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Objective: This study aimed to assess selenium status in South Korean pregnant women and its impact on maternal thyroid function and pregnancy outcomes. Methods: ‘Ideal Breast Milk (IBM) Cohort Study’ included 367 pregnant women out of 442 participants and categorized into three groups based on plasma selenium levels: deficient (< 70 μg/L), suboptimal (70–99 μg/L), and optimal (≥ 100 μg/L). During the second or third trimester, various blood parameters, including selenium, thyroid-stimulating hormone, free T4, free T3, and anti-thyroid peroxidase antibody levels, were measured. Thyroid parenchymal echogenicity was assessed as another surrogate marker for thyroid autoimmunity using ultrasonography. Results: The median plasma selenium was 98.8 (range: 46.7–206.4) μg/L, and 30 individuals (8%) were categorized as deficient, while 164 (45%) were classified in the suboptimal group. Selenium deficiency was associated with markers of autoimmune thyroiditis, including positive anti-thyroid peroxidase antibody results (13.3 (deficient) vs 4.6 (optimal) %, P = 0.031) and thyroid parenchymal heterogeneity on ultrasound (33.3 (deficient) vs 14.6 (suboptimal) vs 17.3 (optimal) %, P = 0.042), independently of gestational age. The incidence of severe preeclampsia was higher in the group not taking selenium supplements, particularly among those with twin pregnancies, compared to the group taking selenium supplements (0 (selenium supplement) vs 9.0 (no supplement) %, P = 0.015). Conclusion: Pregnant women experience mild selenium deficiency, which can lead to significant health issues including maternal thyroid autoimmunity and obstetrical complications during pregnancy. Guidelines for appropriate selenium intake according to the stage of pregnancy and the number of fetuses are needed.

Selenium is an important micronutrient that plays key functions in antioxidant defense, immune function, and thyroid health. However, its benefits and risks are closely linked to selenium methylation, a process that significantly influences its biological activity and potential toxicity. This review critically analyse the role of selenium methylation in modulating selenium’s effects on health, highlighting its impact on both protective and adverse outcomes. it also discusses the current understanding of selenium’s essential functions and toxicity risks, emphasizing the complexities of Se methylation. The review addresses notable research gaps and controversies, including inconsistent findings on selenium’s cancer-preventive properties, the diverse biological activities of different selenium species, and the challenges in determining optimal selenium intake levels. By synthesizing existing knowledge and identifying key areas for further investigation, this review aims to advance readers’ understanding of selenium’s multifaceted roles that guide future research and public health strategies.

Irritable bowel syndrome (IBS) patients exhibit significantly lower levels of serum selenium (Se) compared to healthy controls. This study integrates a prospective cohort analysis and animal experiments to investigate Se deficiency as a potential risk factor for IBS. Using data from the UK Biobank, a longitudinal analysis was conducted to explore the associations between dietary Se intake and the risk of incident IBS. In animal study, C57BL/6 mice were fed diets with normal (0.2 ppm) or low (0.02 ppm) Se levels to assess the impacts of Se deficiency on IBS symptoms. Furthermore, we performed 16 S rRNA sequencing, untargeted colonic fecal metabolomics analysis, and colon transcriptome profiling to uncover the regulatory mechanisms underlying Se deficiency-induced IBS. The analysis of UK Biobank data revealed a significant correlation between low dietary Se levels and an increased incidence of IBS. In the experimental study, a low Se diet induced IBS symptoms, evidenced by elevated abdominal withdrawal reflex scores, colon inflammation, and severe pathological damage to the colon. Additionally, the low Se diet caused disturbances in gut microbiota, characterized by an increase in Faecalibaculum and Helicobacter, and a decrease in Bifidobacterium and Akkermansia. Combined colonic fecal metabolomics and colon transcriptome analysis indicated that Se deficiency might trigger IBS through disruptions in pathways related to ''bile excretion'', ''steroid hormone biosynthesis'', ''arachidonic acid metabolism'', and ''drug metabolism-cytochrome P450''. These findings underscore the significant adverse effects of Se deficiency on IBS and suggest that Se supplementation should be considered for IBS patients.

Mollisols rich in natural organic matter are a significant sink of carbon (C) and selenium (Se). Climate warming and agricultural expansion to the cold Mollisol regions may enhance soil respiration and biogeochemical cycles, posing a growing risk of soil C and Se loss. Through field-mimicking incubation experiments with uncultivated and cultivated soils from the Mollisol regions of northeastern China, this research shows that soil respiration remained significant even during cold seasons and caused co-emission of greenhouse gases (CO2 and CH4) and methylated Se. Such stimulus effects were generally stronger in the cultivated soils, with maximum emission rates of 7.45 g/m2/d C and 1.42 μg/m2/d Se. For all soil types, the greatest co-emission of CO2 and dimethyl selenide occurred at 25 % soil moisture, whereas measurable CH4 emission was observed at 40 % soil moisture with higher percentages of dimethyl diselenide volatilization. Molecular characterization with three-dimensional fluorescence and ultra-high resolution mass spectrometry suggests that CO2 emission is sensitive to the availability of microbial protein-like substances and free energy from organic carbon biodegradation under variable moisture conditions. Predominant Se binding to biodegradable organic matter resulted in high dependence of Se volatilization on rates of greenhouse gas emissions. These findings together highlight the importance of dynamic organic carbon quality for soil respiration and consequent Mollisol Se loss risk, with implications for science-based management of C and Se resources in agricultural lands to combat with Se deficiency.

