; p = 0.50) or HOMA-IR (SMD=-0.51; 95% CI=-3.79 to 2.77; p = 0.76). Conclusions: Selenium supplementation may be able to improve the metabolic response for polycystic ovary syndrome, and this finding should be interpreted with caution.

Genome-Wide Association Study of Response to Selenium Supplementation and Circulating Selenium Concentrations in Adults of European Descent.

BACKGROUND: Selenium (Se) is a trace element that has been linked to many health conditions. Genome-wide association studies (GWAS) have identified variants for blood and toenail Se levels, but no GWAS has been conducted to date on responses to Se supplementation. OBJECTIVES: A GWAS was performed to identify the single nucleotide polymorphisms (SNPs) associated with changes in Se concentrations after 1 year of supplementation. A GWAS of basal plasma Se concentrations at study entry was conducted to evaluate whether SNPs for Se responses overlap with SNPs for basal Se levels. METHODS: A total of 428 participants aged 40-80 years of European descent from the Selenium and Celecoxib Trial (Sel/Cel Trial) who received daily supplementation with 200 µg of selenized yeast were included for the GWAS of responses to supplementation. Plasma Se concentrations were measured from blood samples collected at the time of recruitment and after 1 year of supplementation. Linear regression analyses were performed to assess the relationship between each SNP and changes in Se concentrations. We further examined whether the identified SNPs overlapped with those related to basal Se concentrations. RESULTS: No SNP was significantly associated with changes in Se concentration at a genome-wide significance level. However, rs56856693, located upstream of the NEK6, was nominally associated with changes in Se concentrations after supplementation (P = 4.41 × 10-7), as were 2 additional SNPs, rs11960388 and rs6887869, located in the dimethylglycine dehydrogenase (DMGDH)/betaine-homocysteine S-methyltransferase (BHMT) region (P = 0.01). Alleles of 2 SNPs in the DMGDH/BHMT region associated with greater increases in Se concentrations after supplementation were also strongly associated with higher basal Se concentrations (P = 8.67 × 10-8). CONCLUSIONS: This first GWAS of responses to Se supplementation in participants of European descent from the Sel/Cel Trial suggests that SNPs in the NEK6 and DMGDH/BHMT regions influence responses to supplementation.

Selenium supplementation in patients with peripartum cardiomyopathy: a proof-of-concept trial.

BACKGROUND: We studied the efficacy and safety of selenium supplementation in patients who had peripartum cardiomyopathy (PPCM) and selenium deficiency. METHODS: We randomly assigned 100 PPCM patients with left ventricular ejection fraction (LVEF) < 45% and selenium deficiency (< 70 µg/L) to receive either oral Selenium (L-selenomethionine) 200 µg/day for 3 months or nothing, in addition to recommended therapy, in an open-label randomised trial. The primary outcome was a composite of persistence of heart failure (HF) symptoms, unrecovered LV systolic function (LVEF < 55%) or death from any cause. RESULTS: Over a median of 19 months, the primary outcome occurred in 36 of 46 patients (78.3%) in the selenium group and in 43 of 54 patients (79.6%) in the control group (hazard ratio [HR] 0.69; 95% confidence interval [CI] 0.43-1.09; p = 0.113). Persistence of HF symptoms occurred in 18 patients (39.1%) in the selenium group and in 37 patients (68.5%) in the control group (HR 0.53; 95% CI 0.30-0.93; p = 0.006). LVEF < 55% occurred in 33 patients (71.7%) in the selenium group and in 38 patients (70.4%) in the control group (HR 0.91; 95% CI 0.57-1.45; p = 0.944). Death from any cause occurred in 3 patients (6.5%) in the selenium group and in 9 patients (16.7%) in the control group (HR 0.37; 95% CI 0.10-1.37; p = 0.137). CONCLUSIONS: In this study, selenium supplementation did not reduce the risk of the primary outcome, but it significantly reduced HF symptoms, and there was a trend towards a reduction of all-cause mortality. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT03081949.

Selenium supplementation during pregnancy and lactation promotes metabolic changes in Wistar rats' offspring.

