Se-deficient Diet Research Articles

Selenium Deficiency Augments the Levels of Inflammatory Factors and Heat Shock Proteins via the Redox Regulatory Pathway in the Skeletal Muscles of Mice.

Dietary selenium (Se) deficiency is known to cause myodynia syndrome and Se influences immune responses by changing the expression of inflammatory cytokines and heat shock proteins (Hsps), but the details are not completely elucidated. In the present study, 72 1-day-old mice were divided into two groups; the first group was fed a Se-sufficient diet, while the second group was fed a Se-deficient diet. Skeletal muscles and blood samples were taken from all mice after 42days of treatment. The activities of glutathione peroxidase (GPX) and glutathione (GSH), mRNA and protein expression levels of inflammatory cytokines (including TNF-α, inducible NO synthase, cyclooxygenase-2, and prostaglandin E synthases), protein expression levels of NF-κB, and the mRNA expression levels of Hsps in the skeletal muscles of mice were examined. The results showed that GPX and GSH activities were decreased, while the mRNA and protein expression levels of inflammatory cytokines and the mRNA levels of Hsps were increased by Se deficiency in mouse skeletal muscles. In the present study, the protective role of Se in oxidative stress, inflammatory cytokines, and Hsps in the skeletal muscles of mice was summarized.

Pancreatic atrophy caused by dietary selenium deficiency induces hypoinsulinemic hyperglycemia via global down-regulation of selenoprotein encoding genes in broilers.

This study was envisaged to comprehensively profile genes in selected tissues along with a few biochemical indicators and integrate resulting information with dietary selenium (Se) deficiency symptoms in broilers. A total of 120 one-day-old Cobb male broilers were equally divided into two groups and fed a Se deficient corn-soybean-based basal diet supplemented with 0.3 mg/kg sodium selenite (Control, Se adequate) or without selenite (Se deficiency) for five weeks. Effects of Se deficiency on mRNA abundance of twenty-three selenoprotein encoding genes and seventeen insulin signaling related genes were studied at day 35 in pancreas, liver and muscle along with plasma biochemical constituents and enzyme activities. Compared to healthy birds in control diet, Se deficient diet induced deficiency symptoms in 90% birds and classic nutritional pancreatic atrophy, depressed growth performance of broilers, and decreased (P < 0.01 to P < 0.05) total antioxidant capacity and activities of superoxide dismutase and glutathione peroxidase in plasma and three other tissues. Se deficiency resulted in 58% higher mortality than control birds. Dietary Se deficiency down-regulated (P < 0.01–0.05) eighteen selenoprotein encoding genes in pancreas, fourteen genes in muscle and nine genes in liver, and up-regulated (P < 0.05) Txnrd1 and Selx in liver. Meanwhile, six, thirteen and five insulin signaling related genes were down-regulated (P < 0.01–0.05) in pancreas, muscle and liver, respectively, and three genes were up-regulated (P < 0.01) in liver. The decrease (P < 0.05) in levels of plasma insulin, total triglyceride and total cholesterol, and concurrent elevated (P < 0.05) levels of plasma glucose and inflammatory cytokines accompanied the global down-regulation of selenoprotein encoding- and insulin signaling related- genes in Se deficient birds. It was concluded that dietary Se deficiency induces nutritional pancreatic atrophy and metabolic disorder of glucose and lipid in broilers via down-regulation of selenoprotein encoding- and insulin signaling related- genes, indicating potential roles of these genes in metabolic regulation.