ABSTRACT Although Selenium (Se) plays a role as a micronutrient for humans through vegetable consumption, it is also recognized as toxic when present in excessive quantities. Therefore, quantifying Se contents in soils can prevent diseases influenced by crop Se deficiency or excess. We aimed to measure background contents, establish quality reference values (QRV) for Se in soils from two Brazilian biomes (Cerrado and Caatinga), and assess how geopedological factors affect Se content and spatial variability. Two hundred and eight composite topsoil samples were analyzed for Se content, covering an area of about 251,578 km². Sampling sites were under the minimal anthropogenic influence to represent Se background contents. Selenium contents were determined by hydride generation atomic absorption spectroscopy (HGAAS), ranging from 0.002 to 4.78 mg kg-1. Most soils had contents below the world average of 0.44 mg kg-1 but still above the soil content that causes human Se deficiency (0.125 mg kg-1). Soils from Cerrado and Caatinga biomes showed similar average contents of Se, 0.41 and 0.47 mg kg-1, respectively. Organic carbon content and soil particle size (clay fraction) were the main factors governing Se content in the soils. Our results contribute to understanding the Se content and spatial distribution in tropical soils and the factors governing them. They also provide a tool for agriculture and environmental decision-makers to plan public policies regarding the management of Se levels in these and similar tropical soils in the world.

Peng Ju Liu,1 Liangkun Ma,2 Rui Li,1 Yanping Liu1 1Department of Clinical Nutrition, Peking Union Medical College Hospital, China Academic Medical Science and Peking Union Medical College, Beijing, People’s Republic of China; 2Department of Gynaecology and Obstetrics, Peking Union Medical College Hospital, China Academic Medical Science and Peking Union Medical College, Beijing, People’s Republic of ChinaCorrespondence: Yanping Liu, Tel/Fax +86-10-69155535, Email liuyp1227@vip.sina.comPurpose: The role of imbalanced one-carbon nutrients in gestational diabetes mellitus (GDM) risk has garnered significant interest, yet existing studies yield inconsistent results. Our objective was to assess whether the association between an unbalanced ratio of folate to vitamin B12 and GDM risk is influenced by the status of other micronutrients.Methods: This cohort study included 366 singleton-pregnancy Han women enrolled at the Shunyi District Maternal and Child Health Hospital in Beijing, China. During the first trimester of pregnancy, we measured red blood cell (RBC) folate, serum levels of vitamin B12, vitamin D, and selenium. We examined the association between the imbalanced status of RBC folate and vitamin B12 and GDM risk using logistic regression, stratified by serum selenium or vitamin D status.Results: Among the 366 women, 67 (18.3%) were diagnosed with GDM, 201 (54.9%) had vitamin D deficiency, and 245 (66.9%) had selenium deficiency. Overall, women with higher RBC folate/vitamin B12 ratios did not exhibit a significantly higher risk of GDM compared to those in reference tertile (all P > 0.05). Subsequently, we divided women into deficient and non-deficient groups based on serum selenium or vitamin D levels. In women with selenium deficiency, those in the highest tertile of the RBC folate/vitamin B12 ratio had the highest odds of GDM [OR: 3.40 (1.16– 9.97), P=0.026] after adjusting for covariates. However, similar findings were not observed in pregnancies with normal selenium status. Irrespective of vitamin D status, women with higher RBC folate/vitamin B12 ratios did not exhibit a significantly increased risk of GDM.Conclusion: Micronutrient deficiencies are common in early pregnancy. Women with a higher folate/vitamin B12 ratio coupled with selenium deficiency in early pregnancy have a higher GDM risk. These findings underscore the importance of micronutrient assessment in early pregnancy and subsequent interventions for micronutrient deficiencies.Keywords: gestational diabetes mellitus, folate, vitamin B12, early pregnancy, selenium deficiency

IntroductionThe current study investigated the value of urine selenium (Se) concentration as a biomarker of population Se status in rural sub-Saharan Africa.MethodUrine and plasma Se concentrations were measured among children aged 6–59 months (n = 608) and women of reproductive age (WRA, n = 781) living in rural Zimbabwe (Murehwa, Shamva, and Mutasa districts) and participating in a pilot national micronutrient survey. Selenium concentrations were measured by inductively coupled plasma-mass spectrometry (ICP-MS), and urine concentrations were corrected for hydration status.ResultsThe median (Q1, Q3) urine Se concentrations were 8.4 μg/L (5.3, 13.5) and 10.5 μg/L (6.5, 15.2) in children and WRA, respectively. There was moderate evidence for a relationship between urine Se concentration and plasma Se concentration in children (p = 0.0236) and WRA (p = < 0.0001), but the relationship had poor predictive value. Using previously defined thresholds for optimal activity of iodothyronine deiodinase (IDI), there was an association between deficiency when indicated by plasma Se concentrations and urine Se concentrations among WRA, but not among children.DiscussionUrine Se concentration poorly predicted plasma Se concentration at sub-district scales in Zimbabwe, limiting its value as a biomarker of population Se status in this context. Further research is warranted at wider spatial scales to determine the value of urine Se as a biomarker when there is greater heterogeneity in Se exposure.