Epidemiological and animal studies have demonstrated a strong association between selenium (Se) supplementation and metabolic disorders, we aimed to evaluate whether maternal Se supplementation was able to change metabolic parameters in rats' offspring. Moreover, as Se is a deiodinase (DIO) cofactor, we decided to investigate how thyroid hormones (THs) would be involved in such metabolic changes. Thereby, two groups (n = 6, ~250 g) of female Wistar rats underwent isotonic saline or sodium selenite (1 mg/kg, p.o.) treatments. Although there were no significant differences in body weight between groups, the Se treatment during pregnancy and lactation increased milk intake and the visceral white adipose tissue (WAT) in offspring. The rats whose mothers were treated with Se also presented an improvement in the glucose tolerance test and in the glucose-stimulated insulin secretion. Regarding the lipid metabolism, the Se group had a reduction of triglycerides in the liver and in WAT. These metabolic changes were accompanied by an increase in serum triiodothyronine (T3 ) and in DIO 2 expression in brown adipose tissue (BAT). We further demonstrate an increased expression of peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α) and nuclear respiratory factor-1 (NRF-1) mRNA in the liver. In adulthood offspring, Se supplementation programs thyroid function, glucose homeostasis, and feeding behaviour. Taken together, there is no indication that Se programming causes insulin resistance. Moreover, we conjecture that these metabolic responses are induced by increased thyroxine (T4 ) to T3 conversion by DIO2 in BAT and mediated by altered transcription factors expression associated with oxidative metabolism control in the liver.

Biological implications of selenium in adolescent rats exposed to binge drinking: Oxidative, immunologic and apoptotic balance.

Alcohol intermittent binge drinking (BD) during adolescence decreases the levels of selenium (Se), a trace element that plays a key biological role against oxidative damage in hepatocytes through different selenoproteins such as the antioxidant enzymes glutathione peroxidases (GPx1 and Gpx4) and selenoprotein P (SelP). In this context, it has been found that GPx4 has an essential antioxidant role in mitochondria modulating the apoptosis and NF-kB activation (a factor intimately related to apoptosis and immune function). To further investigate the effectiveness of selenium supplementation in oxidative balance, inflammation and apoptosis, the present study examined the protective effects of 0.4ppm of dietary selenite administrated to adolescent rats exposed to BD. BD consumption depleted Se deposits in all the tissues studied. In liver, GPx1 activity and expression were decreased leading to protein and lipid hepatic oxidation. Moreover GPx4 and NF-kB expression were also decreased in liver, coinciding with an increase in caspase-3 expression. This hepatic profile caused general liver damage as shown the increased serum transaminases ratio AST/ALT. Proinflammatory serum citokines and chemocines were decreased. Se supplementation therapy used restored all these values, even AST levels. These findings suggest for first time that Se supplementation is a good strategy against BD liver damage during adolescence, since it increases GPx1 and GPx4 expression and avoids NF-kB downregulation and caspase-3 upregulation, leading to a better oxidative, inflammatory and apoptotic liver profile. The therapy proposed could be considered to have a great biological efficacy and to be suitable for BD exposed teenagers in order to avoid future hepatic complications.

Methods of Selenium Supplementation: Bioavailability and Determination of Selenium Compounds.

Selenium, a "dual-surface" element, maintains a very thin line between a level of necessity and harmfulness. Because of this, a deficiency or excess of this element in an organism is dangerous and causes health-related problems, both physically and mentally. The main source of selenium is a balanced diet, with a proper selection of meat and plant products. Meanwhile, the proper assimilation of selenium into these products depends on their bioavailability, bioaccessibility, and/or bioactivity of a given selenium compound. From the time when it was discovered that selenium and its compounds have a significant influence on metabolic processes and in many countries throughout the world, a low quantity of selenium was found in different parts of the environment, pressure was put upon an effective and fast method of supplementing the environment with the help of selenium. This work describes supplementation methods applied with the use of selenium, as well as new ideas for increasing the level of this element in various organisms. Based on the fact that selenium appears in the environment at trace levels, the determination of total amount of selenium or selenium speciation in a given sample demands the selection of appropriate measurement methods. These methods are most often comprised of a sample preparation technique and/or a separation technique as well as a detection system. The work presents information on the subject of analytical methods used for determining selenium and its compounds as well as examples in literature of their application.

The effects of selenium supplementation on biomarkers of inflammation and oxidative stress in patients with diabetic nephropathy: a randomised, double-blind, placebo-controlled trial.