Increased Chondrocyte Apoptosis in Kashin-Beck Disease and Rats Induced by T-2 Toxin and Selenium Deficiency

ObjectiveTo investigate chondrocyte apoptosis and the expression of biochemical markers associated with apoptosis in Kashin-Beck disease (KBD) and in an established T-2 toxin- and selenium (Se) deficiency-induced rat model. MethodsCartilages were collected from the hand phalanges of five patients with KBD and five healthy children. Sprague-Dawley rats were administered a selenium-deficient diet for 4 weeks prior to T-2 toxin exposure. The apoptotic chondrocytes were observed by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Caspase-3, p53, Bcl-2, and Bax proteins in the cartilages were visualized by immunohistochemistry, their protein levels were determined by Western blotting, and mRNA levels were determined by real-time reverse transcription polymerase chain reaction. ResultsIncreased chondrocyte apoptosis was observed in the cartilages of children with KBD. Increased apoptotic and caspase-3-stained cells were observed in the cartilages of rats fed with normal and Se-deficient diets plus T-2 toxin exposure compared to those in rats fed with normal and Se-deficient diets. Caspase-3, p53, and Bax proteins and mRNA levels were higher, whereas Bcl-2 levels were lower in rats fed with normal or Se-deficiency diets supplemented with T-2 toxin than the corresponding levels in rats fed with normal diet. ConclusionT-2 toxin under a selenium-deficient nutritional status induces chondrocyte death, which emphasizes the role of chondrocyte apoptosis in cartilage damage and progression of KBD.

Selenium Deficiency Induced Injury in Chicken Muscular Stomach by Downregulating Selenoproteins.

The aim of the present study was to examine the effect of selenium (Se) deficiency on the expression of selenoproteins in chicken muscular stomach and to detect the correlation of selenoproteins with muscular stomach injuries. One-day-old broiler chickens were maintained for 55days on a normal diet (0.2mg/kg) or a Se-deficient diet (0.033mg Se/kg). The expression levels of 25 selenoproteins, heat shock proteins (HSPs), and inflammatory factors were then examined by real-time PCR. Following this, the correlation between selenoproteins, HSPs, and inflammatory factors was analyzed by principal component analysis (PCA). The results showed that Se deficiency decreased the expression of 25 selenoproteins (P<0.05), but increased the expression of HSP27, HSP40, HSP60, HSP70, and HSP90, and NF-κB, iNOS, TNF-α, COX-2, and HO-1 (P<0.05). Selenoproteins showed a high negative correlation with HSPs and inflammatory factors. Thus, the results suggested that Se deficiency induced muscular stomach injuries by decreasing the expression of selenoproteins. In addition, selenoproteins play an important role in regulating HSPs and inflammatory response. The muscular stomach is a key target of Se deficiency and may play a special role in response to Se deficiency.

Glutathione Peroxidase 1, Selenoprotein K, and Selenoprotein H May Play Important Roles in Chicken Testes in Response to Selenium Deficiency.

Selenium (Se) deficiency induces testicular functional disturbances, but the molecular mechanism remains unclear. In the present study, 1-day-old broiler chickens were maintained for 55days with a normal diet (0.2mg/kg) and a Se-deficient diet (0.033mg Se/kg). Then, the messenger RNA (mRNA) levels of selenoproteins, heat shock proteins (HSPs), and inflammatory factors were examined. Se deficiency led to decreased selenoproteins (Gpx1, Selk, and Selh) and HSPs (HSP40, HSP60, and HSP90) (P<0.05). However, the expression levels of Gpx2, Sepn1, Seli, Selpb, Sepx1, HSP27, and inflammatory factors (iNOS, TNF-α, COX-2, and HO-1) were increased by Se deficiency (P<0.05). Gpx1, Selk, and Selh showed positive correlation with HSP40, HSP60, and HSP90, but negative correlation with HSP27, HSP70, iNOS, TNF-α, COX-2, and HO-1. However, Gpx2, Spen1, Seli, Selpb, and Sepx1 showed positive correlation with inflammatory factors and HSP27 and HSP70. Selenoproteins showed different correlation with HSPs and inflammatory factors and were classified into different groups in response to Se deficiency. The results suggested that selenoproteins play different roles in chicken testes, and we think that Gpx1 and Selk may play a special role in chicken testes.

