Trace mineral concentrations in Canadian beef calves at weaning.

Objective: To describe the copper and selenium statuses of beef calves at weaning. Animal: Calves (n = 1998) were sampled from 106 Canadian cow-calf herds in the fall of 2021. Procedure: Serum samples from calves were tested for copper, selenium, and molybdenum concentrations. Results: Although the percentages of calves classified as selenium deficient (< 0.025 ppm) were relatively low (0.5% western Canada, 3% eastern Canada), 53% of calves from western Canada and 77% of calves from eastern Canada were classified as having less than adequate selenium concentrations (< 0.08 ppm). Copper deficiency (< 0.5 ppm) was common in calves from both western (17%) and eastern (14%) Canada. High molybdenum concentrations (> 0.10 ppm) were identified in 6% of calves from western Canada and 7% of calves from eastern Canada. Conclusion: Selenium concentrations were higher in calves from western Canada than from those in eastern Canada (P < 0.001). Copper and molybdenum concentrations were not significantly different between western and eastern Canada. Less-than-adequate serum copper was the most common deficiency identified in Canadian beef calves at weaning. Clinical relevance: Trace minerals are important for immune system function in calves at weaning. Selenium concentrations in calves at weaning were lower than in cows from the same herds collected at pregnancy testing 2 y earlier. Copper deficiency was also identified, though less frequently than for mature cows. Supplementation programs for calves should be customized based on testing and recognize both regional and age differences in risk.

Concentrations d'oligo-éléments minéraux chez les veaux de boucherie canadiens au sevrage. Objectif: Décrire les statuts en cuivre et en sélénium des veaux de boucherie au sevrage. Animal: Des veaux (n = 1998) ont été échantillonnés dans 106 troupeaux de type vache-veau canadiens à l'automne 2021. Procédure: Des échantillons de sérum de veaux ont été testés pour déterminer les concentrations de cuivre, de sélénium et de molybdène. Résultats: Même si les pourcentages de veaux classés comme déficients en sélénium (< 0,025 ppm) étaient relativement faibles (0,5 % dans l'ouest du Canada, 3 % dans l'est du Canada), 53 % des veaux de l'ouest du Canada et 77 % des veaux de l'est du Canada étaient classés comme ayant moins des concentrations de sélénium moins qu'adéquates (< 0,08 ppm). Une carence en cuivre (< 0,5 ppm) était courante chez les veaux de l'ouest (17 %) et de l'est (14 %) du Canada. Des concentrations élevées de molybdène (> 0,10 ppm) ont été identifiées chez 6 % des veaux de l'ouest du Canada et 7 % des veaux de l'est du Canada. Conclusion: Les concentrations de sélénium étaient plus élevées chez les veaux de l'ouest du Canada que chez ceux de l'est du Canada (P < 0,001). Les concentrations de cuivre et de molybdène n'étaient pas significativement différentes entre l'ouest et l'est du Canada. Un taux de cuivre sérique nettement insuffisamment était la carence la plus courante identifiée chez les veaux de boucherie canadiens au sevrage. Pertinence clinique: Les oligo-éléments sont importants pour le fonctionnement du système immunitaire des veaux au sevrage. Les concentrations de sélénium chez les veaux au sevrage étaient inférieures à celles des vaches des mêmes troupeaux collectées lors des tests de gestation deux ans plus tôt. Des carences en cuivre ont également été identifiées, quoique moins fréquemment que chez les vaches matures. Les programmes de supplémentation pour les veaux doivent être personnalisés en fonction des tests et reconnaître les différences de risque selon la région et l'âge.(Traduit par Dr Serge Messier).

Maternal selenium deficiency during pregnancy in association with autism and ADHD traits in children: The Odense Child Cohort.