IntroductionWe conducted a study to determine the prevalence of structural heart disease in patients with CF, the characteristics of a cardiomyopathy not previously described in this population, and its possible relationship with nutritional deficiencies in CF.MethodsWe studied 3 CMP CF patients referred for heart-lung transplantation and a prospective series of 120 adult CF patients. All patients underwent a clinical examination, blood tests including levels of vitamins and trace elements, and echocardiography with evaluation of myocardial strain. Cardiac magnetic resonance imaging (CMR) was performed in patients with CMP and in a control group. Histopathological study was performed on hearts obtained in transplant or necropsy.ResultsWe found a prevalence of 10% (CI 4.6%–15.4%) of left ventricular (LV) dysfunction in the prospective cohort. Myocardial strain parameters were already altered in CF patients with otherwise normal hearts. Histopathological examination of 4 hearts from CF CMP patients showed a unique histological pattern of multifocal myocardial fibrosis similar to Keshan disease. Four of the five CF CMP patients undergoing CMR showed late gadolinium uptake, with a characteristic patchy pattern in 3 cases (p

As common pathogenic agents in the world and widely distributed globally, T-2 toxin and selenium deficiency might exacerbate toxic effects by combined exposure, posing a dramatic health hazard to humans and animals. In this study, we aim to elucidate the underlying mechanisms of renal fibrosis triggered by T-2 toxin and selenium deficiency exposure. A total of thirty-two rats are randomly divided into the normal control, T-2 toxin, selenium deficiency, and combined intervention groups. T-2 toxin (100 ng/g) is intragastric gavaged to the rats in compliance with the body weight. Both the standard (containing selenium 0.20 mg/Kg) and selenium-deficient (containing selenium 0.02 mg/Kg) diets were manufactured adhering to the AIN-93 formula. After 12 weeks of intervention, renal tissue ultrastructural and pathological changes, inflammatory infiltration, epithelial mesenchymal transition (EMT), and extracellular matrix (ECM) deposition are evaluated, respectively. Metabolomics analysis is conducted to explore the underlying pathology of renal fibrosis, followed by the validation of potential mechanisms at gene and protein levels. T-2 toxin and selenium deficiency exposure results in podocyte foot process elongation or fusion, tubular vacuolization and dilatation, and collagen deposition in the kidneys. Additionally, it also increases inflammatory infiltration, EMT conversion, and ECM deposition. Metabolomics analysis suggests that T-2 toxin and selenium deficiency influence amino acid and cholesterol metabolism, respectively, and the estrogen signaling pathway is probably engaged in renal fibrosis progression. Moreover, T-2 toxin and selenium deficiency are found to regulate the expressions of the ERα/PI3K/Akt signaling pathway. In conclusion, T-2 toxin and selenium deficiency synergistically exacerbate renal fibrosis through regulating the ERα/PI3K/Akt signaling pathway, and inflammatory infiltration, EMT and ECM deposition are involved in this process.

Abstract Background There have been reports of isolated trace elements or vitamin deficiencies due to imbalanced diets, but no cases of selenium deficiency combined with scurvy have been reported. Case presentation A 7 year-old boy diagnosed with autistic spectrum disorder and mild psychomotor retardation, started an imbalanced diet including specific snacks and lacto-fermenting drinks from 5 years of age. Gingival hemorrhage and perioral erosions occurred at 6 years and 8 months of age, and he was referred to our hospital at 7 years of age. Slight tachycardia was found. Serum vitamin C level was 1.1 µg/dL (reference range (rr): 5–17.5 µg/dL), and selenium level was 2.8 µg/dL (rr: 7.7–14.8 µg/dL). He was diagnosed with both selenium deficiency and scurvy. Multivitamins and sodium selenate were administered for 12 days during admission, and symptoms of selenium deficiency and scurvy improved. After discharge, symptoms abated following the administration of multivitamins and regular administration of sodium selenate every 3 months. Conclusions We report a complicated case of both selenium deficiency and scurvy due to an imbalanced diet of snacks and lacto-fermenting drinks in a 7-year-old boy with autism spectrum disorder. In patients with imbalanced diet, regular blood tests including trace elements and vitamins are necessary.

IntroductionSelenium (Se) deficiency is increasingly recognized as a public health problem in sub-Saharan Africa.MethodsThe current cross-sectional study assessed the prevalence and geospatial patterns of Se deficiency among children aged 6–59 months (n = 741) and women of 15–49 years old (n = 831) selected by simple random sampling in rural Zimbabwe (Murewa, Shamva, and Mutasa districts). Venous blood samples were collected and stored according to World Health Organization guidelines. Plasma Se concentration was determined by inductively coupled plasma-mass spectrometry.ResultsMedian, Q1, and Q3 plasma Se concentrations were 61.2, 48.7, and 73.3 μg/L for women and 40.5, 31.3, and 49.5 μg/L for children, respectively. Low plasma Se concentrations (9.41 μg/L in children and 10.20 μg/L in women) indicative of severe Se deficiency risk was observed. Overall, 94.6% of children and 69.8% of women had sub-optimal Se status defined by plasma Se concentrations of