Interplay between autophagy and apoptosis in selenium deficient cardiomyocytes in chicken

Dietary selenium (Se) deficiency can cause heart dysfunction, however the exact mechanism remains unclear. To understand this mechanism, 180day-old chicks, divided into two groups, C (control group) and L (low Se group), were fed with either a Se-sufficient (0.23mg/kg) or Se-deficient (0.033mg/kg) diets for 25days, respectively. Heart tissues and blood samples were collected. In L group, the activities of serum creatine kinase (CK) and creatine kinase-myoglobin (CK-MB) increased and typical ultrastructural apoptotic features were observed. Se deficiency up-regulated the mRNA levels of Cysteinyl aspartate specific proteinase 3 (Caspase-3), Cysteinyl aspartate specific proteinase 8 (Caspase-8), Cysteinyl aspartate specific proteinase 9 (Caspase-9), B cell lymphoma/leukemia 2 (Bcl-2), Bcl-2 Associated X Protein (Bax), (P<0.05), whereas, the mRNA levels of Microtubuleassociated protein light chains 3-1 (LC3-1), Autophagy associated gene 5 (ATG-5), Mammalian target of rapamycin (mTOR), Dynein and Becline-1 were down-regulated (P<0.05). Noticeably, Microtubuleassociated protein light chains 3-2 (LC3-2) mRNA level increased (P<0.05) by 20%. Western blot results showed that Se deficiency decreased the expression of Becline-1 and LC3-1 protein, however, the expression of Bax, Caspase-3 and Cysteinyl aspartate specific proteinase 12 (Caspase-12) increased at protein levels. The present study revealed that Se deficiency induced apoptosis while inhibited autophagy in chicken cardiomyocytes through Bax/Bcl-2 inhibition and caspases-mediated cleavage of Becline-1. Moreover, correlation analysis illustrates that apoptosis and autophagy might function contradictorily. Altogether we conclude that Se deficient chicken cardiomyocytes experienced apoptosis rather than autophagy which is considered to be more pro-survival.

Disbalance of calcium regulation-related genes in broiler hearts induced by selenium deficiency

ABSTRACTDietary selenium (Se) deficiency may influence the calcium (Ca) homeostasis in broilers. Our objective was to investigate the effects of Se deficiency on Ca regulation-related genes in broiler hearts. In the present study, 1-day-old broilers were fed either a commercial diet (as control group) with 0.15 mg/kg Se or a Se-deficient diet (as L group) with 0.033 mg/kg Se for 35 days. We examined the mRNA expression levels of 15 Ca regulation-related genes (ITPR 1, ITPR 2, ITPR3, RyR2, RyR3, SERCA1s, SLC8A1, PMCA1, CACNA1S, TRPC1, TRPC3, stromal interacting molecule 1, ORAI1, calmodulin (CaLM) and calreticulin (CRT) in broiler hearts. Then, Kyoto Encyclopedia of Genes and Genomes analysis, protein–protein interactions (PPI) analysis and correlation analysis were performed to analyse the relationships between these genes. The results showed that the mRNA expression levels of ITPR 1, ITPR 2, RyR2, RyR3, SERCA1s, SLC8A1, PMCA1, CACNA1S, CaLM and CRT were generally decreased by Se deficiency, while mRNA expression levels of TRPC1, TRPC3, stromal interacting molecule 1, ORAI1 and ITPR3 were increased by Se deficiency. Kyoto Encyclopedia of Genes and Genomes and PPI analysis showed that these Ca regulation-related genes are involved in the Ca signalling pathway and a total of 15 PPIs with a combined score of >0.4 were obtained. In conclusion, the results demonstrated that Se deficiency might cause heart injury via modulating the Ca-related pathway genes, and then induce Ca2+ overload in the heart of broilers.