This study was carried out to assess the effects of Se supplementation on biomarkers of inflammation and oxidative stress in patients with diabetic nephropathy (DN). This randomised, double-blind, placebo-controlled clinical trial was conducted among sixty patients with DN. Patients were randomly divided into two groups to take either 200 µg/d Se supplements as Se yeast (n 30) or placebo (n 30) for 12 weeks. In unadjusted analyses, compared with the placebo, Se supplementation led to a significant reduction in high-sensitivity C-reactive protein (hs-CRP) (-1069·2 (sd 1752·2) v. -135·3 (sd 1258·9) ng/ml, P=0·02), matrix metalloproteinase-2 (MMP-2) (-612·3 (sd 679·6) v. +76·0 (sd 309·1) ng/ml, P<0·001) and plasma malondialdehyde (MDA) concentrations (-0·1 (sd 0·7) v. +0·4 (sd 0·9) µmol/l, P=0·01). In addition, a significant increase in plasma total antioxidant capacity (TAC) (+174·9 (sd 203·9) v. +15·8 (sd 382·2) mmol/l, P=0·04) was observed following supplementation with Se compared with the placebo. Subjects who received Se supplements experienced a borderline statistically significant decrease in serum protein carbonyl (PCO) levels (P=0·06) compared with the placebo. When we adjusted the analysis for baseline values of biochemical parameters, age and BMI, serum hs-CRP (P=0·14) and MDA levels (P=0·16) became non-significant, whereas plasma nitric oxide (NO) (P=0·04) and glutathione (GSH) (P<0·001) became statistically significant, and other findings did not change. Supplementation with Se had no significant effect on NO, transforming growth factor ß (TGF-ß), advanced glycation end products (AGE), PCO and GSH compared with the placebo. Overall, our study demonstrated that Se supplementation among DN patients had favourable effects on serum MMP-2, plasma NO, TAC and GSH, but did not affect hs-CRP, TGF-ß, AGE, PCO and MDA.

DNA damage and oxidative stress response to selenium yeast in the non-smoking individuals: a short-term supplementation trial with respect to GPX1 and SEPP1 polymorphism.

PURPOSE: Selenium, both essential and toxic element, is considered to protect against cancer, though human supplementation trials have generated many inconsistent data. Genetic background may partially explain a great variability of the studies related to selenium and human health. The aim of this study was to assess whether functional polymorphisms within two selenoprotein-encoding genes modify the response to selenium at the level of oxidative stress, DNA damage, and mRNA expression, especially in the individuals with a relatively low selenium status. METHODS: The trial involved 95 non-smoking individuals, stratified according to GPX1 rs1050450 and SEPP1 rs3877899 genotypes, and supplemented with selenium yeast (200 µg) for 6 weeks. Blood was collected at four time points, including 4 weeks of washout. RESULTS: After genotype stratification, the effect of GPX1 rs1050450 on lower GPx1 activity responsiveness was confirmed; however, in terms of DNA damage, we failed to indicate that individuals homozygous for variant allele may especially benefit from the increased selenium intake. Surprisingly, considering gene and time interaction, GPX1 polymorphism was observed to modify the level of DNA strand breaks during washout, showing a significant increase in GPX1 wild-type homozygotes. Regardless of the genotype, selenium supplementation was associated with a selectively suppressed selenoprotein mRNA expression and inconsistent changes in oxidative stress response, indicating for overlapped, antioxidant, and prooxidant effects. Intriguingly, DNA damage was not influenced by supplementation, but it was significantly increased during washout. CONCLUSIONS: These results point to an unclear relationship between selenium, genotype, and DNA damage.

The favourable effects of long-term selenium supplementation on regression of cervical tissues and metabolic profiles of patients with cervical intraepithelial neoplasia: a randomised, double-blind, placebo-controlled trial.