Objectives: Selenium deficiency can be associated with increased susceptibility to some viral infections and even more severe diseases. In this study, we aimed to examine whether this association applies to severe fever with thrombocytopenia syndrome (SFTS). Method: An observational study was conducted based on the data of 13,305 human SFTS cases reported in mainland China from 2010 to 2020. The associations among incidence, case fatality rate of SFTS, and crop selenium concentration at the county level were explored. The selenium level in a cohort of patients with SFTS was tested, and its relationship with clinical outcomes was evaluated. Results: The association between selenium-deficient crops and the incidence rate of SFTS was confirmed by multivariate Poisson analysis, with an estimated incidence rate ratio (IRR, 95% confidence interval [CI]) of 4.549 (4.215−4.916) for moderate selenium-deficient counties and 16.002 (14.706−17.431) for severe selenium-deficient counties. In addition, a higher mortality rate was also observed in severe selenium-deficient counties with an IRR of 1.409 (95% CI: 1.061−1.909). A clinical study on 120 patients with SFTS showed an association between serum selenium deficiency and severe SFTS (odds ratio, OR: 2.94; 95% CI: 1.00–8.67) or fatal SFTS (OR: 7.55; 95% CI: 1.14–50.16). Conclusion: Selenium deficiency is associated with increased susceptibility to SFTS and poor clinical outcomes.

Selenium is an integral component of vital biologically active compounds of the human body. Currently, the population of many countries is characterized by selenium deficiency. In this regard, many preparations of inorganic and organic forms of selenium have been developed. Nevertheless, it is evident that the most effective solution to the problem is to enrich the diet with bioavailable forms of selenium. Thus, this work aimed to synthesize and study the antioxidant and immunomodulatory effects of the molecular complex of selenium nanoparticles (Se NPs) and chitosan in laboratory rats with induced hyposelenosis. During the experiment with animals, we found that as a result of 70-day consumption of food with a low selenium content, rats develop an alimentary selenium deficiency state, as evidenced by a significant decrease in the content of this trace element in control group rats to 48.2 ±6.71 µg/kg versus 149.3 ±21.63 µg/kg in intact animals. Course, administration of the molecular complex Se NPs- Chitosan to rats of the experimental group, contributed to the replenishment of selenium deficiency: its concentration in the blood of animals was 96.6 ±3.57 µg/kg. Thus, in animals of the control group, there was a decrease in the total number of lymphocytes by 2.7 times, T-lymphocytes – by 1.8 times, and B-lymphocytes – by 2.3 times compared with similar data in intact animals. In the context of hyposelenosis, it is worth mentioning that there was a slight increase in the content of T-helper cells and cytotoxic T-lymphocytes. The synthesized Se NPs – Chitosan complex administration during hyposelenosis demonstrated a notable immunomodulatory effect by restoring the body's immune response indicators. Thus, the total number of lymphocytes increased by 3 times, T-lymphocytes – by 1.9 times, and B-lymphocytes – by 2 times. The number of T-helper cells and cytotoxic T-lymphocytes increased by 1.9 times compared to the group of intact animals and 1.6 times compared to selenium-deficient rats. Thus, the course introduction of the molecular complex Se NPs – Chitosan against the background of selenium deficiency was accompanied by inhibition of free radical oxidation processes, activation of the antioxidant system and restoration of the immune status of the organism of laboratory animals.

Selenium (Se) deficiency disrupts intracellular REDOX homeostasis and severely deteriorates immune and anti-inflammatory function in high-yielding periparturient dairy cattle. To investigate the damage of extracellular vesicles derived from Se-deficient MAC-T cells (SeD-EV) on normal mammary epithelial cells, an in vitro model of Se deficiency was established. Se-deficient MAC-T cells produced many ROS, promoting apoptosis and the release of inflammatory factors. Extracellular vesicles were successfully isolated by ultrahigh-speed centrifugation and identified by transmission electron microscopy, particle size analysis, and surface markers (CD63, CD81, HSP70, and TSG101). RNA sequencing was performed on exosomal RNA. A total of 9393 lncRNAs and 63,155 mRNAs transcripts were identified in the SeC and SeD groups, respectively, of which 126 lncRNAs and 955 mRNAs were differentially expressed. Furthermore, SeD-EV promoted apoptosis of normal MAC-T cells by TUNEL analysis. SeD-EV significantly inhibited Bcl-2, while Bax and Cleaved Caspase3 were greatly increased. Antioxidant capacity (CAT, T-AOC, SOD, and GSH-Px) was inhibited in SeD-EV-treated MAC-T cells. Additionally, p-PERK, p-eIF2α, ATF4, CHOP, and XBP1 were all elevated in MAC-T cells supplemented with SeD-EV. In addition, p-PI3K, p-Akt, and p-mTOR were decreased strikingly by SeD-EV. In conclusion, SeD-EV caused oxidative stress, thus triggering apoptosis and inflammation through endoplasmic reticulum stress and the PI3K-Akt-mTOR signaling pathway, which contributed to explaining the mechanism of Se deficiency causing mastitis.