BACKGROUND: Selenoproteins regulate pathways controlling neurodevelopment, e.g., redox signaling and thyroid hormone metabolism. However, studies investigating maternal selenium in relation to child neurodevelopmental disorders are scarce. METHODS: 719 mother-child pairs from the prospective population-based Odense Child Cohort study in Denmark were included. Three selenium biomarkers, i.e. concentrations of serum selenium, selenoprotein P (SELENOP), and activity of glutathione peroxidase 3 (GPX3), along with serum copper, zinc and iron were measured in early third trimester (at 28.9+/-0.8 weeks of pregnancy). ADHD and ASD traits in children were assessed systematically using the established Child Behaviour Checklist at 5 years of age, based on a Danish reference cohort with cut-off at 90th percentile. Multivariable regression models adjusted for biologically relevant confounders were applied. RESULTS: 155 of 719 (21.6 %) children had ASD traits and 59 of 719 (8.2 %) children had traits of ADHD at 5 years of age. In crude and adjusted models, all three selenium biomarkers associated inversely with ADHD traits. For ADHD, fully adjusted OR for 10 µg/L increment in selenium was 0.76 (95 % CI 0.60, 0.94), for one mg/L increment in SELENOP was 0.73 (0.56, 0.95), and for 10 U/L increment in GPx3 was 0.93 (0.87,1.00). Maternal total selenium was inversely associated with child ASD traits, OR per 10 µg/L increment was 0.85 (0.74, 0,98). SELENOP and GPx3 were not associated with ASD traits. The associations were specific to selenium, as other trace elements such as copper, zinc, or iron were not associated with the outcomes. CONCLUSIONS: The results provide coherent evidence for selenium deficiency as a risk factor for ADHD and ASD traits in an environment with borderline supply, the causality of which should be elucidated in a randomized controlled trial.

LLL 44-1 Micronutrients in clinical nutrition: Trace elements.

BACKGROUND: Trace elements are an essential component of metabolism and medical nutrition therapy, with key roles in metabolic pathways, antioxidation, and immunity, which the present course aims at summarizing. RESULTS: Medical nutrition therapy includes the provision of all essential trace elements. The clinical essential issues are summarized for Copper, Iron, Selenium, Zinc, Iodine, Chromium, Molybdenum, and Manganese: the optimal analytical techniques are presented. The delivery of all these elements occurs nearly automatically when the patient is fed with enteral nutrition, but always requires separate prescription in case of parenteral nutrition. Isolated deficiencies may occur, and some patients have increased requirements, therefore a regular monitoring is required. The clinicians should always consider the impact of inflammation on blood levels, mostly lowering them even in absence of deficiency. CONCLUSION: This text summarises the most relevant clinical manifestations of trace element depletion and deficiency, the difficulties in assessing status, and makes practical recommendations for provision for enteral and parenteral nutrition.

Lrp8 knockout mice fed a selenium-replete diet display subtle deficits in their spatial learning and memory function.

Selenium is an essential trace element that is delivered to the brain by the selenium transport protein selenoprotein P (SEPP1), primarily by binding to its receptor low-density lipoprotein receptor-related protein 8 (LRP8), also known as apolipoprotein E receptor 2 (ApoER2), at the blood-brain barrier. Selenium transport is required for several important brain functions, with transgenic deletion of either Sepp1 or Lrp8 resulting in severe neurological dysfunction and death in mice fed a selenium-deficient diet. Previous studies have reported that although feeding a standard chow diet can prevent these severe deficits, some motor coordination and cognitive dysfunction remain. Importantly, no single study has directly compared the motor and cognitive performance of the Sepp1 and Lrp8 knockout (KO) lines. Here, we report the results of a comprehensive parallel analysis of the motor and spatial learning and memory function of Sepp1 and Lrp8 knockout mice fed a standard mouse chow diet. Our results revealed that Sepp1 knockout mice raised on a selenium-replete diet displayed motor and cognitive function that was indistinguishable from their wild-type littermates. In contrast, we found that although Lrp8-knockout mice fed a selenium-replete diet had normal motor function, their spatial learning and memory showed subtle deficits. We also found that the deficit in baseline adult hippocampal neurogenesis exhibited by Lrp8-deficit mice could not be rescued by dietary selenium supplementation. Taken together, these findings further highlight the importance of selenium transport in maintaining healthy brain function. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Bisphenol A and selenium deficiency exposure induces pyroptosis and myogenic differentiation disorder in chicken muscle stomach.