This study was conducted to assess the effects of long-term Se administration on the regression and metabolic status of patients with cervical intraepithelial neoplasia grade 1 (CIN1). This randomised, double-blind, placebo-controlled trial was carried out among fifty-eight women diagnosed with CIN1. To diagnose CIN1, we used specific diagnostic procedures of biopsy, pathological diagnosis and colposcopy. Patients were randomly assigned to two groups to receive 200 µg Se supplements as Se yeast (n 28) or placebo (n 28) daily for 6 months. After 6 months of taking Se supplements, a greater percentage of women in the Se group had regressed CIN1 (88·0 v. 56·0 %; P=0·01) compared with those in the placebo group. Long-term Se supplementation, compared with the placebo, resulted in significant decreases in fasting plasma glucose levels (-0·37 (sd 0·32) v. +0·07 (sd 0·63) mmol/l; P=0·002), serum insulin levels (-28·8 (sd 31·2) v. +13·2 (sd 40·2) pmol/l; P<0·001), homeostatic model assessment of insulin resistance values (-1·3 (se 1·3) v. +0·5 (se 1·4); P<0·001) and a significant elevation in quantitative insulin sensitivity check index (+0·03 (sd 0·03) v. -0·01 (sd 0·01); P<0·001). In addition, patients who received Se supplements had significantly decreased serum TAG (-0·14 (sd 0·55) v. +0·15 (sd 0·38) mmol/l; P=0·02) and increased HDL-cholesterol levels (+0·13 (sd 0·21) v. -0·01 (sd 0·15) mmol/l; P=0·003). In addition, compared with the placebo group, there were significant rises in plasma total antioxidant capacity (+186·1 (sd 274·6) v. +42·8 (sd 180·4) mmol/l; P=0·02) and GSH levels (+65·0 (sd 359·8) v. -294·2 (sd 581·8) µmol/l; P=0·007) and a significant decrease in malondialdehyde levels (-1·5 (sd 2·1) v. +0·1 (sd 1·4) µmol/l; P=0·001) among those who took Se supplements. Overall, taking Se supplements among patients with CIN1 led to its regression and had beneficial effects on their metabolic profiles.

Randomised controlled trial of the effect of long-term selenium supplementation on plasma cholesterol in an elderly Danish population.

Although cross-sectional studies have shown a positive association between Se and cholesterol concentrations, a recent randomised controlled trial in 501 elderly UK individuals of relatively low-Se status found that Se supplementation for 6 months lowered total plasma cholesterol. The Danish PRECISE (PREvention of Cancer by Intervention with Selenium) pilot study (ClinicalTrials.gov ID: NCT01819649) was a 5-year randomised, double-blinded, placebo-controlled trial with four groups (allocation ratio 1:1:1:1). Men and women aged 60-74 years (n 491) were randomised to 100 (n 124), 200 (n 122) or 300 (n 119) µg Se-enriched yeast or matching placebo-yeast tablets (n 126) daily for 5 years. A total of 468 participants continued the study for 6 months and 361 participants, equally distributed across treatment groups, continued for 5 years. Plasma samples were analysed for total and HDL-cholesterol and for total Se concentrations at baseline, 6 months and 5 years. The effect of different doses of Se supplementation on plasma lipid and Se concentrations was estimated by using linear mixed models. Plasma Se concentration increased significantly and dose-dependently in the intervention groups after 6 months and 5 years. Total cholesterol decreased significantly both in the intervention groups and in the placebo group after 6 months and 5 years, with small and nonsignificant differences in changes in plasma concentration of total cholesterol, HDL-cholesterol, non-HDL-cholesterol and total:HDL-cholesterol ratio between intervention and placebo groups. The effect of long-term supplementation with Se on plasma cholesterol concentrations or its sub-fractions did not differ significantly from placebo in this elderly population.

Effect of feed selenium supplementation on milk selenium distribution and mozzarella quality.

In the present study, the effect of feed Se supplementation on the Se content of raw milk and mozzarella cheese as well as the effect on cheese quality and functionality were determined. The Se milk was produced by supplying dairy cow feed with Se yeast (0.3mg of Se/kg of dry matter), resulting in a Se concentration in milk of 35.81µg/L. The fat, casein, and whey protein of Se milk were separated by ultracentrifugation, and the Se content was determined by atomic absorption spectroscopy. The Se distribution in different milk fractions of fat, casein, and whey protein were 9.82, 45.56, and 44.62%, respectively. The Se mozzarella cheese was made by Se milk, and the composition and texture of Se cheese did not significantly differ from that of the control. However, the functional properties (meltability, flowability, and stretchability) of the Se cheese were better after 8 wk of storage. Moreover, the pH and water activity were lower in Se cheese, which decreased the total plate count. The Se content in mozzarella cheese was 4 fold higher than that in milk, and Se was found in the whey, hot water, and brine collected during cheesemaking. Organic and inorganic Se was found in the Se cheese after 8 wk of storage, and most Se peptides detected after storage were Se-Met and Se-Cys. The results of this study show that feed Se supplementation can improve the Se content of milk and cheese without affecting mozzarella cheese quality.