ABSTRACT: Selenium (Se) has been proven to be an essential trace element for organism. Se deficiency in poultry can cause widespread damage, such as exudative diathesis. The liver is not only the main organ of metabolism, but also one of the organs with high Se content in organism. Recent studies have shown that solute carrier family 7 member 11 (SLC7A11) plays a key role in the negative regulation of ferroptosis. In order to explore the mechanism of Se deficiency induces liver ferroptosis in broilers, and the role of microRNAs (miRNAs) in this process, we divided broilers into 2 groups: control group (0.2 mg/kg Se) and Se deficiency group (0.03 mg/kg Se). Hematoxylin-Eosin staining detected liver tissue damage in broilers. Predicted and verified the targeting relationship between miR-129-3p and SLC7A11 through miRDB and dual luciferase report experiments. The genes related to ferroptosis were detected by qRT-PCR and Western Blot. The results showed that the expression level of miR-129-3p mRNA in Se-deficient liver was significantly increased. To understand whether the miR-129-3p/SLC7A11 axis could involve in the process of ferroptosis, our further research showed that overexpression of miR-129-3p could reduce the expression of SLC7A11 and its downstream GCL, GSS, and GPX4, thereby inducing ferroptosis. These data indicates that miR-129-3p affected ferroptosis under Se deficiency conditions through the SLC7A11 pathway. Our research provides a new perspective for the mechanism of Se deficiency on the liver damage.

ObjectiveIn order to assess selenium (Se) flux through the soil-plant-human chain in Tibet plateau and explore the reason why local Tibetan adult residents from large scale agricultural production areas in Tibet lacked daily Se intake.MethodsA total of 210 intact highland barley plants and their corresponding cultivated topsoil samples were collected in fields of 14 agricultural counties along Yalung Zangpo River and quantitative dietary data were collected from a cross-sectional survey using a cultural-specific food frequency questionnaire that contained all local Tibetan foods in 2020.ResultsThe mean value of The estimated daily Se dietary intake by each participant was 17.1 ± 1.9 μg/day/adult, the Se concentration in topsoil and highland barley grain were 0.128 ± 0.015 mg/kg and 0.017 ± 0.003 mg/kg, respectively. Although highland barley was the first contributor of dietary Se in local adult residents (34.2%), the dietary Se intake provided by highland barley only about 10% of the EAR value (50 μg/day/adult) currently. A significantly positive relationship was determined between soil total Se content (STSe), available Se content (SASe) and highland barley grain Se content (GSe). The amount of Se in food system depends on a number of soil properties (TOC, pH, clay content, Fe/Mn/Al oxides), climate variables (MAP, MAT) and terrain factor (altitude).ConclusionTo sum up, it can be inferred that the insufficient dietary Se intake of Tibetan adult population living along Yalung Zangbo River is mainly caused by the low Se content in highland barley grain, which was result from the low Se content in cultivated soil. In order to enable adult participants in the present study to achieve recommended dietary Se-intake levels, agronomic fortification with selenised fertilizers applied to highland barley could be a great solution. It is necessary to combine the influencing factors, and comprehensively consider the spatial variation of local soil properties, climatic and topographic conditions, and planting systems.

Introduction and purpose: Selenium is essential for the proper course of many physiological and biochemical processes in the human body. It plays a large role in ensuring proper immunoendocrine function. The organ with the greatest amount of selenium per gram of tissue is the thyroid gland. This element builds enzymes involved in antioxidant processes - peroxidase, as well as deiodinases involved in the metabolism of thyroid hormones. There are scientific reports showing a beneficial effect of selenium supplementation in autoimmune diseases of the thyroid gland. The aim of this study is to summarize the current knowledge on the relationship between selenium deficiency and the development of thyroid dysfunction. Description of the state of knowledge: There is a correlation between selenium deficiency and the functioning of the thyroid gland. It has been shown that selenium levels are often lowered in patients with autoimmune thyroiditis. Research shows that selenium supplementation may lower TPOAb and TgAb antibody levels in patients with Hashimoto's disease. In patients with Graves' orbitopathy, administration of selenium resulted in delayed progression of orbitopathy and less disease severity. There are reports that supplementation with this element may also increase the effectiveness of antithyroid drugs in patients with Graves-Basedow disease. There was also an association between selenium deficiency and the development of goiter and thyroid nodules. Conclusions: Selenium plays an important role in the proper functioning of the thyroid gland. Although the specific role of selenium in the pathogenesis of thyroid disease is still under investigation, there are numerous reports saying that its deficiency may affect it. More research is needed on the relationship between selenium concentration and the regulation of thyroid function, because introducing it into the treatment regimen of thyroid disorders may give hope for better therapeutic effects.

Abstract Background The immune system is one aspect of health that is affected by dietary selenium (Se) levels and selenoprotein expression. Spleen is an important immune organ of the body, which is directly involved in cellular immunity. However, there are limited reports on Se levels and spleen health. Therefore, this study established a Se-deficient pig model to investigate the mechanism of Se deficiency-induced splenic pathogenesis. Methods Twenty-four pure line castrated male Yorkshire pigs (45 days old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into two equal groups and fed Se-deficient diet (0.007 mg Se/kg) or Se-adequate diet (0.3 mg Se/kg) for 16 weeks. At the end of the trial, blood and spleen were collected to assay for erythroid parameters, the osmotic fragility of erythrocytes, the spleen index, histology, terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) staining, Se concentrations, the selenogenome, redox status, and signaling related inflammation and apoptosis. Results Dietary Se deficiency decreased the erythroid parameters and increased the number of osmotically fragile erythrocytes (P

The clinical lecture is a continuation of our report on antioxidants published in one of the preceding issues of the magazine. In the current context of COVID-19 epidemic, the efforts to struggle for preservation of human life and health using all possible sanitary and anti-epidemic (preventive) measures, as well as advanced diagnostic and therapeutic tools, imply fertility preservation in the population together with positive solutions to national demographic challenges in the long term. Testicles are one of the reservoirs for the virus in the male body. This is indirectly confirmed by the sex hormone level alterations in COVID-19 survivors compared to healthy people. Oxidative stress associated with impaired fertility results from antioxidant and trace mineral deficiency. The role of trace minerals, zinc and selenium, in these processes together with possible approaches to adjustment of their levels in the context of COVID-19 pandemic are discussed in detail.