Bisphenol A (BPA), which is commonly found in the environment due to its release from the use of plastics and food overpacks, has become a major stressor for environmental sustainability and livestock and poultry farming health. Selenium (Se) deficiency causes structural damage and inflammatory responses to the digestive system and muscle tissue, and there is a potential for concurrent space-time exposure to nutritional deficiency diseases and environmental toxicants in livestock and poultry. The mechanisms of damage to chicken muscular stomach from BPA or/and Se deficiency treatment are still not known. Here, we established a chicken model of BPA (20 mg/kg) or/and Se deficiency (0.039 mg/kg) exposure, and detected histopathological changes in the muscular stomach tissue, the levels of iNOS/NO pathway, IL-6/JAK/STAT3 pathway, pyroptosis, and myogenic differentiation by H&E staining, immunofluorescence staining, real-time quantitative PCR, and western blot methods. The data revealed that BPA or Se deficiency exposure caused gaps between muscle fibers with inflammatory cell infiltration; up-regulation of the iNOS/NO pathway and IL-6/JAK/STAT3 pathway; up-regulation of NLRP3/Caspase-1-dependent pyroptosis related genes; down-regulation of muscle-forming differentiation (MyoD, MyoG, and MyHC) genes. The combination of BPA and Se deficiency was associated with higher toxic impairment than alone exposure. In conclusion, we discovered that BPA and Se deficiency caused myogastric pyroptosis and myogenic differentiation disorder. These findings provide a theoretical basis for the co-occurrence of animal nutritional deficiency diseases and environmental toxicant exposures in livestock and poultry farming, and may provide important insights into limiting the production of harmful substances.

Selenium deficiency causes hypertension by increasing renal AT1 receptor expression via GPx1/H2O2/NF-κB pathway.

Epidemiological studies show an association between low body selenium and the risk of hypertension. However, whether selenium deficiency causes hypertension remains unknown. Here, we report that Sprague-Dawley rats fed a selenium-deficient diet for 16 weeks developed hypertension, accompanied with decreased sodium excretion. The hypertension of selenium-deficient rats was associated with increased renal angiotensin II type 1 receptor (AT1R) expression and function that was reflected by the increase in sodium excretion after the intrarenal infusion of the AT1R antagonist candesartan. Selenium-deficient rats had increased systemic and renal oxidative stress; treatment with the antioxidant tempol for 4 weeks decreased the elevated blood pressure, increased sodium excretion, and normalized renal AT1R expression. Among the altered selenoproteins in selenium-deficient rats, the decrease in renal glutathione peroxidase 1 (GPx1) expression was most prominent. GPx1, via regulation of NF-κB p65 expression and activity, was involved in the regulation of renal AT1R expression because treatment with dithiocarbamate (PDTC), an NF-κB inhibitor, reversed the up-regulation of AT1R expression in selenium-deficient renal proximal tubule (RPT) cells. The up-regulation of AT1R expression with GPx1 silencing was restored by PDTC. Moreover, treatment with ebselen, a GPX1 mimic, reduced the increased renal AT1R expression, Na+-K+-ATPase activity, hydrogen peroxide (H2O2) generation, and the nuclear translocation of NF-κB p65 protein in selenium-deficient RPT cells. Our results demonstrated that long-term selenium deficiency causes hypertension, which is due, at least in part, to decreased urine sodium excretion. Selenium deficiency increases H2O2 production by reducing GPx1 expression, which enhances NF-κB activity, increases renal AT1R expression, causes sodium retention and consequently increases blood pressure.

Population status of selenium in Colombia and associated factors: a cross-sectional study.

OBJECTIVES: This study aims to investigate the population status of selenium in Colombia and other associated factors. METHODS: Cross-sectional study, in population of urban or rural origin (n=412). Main outcome measures were: median serum selenium, thyrotropin, the prevalence of and positivity of anti-thyroid peroxidase, anti-thyroglobulin, and anti-TSH receptor. RESULTS: This study found that 96.6% of the subjects had normal selenium levels, and no significant associations were found between the population median of selenium and overweight/obesity, sociodemographic variables, age, goiter, and thyroid antibody positivity. CONCLUSIONS: In Colombia, the population status of selenium is normal, and the geological characteristics may contribute to the state of selenium in this population. However, additional studies are required to evaluate the content of selenium in plants and other foods.