Influence of selenium supplementation on fatty acids profile and biological activity of four edible amaranth sprouts as new kind of functional food.

Suitability assessment of amaranth sprouts as a new functional food was carried out. The optimisation of sprouting process and the influence of selenium supplementation, in doses 10, 15, and 30 mg/l of selenium as sodium selenite, on amaranth growth and fatty acid profile were examined. Methods such as FRAP, DPPH, polyphenols content and GPX activity were applied to characterize antioxidant potential of seeds and sprouts of four different edible amaranth genera. E. coli, S. aureus, C. albicans were used to evaluate amaranth sprouts antimicrobial properties. Interaction between amaranth sprouts and biological systems was assessed by analysing antibacterial and antifungal properties with a disc diffusion test. The studies proved amaranth sprouts to be potentially attractive as functional food. As confirmed by all the data amaranth sprouts are suitable as a moderate selenium accumulator and are rich in essential fatty acids, especially linoleic and alpha-linolenic acids, which are precursors of long chain polyunsaturated fatty acids. Thus, it opens dietary opportunities for amaranth sprouts. They can also serve as a moderate source of antioxidant compounds. Nevertheless, the experiments revealed neither antibacterial, nor antifungal properties of sprouts. In general, amaranth sprouts biological activity under evaluation has failed to prove to be significantly impacted by selenium fertilization.

The effects of di(2-ethylhexyl)phthalate on rat liver in relation to selenium status.

This study was performed to determine the hepatotoxicity of di(2-ethylhexyl)phthalate (DEHP) in relation to selenium status. In 3-week-old Sprague-Dawley rats, selenium deficiency was induced by a ≤0.05 selenium mg/kg. A selenium supplementation group was given 1 mg selenium/kg diet for 5 weeks. Di(2-ethylhexyl)phthalate-treated groups received 1000 mg/kg dose by gavage during the last 10 days of the experiment. Histopathology, peroxisome proliferation, catalase (CAT) immunoreactivity and activity and apoptosis were assessed. Activities of antioxidant selenoenzymes [glutathione peroxidase 1 (GPx1), glutathione peroxidase 4 (GPx4), thioredoxin reductase (TrxR1)], superoxide dismutase (SOD), and glutathione S-transferase (GST); aminotransferase, total glutathione (tGSH), and lipid peroxidation (LP) levels were measured. Di(2-ethylhexyl)phthalate caused cellular disorganization while necrosis and inflammatory cell infiltration were observed in Se-deficient DEHP group (DEHP/SeD). Catalase activity and immunoreactivity were increased in all DEHP-treated groups. Glutathione peroxidase 1 and GPx4 activities decreased significantly in DEHP and DEHP/SeD groups, while GST activities decreased in all DEHP-exposed groups. Thioredoxin reductase activity increased in DEHP and DEHP/SeS, while total SOD activities increased in all DEHP-treated groups. Lipid peroxidation levels increased significantly in SeD (26%), DEHP (38%) and DEHP/SeD (71%) groups. Selenium supplementation partially ameliorated DEHP-induced hepatotoxicity; while in DEHP/SeD group, drastic changes in hepatic histopathology and oxidative stress parameters were observed.

Effects of the consumption of rice from non-KBD areas and selenium supplementation on the prevention and treatment of paediatric Kaschin-Beck disease: an epidemiological intervention trial in the Qinghai Province.