Delineating hierarchy of selenotranscriptome expression and their response to selenium status in chicken central nervous system

Selenium (Se) incorporated in selenoproteins as selenocysteine and supports various important cellular and organismal functions. We recently reported that chicken brain exhibited high priority for Se supply and retention under conditions of dietary Se deficiency and supernutrition Li et al. (2012) . However, the selenotranscriptome expressions and their response to Se status in chicken central nervous system (CNS) are unclear. To better understand the relationship of Se homeostasis and selenoproteins expression in chicken CNS, 1day-old HyLine White chickens were fed a low Se diet (Se-L, 0.028mg/g) supplemented with 4 levels of dietary Se (0 to 5.0mgSe/kg) as Na2SeO3 for 8weeks. Then chickens were dissected for getting the CNS, which included cerebral cortex, cerebellum, thalamus, bulbus cinereus and marrow. The expressions of selenoproteome which have 24 selenoproteins were detected by the quantitative real-time PCR array. The concept of a selenoprotein hierarchy was developed and the hierarchy of different regions in chicken CNS was existence, especially cerebral cortex and bulbus cinereus. The expression of selenoproteins has a hierarch while changing Se content, and Selenoprotein T (Selt), Selenoprotein K (Selk), Selenoprotein W (Selw), Selenoprotein U (Selu), Glutathione peroxidase 3 (Gpx3), Glutathione peroxidase 4 (Gpx4), Selenoprotein P (Sepp1), Selenoprotein O (Selo), Selenoprotein 15 (Sel15), Selenoprotein N (Seln), Glutathione peroxidase 2 (Gpx2) and Selenoprotein P 2 (Sepp2) take more necessary function in the chicken CNS. Therefore, we hypothesize that hierarchy of regulated the transcriptions of selenoproteome makes an important role of CNS Se metabolism and transport in birds.

Long-Term Selenium-Deficient Diet Induces Liver Damage by Altering Hepatocyte Ultrastructure and MMP1/3 and TIMP1/3 Expression in Growing Rats

The effects of selenium (Se)-deficient diet on the liver were evaluated by using growing rats which were fed with normal and Se-deficient diets, respectively, for 109days. The results showed that rats fed with Se-deficient diet led to a decrease in Se concentration in the liver, particularly among male rats from the low-Se group. This causes alterations to the ultrastructure of hepatocytes with condensed chromatin and swelling mitochondria observed after low Se intake. Meanwhile, pathological changes and increased fibrosis in hepatic periportal were detected by hematoxylin and eosin and Masson's trichrome staining in low-Se group. Furthermore, through immunohistochemistry (IHC) staining, higher expressions of metalloproteinases (MMP1/3) and their tissue inhibitors of metalloproteinases (TIMP1/3) were observed in the hepatic periportal of rats from the low-Se group. However, higher expressions of MMP1/3 and lower expressions of TIMP1/3 were detected in hepatic central vein and hepatic sinusoid. In addition, upregulated expressions of MMP1/3 and downregulated expressions of TIMP1/3 at the messenger RNA (mRNA) and protein levels also appeared to be relevant to low Se intake. In conclusion, Se-deficient diet could cause low Se concentration in the liver, alterations of hepatocyte ultrastructure, differential expressions of MMP1/3 and TIMP1/3 as well as fibrosis in the liver hepatic periportal.

Role of Hydrogen Sulfide on Autophagy in Liver Injuries Induced by Selenium Deficiency in Chickens.

Selenium (Se) is an indispensable trace mineral that was associated with liver injuries in animal models. Hydrogen sulfide (H2S) is involved in many liver diseases, and autophagy can maintain liver homeostasis with a stress stimulation. However, little is known about the correlation between H2S and autophagy in the liver injury chicken models induced by Se deficiency. In this study, we aimed to investigate the correlation between H2S and autophagy in the liver injury chicken models. We randomly divided 120 1-day-old chickens into two equal groups. The control group was fed with complete food with a Se content of 0.15mg/kg, and the Se-deficiency group (lab group) was fed with a Se-deficient diet with a Se content of 0.033mg/kg. When the time comes to 15, 25, and 35days, the chickens were sacrificed (20 each). The liver tissues were gathered and examined for pathological observations, the mRNA and protein levels of H2S synthases (CSE, CBS, and 3-MST) and the mRNA and protein levels of autophagy-related genes. The results showed that the expression of CSE, CBS, and 3-MST and H2S production were higher in the lab group than in the control group. Swellings, fractures, and vacuolizations were visible in the mitochondria cristae in the livers of the lab group and autophagosomes were found as well. In addition, the expression of autophagy-related genes (ATG5, LC3-I, LC3-II, Beclin1, and Dynein) was higher in the lab group than in the control group (p < 0.05) while TOR decreased significantly in the lab group (p < 0.05). The results showed that H2S and autophagy were involved in the liver injury chicken models, and H2S was correlated with autophagy.