The Role of Selenium-Mediated Notch/Hes1 Signaling Pathway in Kashin-Beck Disease Patients and Cartilage Injury Models.

Kashin-Beck disease (KBD) is a nutrition-related osteoarthropathy, and selenium (Se) deficiency is an environmental risk factor for KBD. Notch/Hes1 signaling pathway plays a vital role in regulating cartilage, but its exact mechanisms in KBD remain unknown. The Se contents were determined using the hydride atomic fluorescence spectrometry assay technique, and the mRNA levels were detected via quantitative real-time PCR. The chondrocyte injury models were established by Se deficiency and tert-butyl hydroperoxide (tBHP), respectively; apoptosis and necrosis rates were detected using Hoechst 33,342/PI and Annexin V-FITC/PI. The results showed that the Se levels in the flour of KBD areas were lower than that of the non-KBD areas, and the Se levels in the plasma of KBD patients were lower than that of the controls. The expressions of Notch1, Jagged1, and Hes1 were higher in the whole blood of KBD patients than those of the controls, and Notch1 was negatively correlated with the expression of BCL2, while was positively correlated with BAX. In injury, chondrocytes induced by low Se and tBHP, the expression of Notch1, Jagged1, and Hes1 increased, apoptosis and necrosis rates increased in Se deficiency and tBHP groups, while Se supplementation reversed it. Decreased plasma Se in KBD patients may be related to low dietary Se. Se deficiency might be involved in the pathological process of KBD by activating the Notch/Hes1 signaling pathway to induce excessive apoptosis of chondrocytes, the activation of Notch/Hes1 promotes oxidative injury, and Se supplementation could reverse it. The importance of Notch/Hes1 signaling pathway in KBD development will provide a new potential target for KBD.

Short- and Long-Term Effects of Suboptimal Selenium Intake and Developmental Lead Exposure on Behavior and Hippocampal Glutamate Receptors in a Rat Model.

Selenium (Se) is an essential trace element required for normal development as well as to counteract the adverse effects of environmental stressors. Conditions of low Se intake are present in some European countries. Our aim was to investigate the short- and long-term effects of early-life low Se supply on behavior and synaptic plasticity with a focus on the hippocampus, considering both suboptimal Se intake per se and its interaction with developmental exposure to lead (Pb). We established an animal model of Se restriction and low Pb exposure; female rats fed with an optimal (0.15 mg/kg) or suboptimal (0.04 mg/kg) Se diet were exposed from one month pre-mating until the end of lactation to 12.5 µg/mL Pb via drinking water. In rat offspring, the assessment of motor, emotional, and cognitive endpoints at different life stages were complemented by the evaluation of the expression and synaptic distribution of NMDA and AMPA receptor subunits at post-natal day (PND) 23 and 70 in the hippocampus. Suboptimal Se intake delayed the achievement of developmental milestones and induced early and long-term alterations in motor and emotional abilities. Behavioral alterations were mirrored by a drop in the expression of the majority of NMDA and AMPA receptor subunits analyzed at PND 23. The suboptimal Se status co-occurring with Pb exposure induced a transient body weight increase and persistent anxiety-like behavior. From the molecular point of view, we observed hippocampal alterations in NMDA (Glun2B and GluN1) and AMPA receptor subunit trafficking to the post-synapse in male rats only. Our study provides evidence of potential Se interactions with Pb in the developing brain.

Clinical Usefulness of Blenderized Food for Selenium Deficiency in Pediatric Patients with Severe Motor and Intellectual Disabilities.

