Increase In Selenium Levels Research Articles

Clinical Signs and Laboratory Tests for the Differential Diagnosis ofAndrogenic and Post-COVID-19 Alopecia in Women

Background: Pathological hair loss in women has emerged as a prevalent cause for seeking specialized dermatological and cosmetic services. The most common type of this condition is androgenetic alopecia, which arises due to hormonal and micronutrient imbalances.Furthermore, during the COVID-19 epidemic, there has been a notable increase in the number of female patients with pathological hair loss as a complication of the disease, with some individualsexperiencing alopecia the sole indication of asymptomatic COVID-19. Aims: The aim of the study wassearch for objective criteria for the differential diagnosis of androgenetic alopecia and post-COVID alopecia in women based on informative trichological and laboratory markers. Materials and methods: The including criteria for androgenetic alopecia (AGA) group were elevated dihydrotestosterone (DHT) levels, clinical indications of alopecia corresponding to initial stages of the condition, and a past experience of continuous observation untilFebruary 2020. For the post-COVID alopecia (COVID) group, inclusion criteria were a confirmed diagnosis of COVID-19 using RT-PCR and the presence of alopecia symptoms emerging within a year post-infection. Evaluation of quantitative characteristics of hairs was conducted was carried out based on trichogram and phototrichogram data, followed by image processing using a computer diagnostic program. Key indicators for hair growth were identified in patients' plasma, including DHT, vitamins B9 (folic acid), B12, D (25(OH)-D3 form), E, as well as calcium (Ca), iron (Fe), magnesium (Mg), selenium (Se), copper (Cu), and zinc (Zn). CART algorithm (Classification and Regression Trees) based on recursive partitioning of available data with selection of informative predictors and formation of a tree-like hierarchical structurewas applied to determine criteria to differentiate between patients with androgenetic and post-COVID alopecia. Results: Analysis of trichograms and phototrichograms revealed that unlike androgenetic alopecia, which primarily impacts hair follicles in the telogen and anagen phases in the androgen-dependent zone, post-COVID hair loss presents as a diffuse telogen effluvium pattern, involving the androgen-dependent (parietal) area of the scalp. Notably, patients with post-COVID alopecia exhibited elevated dihydrotestosterone levels compared to reference values, with no significant differencein comparison to AGA. While there were no variations in vitamin and certain trace element levels (Fe, Ca, Mg, Zn), individuals in COVID group have demonstrated a statistically significant reduction in copper content (46.4% lower than AGA; p=0.006) alongside an increase in selenium levels (24.7% higher than AGA; p=0.003). Conclusions: The performed study for the first time presents objective criteria for the differential diagnosis of androgenetic and post-COVID alopecia in women. The data obtained show a diffuse pattern of telogen effluvium after recovering from COVID-19, linked to an imbalance in trace elements - specifically, a decrease in copper (Cu) and an increase in selenium (Se). Based on this fact, the algorithm CART used allows for a highly effective differentiation of the compared variants of pathological hair loss in studied patients and forms the basis for pathogenetically justified conservative therapy.

Enhancing Endothelial Function with Nutrient-Enriched Table Hen Eggs: A Randomized Study in Patients Recovering from Acute Coronary Syndrome.