OBJECTIVE: Based on the aetiological hypothesis of Kaschin-Beck disease (KBD), different interventions were adopted, and the preventive and therapeutic effects of interventions was observed and evaluated in this trial. DESIGN: A total of 358 children from seven villages of Qinghai Province in China were examined, and 280 children aged 6-11 years old were eligible for the trial. The children were divided into three groups that received either no intervention (n = 64), 150 kg/person of rice from non-KBD areas (n = 103) or 7 kg/family of selenium-iodine salt (n = 113) for 12 months. Data were collected and used to calculate the proportion of patients with X-ray lesions, the proportion of new patients and the metaphyseal repair rate. All indicators were analysed with Pearson chi-square or Fisher's exact tests. The registration number of this trial is ChiCTR-PNRC-12002309 (http://www.chictr.org). RESULTS: After interventions, the proportion of patients with X-ray lesions increased dramatically in the control group and decreased significantly in two intervention groups; significant differences were seen between the control group and two intervention groups (P < 0.05). Moreover, significant differences were observed in the proportions of new patients and the metaphyseal repair rates between the control group and two intervention groups (P < 0.05). Additionally, the proportion of new patients was lowest and the metaphyseal repair rate was highest in group B. CONCLUSIONS: The effects of eating rice from non-KBD areas and selenium supplementation on the prevention and treatment of paediatric KBD were notable, the consumption of rice might be the most effective and safest intervention and should be encouraged.

Effects of di(2-ethylhexyl)phthalate on testicular oxidant/antioxidant status in selenium-deficient and selenium-supplemented rats.

Di(ethylhexyl)phthalate (DEHP), the most widely used plasticizer, was investigated to determine whether an oxidative stress process was one of the underlying mechanisms for its testicular toxicity potential. To evaluate the effects of selenium (Se), status on the toxicity of DEHP was further objective of this study, as Se is known to play a critical role in testis and in the modulation of intracellular redox equilibrium. Se deficiency was produced in 3-weeks-old Sprague-Dawley rats feeding them ≤0.05 mg Se /kg diet for 5 weeks, and Se-supplementation group was on 1 mg Se/kg diet. DEHP-treated groups received 1000 mg/kg dose by gavage during the last 10 days of the feeding period. Activities of antioxidant selenoenzymes [glutathione peroxidase 1 (GPx1), glutathione peroxidase 4 (GPx4), thioredoxin reductase (TrxR)], catalase (CAT), superoxide dismutase (SOD), and glutathione S-transferase (GST); concentrations of reduced glutathione (GSH), oxidized glutathione (GSSG), and thus the GSH/GSSG redox ratio; and thiobarbituric acid reactive substance (TBARS) levels were measured. DEHP was found to induce oxidative stress in rat testis, as evidenced by significant decrease in GSH/GSSG redox ratio (>10-fold) and marked increase in TBARS levels, and its effects were more pronounced in Se-deficient rats with ∼18.5-fold decrease in GSH/GSSG redox ratio and a significant decrease in GPx4 activity, whereas Se supplementation was protective by providing substantial elevation of redox ratio and reducing the lipid peroxidation. These findings emphasized the critical role of Se as an effective redox regulator and the importance of Se status in protecting testicular tissue from the oxidant stressor activity of DEHP.

Exploring effects of organic selenium supplementation on pork loin: Se content, meat quality, antioxidant capacity, and metabolomic profiling during storage.

This research was conducted to study the effects of organic selenium (Se) supplements at different levels on pork loin quality during storage. Fifteen pork loins were procured randomly from three groups, Con (fed basal diet), Se15 (fed 0.15 ppm organic Se along with 0.10 ppm inorganic Se), and Se45 (fed 0.45 ppm organic Se along with 0.10 ppm inorganic Se). Each sample was analyzed for Se contents, antioxidant properties (glutathione peroxidase [GPx] activity, 2,2'-azinobis-[3-ethylbenzothiazoline-6-sulfonic acid] [ABTS] and 2,2-diphenyl-1-picrylhydrazyl [DPPH] radical scavenging activities, 2-thiobarbituric acid reactive substances), physicochemical properties (water holding capacity, pH, color), and metabolomic analysis during 14-day storage period. Se45-supplemented group showed significantly higher Se contents and GPx activity than the other groups throughout the storage period. However, other antioxidant properties were not significantly affected by Se supplementation. Selenium supplementation did not have an adverse impact on physicochemical properties. Nuclear Magnetic Resonance-based metabolomic analysis indicated that the selenium supply conditions were insufficient to induce metabolic change. These results suggest that organic Se (0.15 and 0.45 ppm) can accumulate high Se content in pork loins without compromising quality.

The Role of Selenitetriglycerides in Enhancing Antioxidant Defense Mechanisms in Peripartum Holstein-Friesian Cows.