INTRODUCTION: This study aimed to assess the preventive or therapeutic effects of blenderized food (BF) on selenium deficiency in pediatric patients with severe motor and intellectual disabilities (SMID). METHODS: The medical records of all 40 consecutive pediatric patients with SMID who underwent nutritional assessment were retrospectively reviewed and compared between two groups: the enteral formula (EF) group and the BF group fed with BF providing more than 10% of total caloric intake. Next, for the selenium-deficient patients who were newly started on blenderized tube feeds after the first nutritional assessment, improvement of selenium deficiency and change of dietary contents were assessed. RESULTS: The BF group patients had a significantly lower prevalence of selenium deficiency and higher serum selenium levels than the EF group patients. In all 7 selenium-deficient patients who started blenderized tube feeds after the first nutritional assessment, serum selenium levels were significantly increased at the second nutritional assessment, even though total selenium intake, selenium intake by EF, and total caloric intake did not differ significantly, and, in fact, caloric intake was significantly decreased by EF. CONCLUSION: Combined feeding of BFs can be useful for prevention and therapy of selenium deficiency in pediatric SMID patients.

Bisphenol A aggravates renal apoptosis and necroptosis in selenium-deficient chickens via oxidative stress and PI3K/AKT pathway.

Bisphenol A (BPA) in the environment can have deleterious effects on humans and animals. BPA can exert nephrotoxicity by inducing oxidative stress. Selenium (Se) deficiency can specifically impair kidney tissues and additionally show a synergistic effect on the toxicity of several environmental chemicals. However, the toxic effects of BPA on the chicken kidney and whether Se deficiency produces synergistic effects on the toxicity of BPA remain poorly understood. Herein, we established BPA exposure models and Se deficiency model in vivo and in vitro, and described the discovery path of BPA aggravation on apoptosis and necroptosis in Se-deficient chicken kidneys via regulation of oxidative stress and phosphatidylinositol 3-kinase/threonine kinase (PI3K/AKT) signaling pathway. We found that BPA exposure increased reactive oxygen species and malondialdehyde levels, reduced activities of catalase, GPx, and superoxide dismutase, downregulated PI3K and AKT expressions, activated Bcl/Bax-Caspase 9-Caspase 3, and receptor-interacting protein kinase 1/mixed lineage kinase domain-like protein signaling pathways, resulting in apoptosis and necroptosis in the chicken kidney. In addition, Se deficiency significantly promoted the expression of renal apoptosis and necroptosis in BPA-exposed chicken kidneys. Altogether, our results showed that BPA aggravates apoptosis and necroptosis in Se-deficient chicken kidneys via regulation of oxidative stress and PI3K/AKT signaling pathway. Our findings elucidate the mechanism of BPA nephrotoxicity and Se deficiency exacerbation toxicity in chickens and will provide great significance for the protection of the ecological environment and animal health.

Selenium Deficiency in COVID-19-A Possible Long-Lasting Toxic Relationship.

In the last two years, there has been a surge in the number of publications on the trace element selenium (Se) and selenocysteine-containing selenoproteins in human health, largely due to the pandemic and the multiple roles that this micronutrient and Se-dependent selenoproteins play in various aspects of the disease [...].

Selenium Deficiency Causes Inflammatory Injury in the Bursa of Fabricius of Broiler Chickens by Activating the Toll-like Receptor Signaling Pathway.

The aim of our study was to observe the effect of selenium (Se) deficiency on inflammatory injury in the bursa of Fabricius of broiler chickens and to determine the role of the Toll-like receptor (TLR)/myeloid differential protein-88 (MyD88)/nuclear factor-κB (NF-κB) signaling pathway during this process. Here, we revealed that severe inflammatory injury occurred in the broiler bursa of Fabricius with Se deficiency via histopathology. Moreover, the ultrastructural pathological results showed that the nuclear, mitochondrial, endoplasmic reticulum and cytomembrane structures were damaged to varying degrees. Additionally, interleukin-2 (IL-2), interleukin-6 (IL-6), and interferon (IFN-γ) mRNA expression was markedly upregulated in the broiler bursa of Fabricius with Se deficiency. Furthermore, TLR, toll-interleukin-1 receptor domain-containing adapter-inducing interferon-ß (TRIF), MyD88, and NF-κB mRNA expression was also markedly elevated in the broiler bursa of Fabricius with Se deficiency. The above results suggested that Se deficiency increases the expression of numerous proinflammatory cytokines and is probably due to the activation of the TLR/MyD88/NF-κB signaling pathway, which causes inflammatory injury in the bursa of Fabricius of broiler chickens. Our findings provide a theoretical reference for further studying the underlying mechanism of Se deficiency-induced inflammatory injury in the bursa of Fabricius of broiler chickens.