Abstract Background Recumbent cows are a diagnostic challenge because of a wide range of differential diagnoses, which include trauma, neurological and metabolic disorders, malnutrition and mineral deficiencies. This case report describes recumbent suckler cows that presented as a herd problem. In addition to weakness due to inanition, Cu and Se deficiencies were considered as possible aetiologies of the recumbency. Furthermore, Trypanosoma (T.) theileri, a blood parasite of unknown importance in Germany, was detected in the blood of some cows. Case presentation Three recumbent cows were referred to the Clinic for Ruminants and Swine, Faculty of Veterinary Medicine of the University of Leipzig. They were unable to rise and had low body condition scores and rough hair coats. Haematological and serum biochemical analyses showed neutrophilia, electrolyte imbalances, increased activities of muscle and liver enzymes and decreased concentrations of trace elements, especially Copper (Cu) and Selenium (Se). T. theileri was detected in a routine blood smear from one cow. The cows did not respond to an intensive care protocol, which included intravenous fluids and electrolytes, mineral substitution, non-steroidal anti-inflammatories and antibiotics, and were therefore euthanized or died. Postmortem examination showed cachexia, subcutaneous and scleral oedema and muscular dystrophy, especially in the hind limbs. Follow-up examination of the herd of origin produced similar findings including the detection of T. theileri in a large proportion of the herd. Ration analysis revealed considerable undersupply of several nutrients. Conclusions Based on all findings, an aetiological diagnosis of trace mineral and nutrient deficiency with possible involvement of T. theileri was made.

Background: Selenium (Se) is a trace element found in many foodstuffs and critical for antioxidant and immune functions. Widespread Se deficiency has been noted in populations of some sub-Saharan African countries including Ethiopia and Malawi. As a first step towards developing a fuller understanding of problems with the availability of Se in the diet in Lusaka province, Zambia, we measured plasma Se in adults and children in this geographic area. Methods: Total plasma Se was measured using inductively coupled plasma optical emission spectrometry (ICP-OES) in several groups of adults recruited to various pre-existing studies, including those of high and low socioeconomic status (SES) and pregnant women, and children with a range of nutritional states (healthy, stunted or wasted). Results: A total of 660 plasma samples from 391 adults and 269 children were included. Adults had a median plasma Se concentration of 0.27 μmol/l (IQR 0.14–0.43). Concentrations consistent with deficiency (

Selenium is an essential trace element for health that can only be obtained through food. However, the pathological processes of selenium deficiency in cattle have received little attention. This study investigated the effects of selenium deficiency on oxidative stress, apoptosis, inflammation, and necroptosis in the lungs of weaning calves compared with healthy calves as controls. The lung selenium content and the expression of 11 selenoproteins mRNA in selenium-deficient calves were substantially reduced compared with the controls. Pathological results showed engorged alveolar capillaries, thickened alveolar septa, and diffuse interstitial inflammation throughout the alveolar septa. The levels of GSH and T-AOC, as well as the CAT, SOD, and TrxR activities, were significantly decreased compared with healthy calves. MDA and H2O2 were significantly elevated. Meanwhile, the apoptosis activation in the Se-D group was validated. Next, in the Se-D group, several pro-inflammatory cytokines showed higher expression. Further research revealed that the lungs in the Se-D group experienced inflammation via hyperactive NF-κB and MAPK pathways. The high level of expression of c-FLIP, MLKL, RIPK1, and RIPK3 indicated that necroptosis also causes lung damage during selenium deficiency.

Selenium (Se) is a beneficial microelement for humans, and its varying abundances and shortages have attracted widespread concern. The accumulation process of soil Se is quite complicated, being controlled by multiple factors. However, the influence mechanism of soil properties, climate, and topographic conditions on Se distribution is still unclear in Se-deficient areas. For this study, we collected 2804 samples from cropland soil to assess the levels of Se and the factors that influence those levels in Se-deficient areas of southwestern China. The Se content in this area (0.17 mg/kg) was less than the mean value of China as a whole (0.29 mg/kg). Moran’s I index and a random forest (RF) model showed that higher Se levels were mostly observed in the southern and northern sections of the area we studied. The RF model had excellent performance in predicting soil Se content, with an accuracy of 64%. The use of Shapley additive explanations indicated that soil organic matter (SOM) and mean annual precipitation (MAP) were the critical factors determining Se distribution. The areas with high SOM and MAP showed high Se levels. The information obtained from this work can provide guidance for agricultural planning in Se-deficient areas.

Selenium (Se) deficiency and poor plasma Se levels can cause cardiovascular diseases by decreasing selenoprotein levels. Neutrophil extracellular traps (NETs) may be the vicious cycle center of inflammation in vasculitis. Here, we show that Se deficiency induced arteritis mainly by reducing selenoprotein S (SelS), and promoted the progression of arteritis by regulating the recruitment of neutrophils and NET formation. Silencing SelS induced chicken arterial endothelial cells (PAECs) to secrete cytokines, and activated neutrophils to promote NET formation. Conversely, scavenging DNA-NETs promoted cytokine secretion in PAECs. The NET formation regulated by siSelS was dependent on a reactive oxygen species (ROS) burst. We also found that the PPAR pathway was a major mediator of NET formation induced by Se-deficient arteritis. Overall, our results reveal how Se deficiency regulates NET formation in the progression of arteritis and support silencing-SelS worsens arteritis.