This study investigated the effect of consumption of table eggs enriched with n-3 polyunsaturated fatty acids (n-3 PUFA), lutein, vitamin E and selenium on microvascular function, oxidative stress and inflammatory mediators in patients after acute coronary syndrome (ACS). In a prospective, randomized, interventional, double-blind clinical trial, ACS patients were assigned to either the Nutri4 (N=15, mean age: 57.2±9.2 years), or the Control group (N=13; mean age 56.8±9.6 years). The Nutri4 group consumed three enriched hen eggs daily for three weeks, providing approximately 1.785 mg of vitamin E, 0.330 mg of lutein, 0.054 mg of selenium and 438 mg of n-3 PUFAs. Biochemical parameters, including serum lipids, liver enzymes, nutrient concentrations, serum antioxidant enzyme activity (catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD)), and markers of oxidative stress (thiobarbituric acid reactive substances (TBARS) and ferric reducing ability (FRAP)), were assessed before and after the dietary interventions. Additionally, arterial blood pressure, heart rate, body composition, fluid status, anthropometric measurements, and skin microvascular blood flow responses to various stimuli (postocclusive reactive hyperemia (PORH), acetylcholine- (AchID), and sodium nitroprusside- (SNPID)) were measured using laser Doppler flowmetry (LDF) throughout the study. The intake of Nutri4 eggs led to a significant reduction in LDL cholesterol levels, while the levels of total cholesterol remained within the established reference values. Consuming Nutri4 eggs resulted in a 12.7% increase in serum vitamin E levels, an 8.6% increase in selenium levels, and demonstrated a favorable impact on microvascular reactivity, as evidenced by markedly improved PORH and ACh ID. Nutri4 eggs exerted a significant influence on the activity of GPx and SOD, with no observed changes in TBARS or FRAP values. The consumption of Nutri4 eggs positively influenced microvascular function in individuals with ACS, without eliciting adverse effects on oxidative stress.

A new perspective on selenium's impact on renal function: European population-based analysis of plasma proteome-mediated Mendelian randomization study.

The relationship between selenium and renal function has always attracted widespread attention. Increased selenium level has been found to cause impaired renal function in our previous study, but the mechanism is not clear. In this study, we evaluate the potential mediating effects of plasma proteome in the association of selenium level and renal function to understand the mechanisms of selenium's effect on renal function. Utilizing two-sample two-step mediating mendelian randomization (MR) methodology to investigate the genetically causal relationship between selenium level and renal function as well as the role of the plasma proteome in mediating them. Additionally, the mediating proteins were enriched and analyzed through bioinformatics to understand the potential mechanisms of selenium effects on renal function. In the MR analysis, an increase in selenium level was found to decrease estimated glomerular filtration rate (eGFR). Specifically, for each standard deviation (SD) increase in selenium levels, eGFR levels are reduced by 0.003 SD [Beta (95% CI): -0.003 (-0.004 ~ -0.001), P=0.001, with no observed heterogeneity and pleiotropy]. Through mediation analysis, 35 proteins have been determined mediating the genetically causal effects of selenium on the levels of eGFR, including Fibroblast growth factor receptor 4 (FGFR4), Fibulin-1, Cilia- and flagella-associated protein 45, Mothers against decapentaplegic homolog 2 (SMAD2), and E3 ubiquitin-protein ligase ZNRF3, and the mediation effect rates of these proteins ranged from 1.59% to 23.70%. In the enrichment analysis, 13 signal transduction pathways, including FGFR4 mutant receptor activation and Defective SLC5A5 causing thyroid dyshormonogenesis 1, were involved in the effect of selenium on eGFR levels. Our finding has revealed the underlying mechanism by which increased selenium level lead to deterioration of renal function, effectively guiding the prevention of chronic kidney disease and paving the way for future studies.

Prenatal Maternal Low Selenium, High Thyrotropin, and Low Birth Weights.

In consideration of the potential roles of selenoproteins in thyroid function, we aimed to evaluate the association of low selenium status with hypothyroidism during pregnancy and the association of maternal low thyroid function with infant birth size. We conducted a prospective birth cohort study in Shanghai in 2010 and investigated 1931 pregnant mothers of gestational weeks 28-36. Maternal serum selenium and thyrotropin (TSH) levels were determined and birth weights and lengths of newborns were measured. Other covariates were obtained through maternal interviews and medical records. A non-linear association was observed between maternal selenium and TSH levels. Two-piecewise multivariable linear regression models were therefore applied to assess the association of serum selenium with TSH levels, and multivariable linear regression models were applied to assess the association of TSH levels with birth weight/length. Adjusting for potential confounders, when maternal serum selenium levels < 103.7μg/L (P25th), each unit increase in selenium levels (μg/L) was significantly associated with a decrease of 0.014μIU/mL in TSH levels (β = - 0.014, 95%CI - 0.025, - 0.002, P = 0.023). However, when selenium levels ≥ 103.7μg/L, there were no significant relationships between selenium and TSH (β = 0.000, 95%CI - 0.001, 0.002, P = 0.859). Maternal TSH levels were significantly inversely associated with infant birth weight (β = - 0.060, 95%CI - 0.100, - 0.010, P = 0.010). We observed a non-linear association between maternal selenium status and TSH levels. Low selenium status during pregnancy may associate with low thyroid function that was related with low birth weights. Graphical abstract .