COVID-19 and Selenium Deficiency: a Systematic Review.

Several studies have indicated that selenium deficiency may be detrimental in the context of various viral disorders, and in the case of COVID-19, several studies have reported heterogeneous results concerning the association of selenium deficiency with the severity of disease. To summarize the available data surrounding the association of body selenium levels with the outcomes of COVID-19, a systematic search was performed in the Medline database (PubMed), Scopus, Cochrane Library, Embase, and Web of Science using keywords including "SARS-CoV-2," "COVID-19," and "selenium," Studies evaluating the association of COVID-19 with body selenium levels were included. Among 1,862 articles viewed in the database search, 10 articles were included after title, abstract, and full-text review. One study was further included after searching the literature again for any newly published articles. Out of 11 included studies, 10 studies measured serum selenium level, and one study investigated urinary selenium level. Three of 10 studies measured serum SELENOP level as well as selenium level. Glutathione peroxidase-3 level in serum was also assessed in one study. The reported outcomes were severity, mortality, and risk of COVID-19. Nine studies indicated that a lower serum selenium level is associated with worse outcomes. Two studies reported no significant association between serum selenium level and COVID-19. In one study, urinary selenium level was reported to be higher in severe and fatal cases compared to non-severe and recovered patients, respectively. In most cases, selenium deficiency was associated with worse outcomes, and selenium levels in COVID-19 patients were lower than in healthy individuals. Thus, it could be concluded that cautious selenium supplementation in COVID-19 patients may be helpful to prevent disease progression. However, randomized clinical trials are needed to confirm this.

MiR-144-3p targets STC1 to activate PI3K/AKT pathway to induce cell apoptosis and cell cycle arrest in selenium deficiency broilers.

Selenium (Se) is an indispensable trace element in vertebrate. Se deficiency can damage the immune system. Studies have shown that Se deficiency can cause immune organ damage by regulating the expression of microRNA. Bursa of Fabricius is a special immune organ in poultry. In order to explore the mechanism of bursa of Fabricius injury caused by Se deficiency and the role of miRNA in this process. Firstly, we established the Se deficient model of broilers in vivo and found that Se deficiency could induce apoptosis and cell cycle arrest of bursa of Fabricius cells through Phosphoinositide 3-kinase (PI3K)/Protein Kinase B (AKT) pathway. Secondly, we inferred miRNA (miR-144-3p) and target gene Stanniocalcin 1 (STC1) that may regulate PI3K/AKT pathway through biological analysis system, and further predicted and determined the targeting relationship between them through dual luciferase, it was found that miR-144-3p was highly expressed in the process of cell apoptosis and cell cycle arrest induced by Se deficiency. Finally, in order to further understand whether miR-144-3p/STC1 axis is involved in the process, miR-144-3p knockdown and overexpression experiments were carried out, it was found that miR-144-3p inhibitor can reduce the occurrence of cell apoptosis and cell cycle arrest. In conclusion, Se deficiency can induce apoptosis and cell cycle arrest of bursa of Fabricius in Broilers by up regulating miR-144-3p targeting STC1 and activating PI3K/AKT pathway, leading to injury of bursa of Fabricius in broilers.

The Nutritional Supply of Iodine and Selenium Affects Thyroid Hormone Axis Related Endpoints in Mice.

Selenium and iodine are the two central trace elements for the homeostasis of thyroid hormones but additional trace elements such as iron, zinc, and copper are also involved. To compare the primary effects of inadequate intake of selenium and iodine on the thyroid gland, as well as the target organs of thyroid hormones such as liver and kidney, mice were subjected to an eight-week dietary intervention with low versus adequate selenium and iodine supply. Analysis of trace element levels in serum, liver, and kidney demonstrated a successful intervention. Markers of the selenium status were unaffected by the iodine supply. The thyroid gland was able to maintain serum thyroxine levels even under selenium-deficient conditions, despite reduced selenoprotein expression in liver and kidney, including deiodinase type 1. Thyroid hormone target genes responded to the altered selenium and iodine supply, whereas the iron, zinc, and copper homeostasis remained unaffected. There was a notable interaction between thyroid hormones and copper, which requires further clarification. Overall, the effects of an altered selenium and iodine supply were pronounced in thyroid hormone target tissues, but not in the thyroid gland.