Ammara Arif, Attya Bhatti, Peter John Atta-Ur-Rahman School of Applied Biosciences, National University of Sciences and Technology, Islamabad, PakistanCorrespondence: Attya BhattiAtta-ur-Rahman School of Applied Biosciences, National University of Sciences and Technology, H-12, Islamabad, PakistanTel +92 51 90856128Fax +92 51 90856102Email attyabhatti@gmail.comPurpose: Rheumatoid arthritis is an inflammatory autoimmune multifactorial disorder that primarily affects the joints. Currently available treatment options, although effective, still present some side effects. This study proposes an alternative treatment option for rheumatoid arthritis through elucidation of therapeutic potential of Foeniculum vulgare Mill.-derived selenium nanoparticles in arthritic Balb/c mice.Methods: Synthesis and characterization of selenium nanoparticles were followed by their toxicity analysis on healthy mice. Subsequently, anti-arthritic efficacy of two doses (5 mg/kg and 10 mg/kg) of synthesized selenium nanoparticles was checked on arthritic mice using multiple parameters.Results: Selenium nanoparticles in 10 mg/kg dose turned out to be more effective in treatment of rheumatoid arthritis as evident by significant reduction in paw volume and normal clinical chemistry parameters of treated arthritic mice. This dose also showed significant antioxidant activity in 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay.Conclusion: Foeniculum vulgare Mill.-derived selenium nanoparticles retain significant anti-arthritic and antioxidant potential and consequently can further be explored as an alternative treatment option for rheumatoid arthritis.Keywords: rheumatoid arthritis, nanotherapy, selenium deficiency, plant seed extract, Balb/c mice

The work presents a review devoted to the metabolism and the mechanism of toxicity of seleniumcontaining supplements: elemental selenium, sodium selenite, diacetophenonyl selenide, selenopyrane, ebselen, dimethyl dipyrasolyl selenide and selenium-containing amino acids used for correction of selenium deficiency. Elemental selenium penetrating through cell walls, but not through transport channels demonstrates poorly predicted and difficultly regulated bioavailability. Sodium selenate is known to be the most toxic form of selenium in food. The metabolism of xenobiotic diacetophenonyl selenide resembles that of sodium selenide. The xenobiotic reacts with thiols, for instance, with the reduced form of glutathione leading to the formation of hydrogen selenide. Ebselen is not considered to be a well bioavailable form of selenium and thus possesses low toxicity. Xenobiotic selenopyrane eliminates selenium only in processes of xenobiotic liver exchange, and in our investigations - partially in acid-catalyzed hydrolysis. The metabolism of xenobiotic dimethyl dipyrasolyl selenide having low toxicity is poorly investigated. The toxicity of high doses of selenomethionine is determined by the possibility of incorporation in proteins and vitally important enzymes with dramatic changes of protein quaternary structure. The toxicity of high doses of methylselenocysteine seems to be caused by the lack of an exchange pool in the body and quick regeneration of hydrogen selenide from methylselenol which is formed as a result of enzymatic destruction of this amino acid. Also the issue of the most prospect selenium donor is discussed. The physiological compatibility, the low toxicity, the presence of an exchangeable pool in the organism, the antioxidantal properties and the simplicity of production indicate selenocystine as an optimal selenium donor.

Selenium (Se) intake disequilibrium is associated with many human diseases (e.g., Keshan disease and type 2 diabetes). To understand the mechanism of Se deficiency-induced hepatic pathogenesis, a pure line pig model was established by feeding a diet with either 0.07 mg/kg Se or 0.3 mg/kg Se for 16 weeks. The hepatic metabolome, lipidome, global proteome, and whole transcriptome were analyzed. Se deficiency causes a redox imbalance via regulation of selenoproteins at both the mRNA and protein level, and blocks the glutathione anti-oxidant system along with enhanced glutathione synthesis and catabolism. The Warburg effect was observed by enhanced activation of the glycolysis and phosphate pentose pathways. The tricarboxylic acid cycle was dysfunctional since the preliminary metabolites decreased and shifted from using glycolysis origin substrates to a glutamine catabolism-preferred metabolic mode. The reprogrammed central carbon metabolism induced widely restrained lipid synthesis. In addition, a Se deficiency initiated inflammation by activating the NF-κB pathway through multiple mechanisms. These results identified the potential metabolic vulnerability of the liver in response to a Se deficiency-induced redox imbalance and possible therapeutic or intervention targets.