Digital Gene Expression (DGE) Analysis of Nutritional Pancreatic Atrophy of Chicks Induced by the Se/Vitamin E Deficiencies

Nutritional pancreatic atrophy (NPA) is a classical Se/vitamin E deficiency disease of chicks. We previously determined responses of mRNA abundances of 25 selenoprotein genes in various tissues of chicks to the deficiencies of these two nutrients. The present DGE analysis was performed to reveal effects of dietary Se/vitamin E deficiencies on the pancreatic transcriptome of chicks and to identify global gene association with the NPA. We fed 4 groups of day‐old broiler chicks (n = 40/group) with a corn‐soy basal diet (BD: 10 μg Se/kg, no vitamin E added), the BD plus all‐rac‐a‐tocopheryl acetate at 50 mg/kg, Se (as sodium selenite) at 0.3 mg/kg, or both of these nutrients for 6 wk. High incidences of NPA (70%) and mortality (35%) of chicks were induced by BD, starting at wk 3. Both NPA incidences and mortality were prevented by dietary Se supplementation. On day 18, chicks were killed to collect pancreases for the DGE analysis. Pancreatic RNA samples were pooled from five individual chicks into each of the four dietary groups, respectively. Dietary Se deficiency altered expression of 884 unigenes, with 360 unigenes up‐regulated and 524 unigenes down‐regulated. Of the differentially expressed genes, 530 unigenes were annotated and 65 were classified into metabolism pathways. Real‐time PCR analyses of selected four unigenes related to selenocompound metabolic and apoptotic pathways showed consistent results with those obtained from the DGE analysis, which confirms the quality of the sequencing data for further gene expression characterization. In conclusion, our pancreatic transcriptiom data of the chicks fed the four experimental diets will facilliate mechanistic investigation on the pathogenesis of NPA induced by the dietary Se/vitamin E deficiencies.Support or Funding Information(This research is supported in part by a NSFC grant #31320103920).

Selenoprotein Transcript Level and Enzyme Activity as Biomarkers for Selenium Status and Selenium Requirements in the Turkey (Meleagris gallopavo).

The current National Research Council (NRC) selenium (Se) requirement for the turkey is 0.2 μg Se/g diet. The sequencing of the turkey selenoproteome offers additional molecular biomarkers for assessment of Se status. To determine dietary Se requirements using selenoprotein transcript levels and enzyme activities, day-old male turkey poults were fed a Se-deficient diet supplemented with graded levels of Se (0, 0.025, 0.05, 0.1, 0.2, 0.3, 0.4, 0.5, 0.75, 1.0 μg Se/g diet) as selenite, and 12.5X the vitamin E requirement. Poults fed less than 0.05 μg Se/g diet had a significantly reduced rate of growth, indicating the Se requirement for growth in young male poults is 0.05 μg Se/g diet. Se deficiency decreased plasma GPX3 (glutathione peroxidase), liver GPX1, and liver GPX4 activities to 2, 3, and 7%, respectively, of Se-adequate levels. Increasing Se supplementation resulted in well-defined plateaus for all blood, liver and gizzard enzyme activities and mRNA levels, showing that these selenoprotein biomarkers could not be used as biomarkers for supernutritional-Se status. Using selenoenzyme activity, minimum Se requirements based on red blood cell GPX1, plasma GPX3, and pancreas and liver GPX1 activities were 0.29–0.33 μg Se/g diet. qPCR analyses using all 10 dietary Se treatments for all 24 selenoprotein transcripts (plus SEPHS1) in liver, gizzard, and pancreas found that only 4, 4, and 3 transcripts, respectively, were significantly down-regulated by Se deficiency and could be used as Se biomarkers. Only GPX3 and SELH mRNA were down regulated in all 3 tissues. For these transcripts, minimum Se requirements were 0.07–0.09 μg Se/g for liver, 0.06–0.15 μg Se/g for gizzard, and 0.13–0.18 μg Se/g for pancreas, all less than enzyme-based requirements. Panels based on multiple Se-regulated transcripts were effective in identifying Se deficiency. These results show that the NRC turkey dietary Se requirement should be raised to 0.3 μg Se/g diet.