Assessing the Efficacy of Dietary Selenomethionine Supplementation in the Setting of Cardiac Ischemia/Reperfusion Injury.

Oxidative stress is a major hallmark of cardiac ischemia/reperfusion (I/R) injury. This partly arises from the presence of activated phagocytes releasing myeloperoxidase (MPO) and its production of hypochlorous acid (HOCl). The dietary supplement selenomethionine (SeMet) has been shown to bolster endogenous antioxidant processes as well as readily react with MPO-derived oxidants. The aim of this study was to assess whether supplementation with SeMet could modulate the extent of cellular damage observed in an in vitro cardiac myocyte model exposed to (patho)-physiological levels of HOCl and an in vivo rat model of cardiac I/R injury. Exposure of the H9c2 cardiac myoblast cell line to HOCl resulted in a dose-dependent increase in necrotic cell death, which could be prevented by SeMet supplementation and was attributed to SeMet preventing the HOCl-induced loss of mitochondrial inner trans-membrane potential, and the associated cytosolic calcium accumulation. This protection was credited primarily to the direct oxidant scavenging ability of SeMet, with a minor contribution arising from the ability of SeMet to bolster cardiac myoblast glutathione peroxidase (GPx) activity. In vivo, a significant increase in selenium levels in the plasma and heart tissue were seen in male Wistar rats fed a diet supplemented with 2 mg kg−1 SeMet compared to controls. However, SeMet-supplementation demonstrated only limited improvement in heart function and did not result in better heart remodelling following I/R injury. These data indicate that SeMet supplementation is of potential benefit within pathological settings where excessive HOCl is known to be generated but has limited efficacy as a therapeutic agent for the treatment of heart attack.

Dietary supplementation of selenium yeast enhances the antioxidant capacity and immune response of juvenile Eriocheir Sinensis under nitrite stress

This study elucidates the response to nitrite stress and the effect of dietary selenium supplements on the growth, antioxidant activity, immunity and transcriptome of juvenile Chinese mitten crab Eriocheir sinensis. In the control group, the crabs were fed the diet without selenium supplementation and there was no nitrite addition to the water. In the test group, the crabs were fed diets with three levels of selenium 0 (N1), 0.5 (N2) and 1.0 (N3) mg/kg in the water containing 2 mg/L NO2N as a stress factor for eight weeks. Feed conversion ratio (FCR) was improved by adding dietary selenium. There was no significant difference in specific growth rate and weight gain between N1 and the control groups, or among different selenium levels in the test group. The superoxide dismutase (SOD) activity was significantly lower, but malondialdehyde (MDA) was higher in the N1 group than those in the serum and hepatopancreas of the control group. The activities of SOD, glutathione peroxidase (GPx) and acid phosphatase increased at the medium level of selenium but decreased as the level of dietary selenium increased to 1.0 mg/kg. The serum lysozyme (LZM) activity increased but the MDA content in both serum and hepatopancreas decreased with the increase of selenium levels. The total clean reads of the crabs in the control group, N1 and N3 groups reached 390.7M and were assembled into 106 471 transcripts. Compared with the control group, 1196 gene were significantly expressed (588-up and 608-down) in the N1 group under nitrite stress. Between the N1 and N3 groups, the expression of 1537 genes (751-up and 786-down) were significantly different. KEGG pathway analysis reveals that 11 and 19 pathways were significantly different between N1 and control and between N3 and N1 groups, respectively. Transcriptome results demonstrate that nutrient metabolism is much more active in crabs fed additional selenium under nitrite stress. This study indicates that dietary selenium can improve both antioxidant capacity and immune response and alter the protein and carbohydrate metabolism of E. sinensis under nitrite stress.