The transition period in high-yielding dairy cows is a critical phase marked by an elevated risk of oxidative stress. This study evaluated the effect of oral selenitetriglyceride supplementation on oxidative stress management in periparturient cows. A controlled experiment was conducted on 12 cows, divided into two groups: the experimental group (STG) received selenitetriglycerides (0.5 mg Se/kg BW), while the control group (CON) was given a placebo, starting 12 days before calving until the calving day. Blood and liver tissue samples were collected at predetermined intervals around the time of parturition. The study observed a significant increase in serum selenium levels and NEFA stabilization in the STG group compared with the control. Antioxidant parameters indicated elevated GSH-Px and CAT concentrations in the STG group. Liver gene expression analysis revealed a significant increase in SOD2 mRNA levels in the STG group (FC = 4.68, p < 0.01). Conversely, GSH-Px3 expression significantly decreased (FC = 0.10, p < 0.05) on the 7th day postpartum in the CON group. However, SOD1, SOD3, and CAT expressions remained stable in both groups. These findings highlight the beneficial role of selenitetriglycerides in enhancing antioxidant capacity and influencing specific gene expressions associated with oxidative stress management in dairy cows during the peripartum period.

Evaluation of the Neuroprotective Effect of Organic Selenium Compounds: An in Vitro Model of Alzheimer's Disease.

Selenium (Se) is an essential trace element for human health and plays an important role in the development and maintenance of central nervous system functions. Se deficiency has been associated with cognitive decline and increased oxidative stress. The increase in oxidative stress is one of the hypotheses for the emergence and worsening of neurodegenerative diseases, such as Alzheimer's disease (AD). To investigate the neuroprotective effects of organic Se compounds in human neuroblastoma cells (SH-SY5Y) differentiated into cholinergic neurons-like. The SH-SY5Y cells were differentiated into cholinergic neuron-like with retinoic acid (RA) and brain-derived neurotrophic factor (BDNF). AD was mimicked exposing the cells to okadaic acid (OA) and beta-amyloid protein (Aß). The neuroprotective effect of organic Se compounds, selenomethionine (SeMet) and Ebselen, was evaluated through cell viability tests, acetylcholinesterase and antioxidant enzyme activities, and detection of reactive oxygen species (ROS). None of the SeMet concentrations tested protected against the toxic effect of OA + Aß. On the other hand, previous exposure to 0.1 and 1 µM Ebselen protected cells from the toxic effect of OA + Aß. Cell differentiation induced by RA and BDNF exposure was effective, showing characteristics of neuronal cells, and pointing to a promising model of AD. Ebselen showed a protective effect, but more studies are needed to identify the mechanism of action.

The role of selenium in shaping mice brain metabolome and selenoproteome through the gut-brain axis by combining metabolomics, metallomics, gene expression, and amplicon sequencing.

Selenium (Se) is a trace element crucial for human health. Recently, the impact of Se supplementation on gut microbiota has been pointed out as well as its influence on the expression of certain selenoproteins and gut metabolites. This study aims to elucidate the link between Se supplementation, brain selenoproteins and brain metabolome as well as the possible connection with the gut-brain axis. To this end, an in vivo study with 40 BALB/c mice was carried out. The study included conventional (n=20) and mice model with microbiota depleted by antibiotics (n=20) under a regular or Se supplemented diet. Brain selenoproteome was determined by a transcriptomic/gene expression profile, while brain metabolome and gut microbiota profiles were accomplished by untargeted metabolomics and amplicon sequencing, respectively. The total content of Se in brain was also determined. The selenoproteins genes Dio and Gpx isoenzymes, SelenoH, SelenoI, SelenoT, SelenoV, and SelenoW and 31 metabolites were significantly altered in the brain after Se supplementation in conventional mice, while 11 selenoproteins and 26 metabolites were altered in microbiota depleted mice. The main altered brain metabolites were related to glyoxylate and dicarboxylate metabolism, amino acid metabolism, and gut microbiota that have been previously related with the gut-brain axis (e.g., members of Lachnospiraceae and Ruminococcaceae families). Moreover, specific associations were determined between brain selenoproteome and metabolome, which correlated with the same bacteria, suggesting an intertwined mechanism. Our results demonstrated the effect of Se on brain metabolome through specific selenoproteins gene expression and gut microbiota.