The Impact of Selenium Deficiency on Cardiovascular Function.

Selenium (Se) is an essential trace element that is necessary for various metabolic processes, including protection against oxidative stress, and proper cardiovascular function. The role of Se in cardiovascular health is generally agreed upon to be essential yet not much has been defined in terms of specific functions. Se deficiency was first associated with Keshan's Disease, an endemic disease characterized by cardiomyopathy and heart failure. Since then, Se deficiency has been associated with multiple cardiovascular diseases, including myocardial infarction, heart failure, coronary heart disease, and atherosclerosis. Se, through its incorporation into selenoproteins, is vital to maintain optimal cardiovascular health, as selenoproteins are involved in numerous crucial processes, including oxidative stress, redox regulation, thyroid hormone metabolism, and calcium flux, and inadequate Se may disrupt these processes. The present review aims to highlight the importance of Se in cardiovascular health, provide updated information on specific selenoproteins that are prominent for proper cardiovascular function, including how these proteins interact with microRNAs, and discuss the possibility of Se as a potential complemental therapy for prevention or treatment of cardiovascular disease.

Maternal selenium deficiency suppresses proliferation, induces autophagy dysfunction and apoptosis in the placenta of mice.

Selenium deficiency is thought to be associated with the occurrence of gestational complications. However, the underlying mechanism of selenium deficiency impairs placental function remains unclear. In this study, female mice were separately supplemented with a Se-deficient (0.02 mg/kg Se) or control diet (0.2 mg/kg Se) for 12 weeks before mating and throughout gestation. Maternal liver and placentas were collected at embryonic day 15.5 and analyzed for Se content. Oxidative stress status, proliferation capability, autophagy, and apoptosis of the placenta were determined. We found that maternal selenium deficiency decreased placental Se concentration and some antioxidant selenoproteins expressions. The concentrations of catalase and glutathione in selenium-deficient placentas were reduced, along with an increase in hydrogen peroxide (H2O2) content. Selenium deficiency inhibited the expression of proliferating cell nuclear antigen. Autophagosomes, autophagolysosomes, and upregulation of autophagy-related protein microtubule-associated protein 1 light chain 3 alpha II (LC3B), Beclin1, PTEN-induced putative kinase 1 (PINK1), and Parkin were found in the selenium-deficient trophoblasts. Autophagic substrate p62/sequestosome 1 was surprisingly increased, indicating autophagy flux dysfunction. Selenium deficiency increased expressions of B cell leukemia/lymphoma 2 associated X protein (Bax), cleaved caspase-9/-3, and decreased the B cell leukemia/lymphoma 2 (Bcl2) level. Moreover, typical apoptotic ultrastructure and apoptosis-positive cells were observed in the selenium-deficient placenta. Our results suggested that maternal selenium deficiency impaired placental proliferation, induced autophagy dysfunction and apoptosis via increasing oxidative stress, and the Akt/mechanistic target of rapamycin (mTOR) pathway involved in this process. This study revealed a novel mechanism by which maternal selenium deficiency caused impairment of the placenta.

Role for Selenium in Metabolic Homeostasis and Human Reproduction.

Selenium (Se) is a micronutrient essential for life. Dietary intake of Se within the physiological range is critical for human health and reproductive functions. Selenium levels outside the recommended range have been implicated in infertility and variety of other human diseases. However, presently it is not clear how different dietary Se sources are processed in our bodies, and in which form or how much dietary Se is optimum to maintain metabolic homeostasis and boost reproductive health. This uncertainty leads to imprecision in published dietary guidelines and advice for human daily intake of Se and in some cases generating controversies and even adverse outcomes including mortality. The chief aim for this review is to describe the sources of organic and inorganic Se, the metabolic pathways of selenoproteins synthesis, and the critical role of selenprotenis in the thyroid gland homeostasis and reproductive/fertility functions. Controversies on the use of Se in clinical practice and future directions to address these challenges are also described and discussed herein.