25 - Role of selenomethionine supplementation in the modulation of damage during inflammation and myocardial ischemia/reperfusion injury

Oxidative stress is a major hallmark of cardiac ischemia/reperfusion (I/R) injury. This partly arises from the presence of activated phagocytes releasing the heme enzyme myeloperoxidase (MPO) and the associated production of hypochlorous acid (HOCl) and hypothiocyanous acid (HOSCN). The dietary supplement selenomethionine (SeMet) has been shown to both bolster endogenous antioxidant processes and readily react with MPO-derived oxidants, yet its ability to protect against cardiac I/R injury is unknown. The aim of this study was to assess whether supplementation with SeMet could modulate the extent of cellular damage observed in an in vitro cardiac myocyte model exposed to (patho)-physiological levels of HOCl and HOSCN and an in vivo rat model of cardiac I/R injury. Exposure of cardiac myocytes to HOCl resulted in a dose-dependent increase in necrotic cell death, which could be prevented by SeMet supplementation (25 µM). This was attributed to SeMet preventing the HOCl-induced loss of mitochondrial inner trans-membrane potential, and the associated cytosolic calcium accumulation, together with bolstering the activity of the selenium-dependent antioxidant enzyme glutathione peroxidase. In contrast, no apparent protection of SeMet supplementation was evident upon exposure of cells to HOSCN, where higher oxidant concentrations (100 – 125 µM) were required to induce cell death. In vivo, a significant increase in selenium levels in the plasma, brain, kidney, and heart tissue were seen in rats fed a diet supplemented with 2 mg/kg SeMet compared to controls. Echocardiograph assessment of LV function at 4 weeks post-surgical intervention in the I/R injury cohort demonstrated limited improvement in fractional shortening and ejection fraction in SeMet-supplemented fed rats compared to controls. However, a more marked improvement was observed in the sham injury cohort, indicating SeMet supplementation’s potential cardiac health benefit.

Effect of Micronutrient Supplementation on Mood in Nursing Home Residents

One third of older people in nursing and/or residential homes have significant symptoms of depression. In younger people, deficiencies in selenium, vitamin C and folate are associated with depression. This study examines the association between micronutrient status and mood before and after supplementation. The objective was to determine whether the administration of selenium, vitamin C and folate improved mood in frail elderly nursing home residents. Mood was assessed using the Hospital Anxiety and Depression rating scale (HAD), and Montgomery-Åsberg Depression Rating Scale (MADRS). Micronutrient supplementation was provided for 8 weeks in a double-blinded randomised controlled trial. Significant symptoms of depression (29%) and anxiety (24%) were found at baseline. 67% of patients had low serum concentrations of vitamin C, but no-one was below the reference range for selenium. Depression was significantly associated with selenium levels, but not with folate or vitamin C levels. No individual with a HAD depression score of ≧8, had selenium levels >1.2 µM. In those patients with higher HAD depression scores, there was a significant reduction in the score and a significant increase in serum selenium levels after 8 weeks of micronutrient supplementation. Placebo group scores were unchanged. This small study concluded that depression was associated with low levels of selenium in frail older individuals. Following 8 weeks of micronutrient supplementation, there was a significant increase in selenium levels and improved symptoms of depression occurred in a subgroup.

Characteristics of selenazolidine prodrugs of selenocysteine: toxicity, selenium levels, and glutathione peroxidase induction in A/J mice

We have previously reported the synthesis and characterization of two new classes of selenazolidine-4(R)-carboxylic acids (2-oxo and 2-methyl-SCAs) (OSCA and MSCA, respectively), as well as the “parent” compound, selenazolidine-4(R)-carboxylic acid (SCA, selenaproline). These compounds were designed as prodrugs of L-selenocysteine with potential application in cancer chemoprevention or other clinical uses. We will be exploring the chemopreventive activity of the new compounds in the well-established A/J mouse model of tobacco-induced lung carcinogenesis. The objectives of the present study were to investigate several fundamental biochemical endpoints after selenazolidine administration compared with other selenium-containing agents. Groups of mice were fed either AIN-76A diet alone or the diet supplemented with the following selenium compounds (ppm Se): sodium selenite (5), L-selenomethionine (3.75), L-selenocystine (15), Se-methyl-L-selenocysteine (3), MSCA (5, 10, or 15), OSCA (5, 10, or 15), or SCA (5, 10, or 15). After 28 days of supplementation, toxicity of the selenazolidines was not evident, as measured by outward appearance and behavior, body and organ weight changes, and histological evaluation of liver and lung tissue. Select treatment groups showed significant increases in selenium levels in blood and tissues. Increased activity of selenium-dependent glutathione peroxidase (GPx) in blood and liver illustrated that the selenazolidines provided a source of biologically-available selenium.