Background/Aims: Selenium (Se) deficiency can lead to several cardiac diseases, including Keshan disease in humans, mulberry heart disease in pigs and cardiac injury in chickens. MicroRNAs have been a research focus in recent years and have been shown to participate in a new avenue of cell death-autophagy, which can play a significant role in several types of heart disease. Methods: MicroRNAome analysis showed that the expression of miR-2954 was increased in the myocardium of selenium-deficient chickens, and PI3K was predicted to be the target gene. The target relationship between miR-2954 and PI3K was verified with a double fluorescence enzyme assay and RNA Protein Interaction Prediction and molecular docking software. qRT-PCR and western blotting were used to detect the expression of PI3K and related pathway components in selenium-deficient chickens and miR-2954 knockout/overexpression cardiomyocytes. Results: In this study, we observed that miR-2954 overexpression led to inhibition of PI3K pathway in vivo and in vitroled to inhibition of the PI3K pathway in vivo and in vitro. Conclusion: The expression of miR-2954 was increased in selenium-deficient myocardium, whereas overexpression of miR-2954 led to autophagy and apoptosis of myocardial cells during cardiac injury through regulation of the PI3K pathway; whether this phenomenon is a self-protection mechanism of the organism or damage caused by miR-2954 requires further study. Our findings provides new insight apoptosis in cardiomyocytes; additionally, we aim to provide a new direction for the diagnosis and targeted treatment of myocardial diseases.

Enzymes excreted by rumen microbiome facilitate the conversion of ingested plant materials into major nutrients (e.g., volatile fatty acids (VFA) and microbial proteins) required for animal growth. Diet, animal age, and health affect the structure of the rumen microbial community. Pathogenic organisms in the rumen negatively affect fermentation processes in favor of energy loss and animal deprivation of nutrients in ingested feed. Drawing from the ban on antibiotic use during the last decade, the livestock industry has been focused on increasing rumen microbial nutrient supply to ruminants through the use of natural supplements that are capable of promoting the activity of beneficial rumen microflora. Selenium (Se) is a trace mineral commonly used as a supplement to regulate animal metabolism. However, a clear understanding of its effects on rumen microbial composition and rumen fermentation is not available. This review summarized the available literature for the effects of Se on specific rumen microorganisms along with consequences for rumen fermentation and digestibility. Some positive effects on total VFA, the molar proportion of propionate, acetate to propionate ratio, ruminal NH3-N, pH, enzymatic activity, ruminal microbiome composition, and digestibility were recorded. Because Se nanoparticles (SeNPs) were more effective than other forms of Se, more studies are needed to compare the effectiveness of synthetic SeNPs and lactic acid bacteria enriched with sodium selenite as a biological source of SeNPs and probiotics. Future studies also need to evaluate the effect of dietary Se on methane emissions.

After its discovery, selenium was most noted for its harmful effects. Selenium was the first element identified to occur in native vegetation at levels toxic to animals. Poisoning of animals can occur through consumption of plants containing toxic levels of selenium. Livestock consuming excessive amounts of selenized forages are afflicted with “alkali disease” and “blind staggers”. Typical symptoms of these diseases include loss of hair, deformed hooves, blindness, colic, diarrhoea, lethargy, increased heart and respiration rates, and eventually death. On the other hand, selenium deficiency in animal feeds can cause “white muscle disease”, a degenerative disease of the cardiac and skeletal muscles. In this regard, this review paper attempts to summarize the essentiality of selenium for humans, animals, and plants and the role of selenium in plant metabolism and physiology.

Selenium (Se) is an essential trace element for humans. About 70% of the regions in China, including most of the Tibetan Plateau, are faced with Se deficiency problems. Turnip is mainly distributed around the Tibetan Plateau and is one of the few local crops. In the present study, we compared the absorption and translocation differences of Se (IV) selenite and Se (VI) selenate in turnip. The results showed that Se treatment, either by soil addition (0.2–2 mg Se kg−1 dry soil) or by foliar spraying (50–200 mg L−1 Se), could significantly increase the Se concentrations in turnips, and 0.5 mg Se (IV) or Se (VI) kg−1 dry matter in soils could improve the biomasses of turnips. Moreover, turnip absorbed significantly more Se (VI) than Se (IV) at the same concentration and also transferred much more Se (VI) from roots to leaves. Based on the Se concentrations, as well as the bioconcentration factors and translocation coefficients, we considered that turnip might be a potential Se indicator plant. Subsequently, we estimated the daily Se intake for adults based on the Se concentrations in turnip roots. The results indicated that Se (IV) should be more suitable as an artificial Se fertilizer for turnips, although the levels found in most samples in this study could cause selenosis to humans. In addition, we also estimated the optimum and maximum Se concentrations for treating turnips based on the linear relations between Se concentrations in turnip roots and Se treatment concentrations. The results provided preliminary and useful information about Se biofortification in turnips.

The article analyzes the published data concerning the presence of metabolic memory associated with the formation of adaptive reactions to the result of the influence of various environmental factors. In terms of deiodinase selenoproteins, mechanisms of metabolic correction under selenium deficiency confirming the existence of the triage theory were investigated. The data of our own observations which made it possible to draw a preliminary conclusion about the lack of selenium at least in some regions of Ukraine are provided.

Aim: Monitoring was performed in order to determine the Selenium (Se) status of cattle herds in different agricultural areas in Wallonia (Belgium). Materials and Methods: The study included 114 heifers and 184 cows (82 dairy and 102 beef cows) from 66 cattle farms situated in Wallonia. The Se status was assessed by measuring the glutathion peroxydase in red cells and converting it to the equivalent Se blood content. Results: The average blood concentrations of Se were very low. The Ardennes region was an area where the lowest Se status was recorded. The highest levels of Se in dairy cows and beef cows were recorded respectively in the limoneuse region and Famenne areas. The Se content in beef herds was lower compared with that of dairy herds (35 vs. 56 μg/L, p