Characteristics of selenazolidine prodrugs of selenocysteine: toxicity, selenium levels, and glutathione peroxidase induction in A/J mice

We have previously reported the synthesis and characterization of two new classes of selenazolidine-4(R)-carboxylic acids (2-oxo and 2-methyl-SCAs) (OSCA and MSCA, respectively), as well as the “parent” compound, selenazolidine-4(R)-carboxylic acid (SCA, selenaproline). These compounds were designed as prodrugs of L-selenocysteine with potential application in cancer chemoprevention or other clinical uses. We will be exploring the chemopreventive activity of the new compounds in the well-established A/J mouse model of tobacco-induced lung carcinogenesis. The objectives of the present study were to investigate several fundamental biochemical endpoints after selenazolidine administration compared with other selenium-containing agents. Groups of mice were fed either AIN-76A diet alone or the diet supplemented with the following selenium compounds (ppm Se): sodium selenite (5), L-selenomethionine (3.75), L-selenocystine (15), Se-methyl-L-selenocysteine (3), MSCA (5, 10, or 15), OSCA (5, 10, or 15), or SCA (5, 10, or 15). After 28 days of supplementation, toxicity of the selenazolidines was not evident, as measured by outward appearance and behavior, body and organ weight changes, and histological evaluation of liver and lung tissue. Select treatment groups showed significant increases in selenium levels in blood and tissues. Increased activity of selenium-dependent glutathione peroxidase (GPx) in blood and liver illustrated that the selenazolidines provided a source of biologically-available selenium.

Increase in total blood antioxidant status and selenium levels in black patients with active vitiligo.

Oxidative stress could be an important phenomenon leading to melanocyte death in vitiligo. The accumulation of hydrogen peroxide (H2O2) and low catalase levels have recently been demonstrated in the epidermis of vitiligo patients. Few abnormalities of antioxidants have been found in the blood of patients with vitiligo, except for an elevation of selenium. No studies on oxidative stress have been performed so far on patients with skin phototype VI (Fitzpatrick classification). To study the blood antioxidant status of black patients with active generalized vitiligo. Randox total antioxidant status, selenium, ferritin, transferrin, ceruloplasmin, tocopherol, and retinol levels were evaluated in blood samples obtained from 11 dark-skinned patients from the French West Indies (Isle of Martinique) with recent active lesions of vitiligo and from 11 age- and sex-matched healthy volunteers. Total blood antioxidant status and selenium levels were significantly increased in vitiligo patients, compared to those in sex- and age-matched controls (P < 0.01 and P < 0.02, respectively). Blood levels of ferritin, transferrin, ceruloplasmin, retinol, and tocopherol were not significantly modified. This is the first report on the global blood antioxidant status in vitiligo. The increase in total blood antioxidant status observed in black patients was an unexpected result that needs to be confirmed and explained by further studies. The spontaneous increase in selenium levels could be of interest, as it has been recommended in the treatment of vitiligo.

Protective Effect of Melatonin on Antioxidative System in Experimental Ischemia-Reperfusion of Rat Small Intestine

Aims: Effect of exogenously administered melatonin (N-acetyl 5-methoxytryptamine) on antioxidant systems in experimental Ischemia–Reperfusion (I-R) of rat gastrointestinal system (GIS) was examined.Methods: A total of 40 rats were divided into 4 groups: Group 1 (Sham), Group 2 (I-R), Group 3 (I-R + 10 mg/kg melatonin) and Group 4 (I-R + 20 mg/kg melatonin). Activity levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined in small intestines.Results: There was a significant (p<0.05) reduction in GSH-Px levels in Group 2 (64.16±7.02 U/mg protein) compared to Group 1 (80.15±9.32 U/mg protein). We observed a meaningful increase in GSH-Px levels in melatonin applied groups (Group 3: 75.94±9.83 U/mg protein, Group 4: 78.55±9.11 U/mg protein) compared to Group 2. Correspondingly, SOD activity levels were significantly reduced (p<0.001) in Group 2 (24.14±4.35 U/mg protein) compared to controls (52.91±6.13 U/mg protein). A stronger effect (p<0.001) of melatonin was observed on SOD levels compared to GSH-Px levels in both doses (Group 3: 38.96±6.39 U/mg protein, Group 4: 43.07±7.76 U/mg protein). Levels of selenium were reduced significantly in Group 2 (1.11±0.31 μg/g tissue) compared to Group 1 (2.01±0.19 μg/g tissue). Melatonin application in Group 3 (1.13±0.28 μg/g tissue) and Group 4 (1.89±0.48 μg/g tissue) caused an increase in selenium levels. There was a strong correlation between increases in selenium and GSH-Px levels in Group 4 (r:0.651 p<0.01).Conclusions: Melatonin seems to exert its antioxidant effect in GIS tract by stimulating SOD and GSH-Px. Selenium also seems to have an antioxidant contribution on protecting rat gastrointestinal tract I-R injury.

Inhibition of 7,12-dimethylbenz[a]anthracene-induced lipid peroxidation and mammary tumor development in rats by vitamin E in conjunction with selenium.

The effects of combined dietary vitamin E supplementation and a relatively low increase in selenium levels on 7,12-dimethylbenz[a]anthracene (DMBA) induction of lipid peroxidation in the short term and development of mammary tumors in the long term were investigated in female Sprague-Dawley rats. Control animals were fed the basal diet (20 mg/kg vitamin E and 0.6 mg/kg selenium) throughout the experiment. Three other groups received a high vitamin E diet (235 mg/kg vitamin E and 0.6 mg/kg selenium) at different times, the first two from three weeks after DMBA treatment and the other throughout the experiment. When the vitamin E diet with selenium supplementation was applied until three weeks after DMBA or until the termination of the experiment, tumor yields (tumors per rat) were significantly inhibited compared with the control group. On the other hand, delaying the supplementation of vitamin E until three weeks postcarcinogen produced no prophylactic effect. The elevation of lipid peroxidation levels observed immediately after DMBA administration was also significantly inhibited in both mammary fat pads and livers of animals in the high vitamin E group. It was therefore concluded that the inhibitory effect of vitamin E in combination with selenium on tumorigenesis might be causally related to reduction of carcinogen treatment associated with lipid peroxidation, the latter presumably playing an important role in DMBA-induced mammary carcinogenesis.

The protective potency of marine animal meat against the neurotoxicity of methylmercury: Its relationship with the organ distribution of mercury and selenium in the rat

The meats of two marine animals, that were known to contain high levels of both methylmercury and selenium, were compared with respect to their protective potencies against the neurotoxicity of methylmercury. The organ distributions of selenium and mercury in rats given diets containing these meats was also compared. Weanling rats were fed for 12 wk on a diet containing 17·5 ppm methylmercuric chloride and one of two levels of selenium (0·3 or 0·6 ppm) originating from the meat of sebastes ( Sebastes iracundus) or of the sperm whale ( Physeter catodon), or from sodium selenite. The protection conferred by sebastes meat was roughly equal to that of the selenite regarding growth rate but was considerably greater with respect to the neurological signs. By both criteria, sperm-whale meat was less effective than sebastes meat and selenite in providing protection. The organ distribution pattern of selenium and mercury showed that selenium in the blood, brain and spinal cord was positively correlated with neurological protection, while total mercury and methylmercury in those organs were negatively correlated with neurological protection. The level of protection (delay of the neurological manifestations by nearly 7 wk) corresponding with the increase in selenium levels in the nervous system (from about 1 50 to 1 10 of the methylmercury levels on a molar basis) indicated that the protective mechanism was not simply direct conjugation of selenium with methylmercury. It has previously been noted that tuna fish containing high levels of selenium provide protection against methylmercury toxicity and it may be that all marine animals rich in both selenium and methylmercury afford this protection.