Selenium Deficiency-Induced Inflammation and Increased Expression of Regulating Inflammatory Cytokines in the Chicken Gastrointestinal Tract.

Selenium (Se), a nutritionally essential trace element, plays an important role in various aspects of health for a wide range of species, including birds. Se deficiency inhibits the growth of immune organs and decreases immune function, leading to many inflammatory diseases. The present study determined the effects and mechanism of dietary Se deficiency on gastrointestinal tract tissue inflammation. The histopathological changes showed that Se deficiency induced inflammatory lesions in the gastrointestinal tract tissues (glandular stomach, gizzard, duodenum, small intestine, and rectum). The expression levels of PTGE (prostagland E synthase), COX-2 (cyclooxygenase-2), TNF-α (tumor necrosis factor α), and NF-κB (nuclear transfer factor κB) in the gastrointestinal tract tissues (glandular stomach, gizzard, duodenum, small intestine, and rectum) were determined by qPCR on days 15, 25, 35, 45, and 55, respectively. The results showed that Se deficiency induced high expression levels of PTGE, COX-2, TNF-α, and NF-κB in the gastrointestinal tract tissues. The effects were more obvious in the duodenum and small intestine than those in the glandular stomach, gizzard, and rectum. In addition, the expression levels of these proteins in the gastrointestinal tract tissue increased in a time-dependent manner with Se deficiency feeding time. Furthermore, Se deficiency induced the production of pro-inflammatory factors, thus aggravating inflammatory lesions in the gastrointestinal tract. The effect of Se deficiency on inflammation and other gastrointestinal tract diseases should be further studied.

Dietary selenium increases the antioxidant levels and ATPase activity in the arteries and veins of poultry

Selenium (Se) deficiency is associated with the pathogenesis of vascular diseases. It has been shown that oxidative levels and ATPase activity were involved in Se deficiency diseases in humans and mammals; however, the mechanism by how Se influences the oxidative levels and ATPase activity in the poultry vasculature is unclear. We assessed the effects of dietary Se deficiency on the oxidative stress parameters (superoxide dismutase, catalase, and hydroxyl radical) and ATPase (Na(+)K(+)-ATPase, Ca(++)-ATPase, Mg(++)-ATPase, and Ca(++)Mg(++)-ATPase) activity in broiler poultry. A total of 40 broilers (1-day old) were randomly divided into a Se-deficient group (L group, fed a Se-deficient diet containing 0.08mg/kg Se) and a control group (C group, fed a diet containing sodium selenite at 0.20mg/kg Se). Then, arteries and veins were collected following euthanasia when typical symptoms of Se deficiency appeared. Antioxidant indexes and ATPase activity were evaluated using standard assays in arteries and veins. The results indicated that superoxide dismutase activity in the artery according to dietary Se deficiency was significantly lower (p < 0.05) compared with the C group. The catalase activity in the veins and hydroxyl radical inhibition in the arteries and veins by dietary Se deficiency were significantly higher (p < 0.05) compared with the C group. The Se-deficient group showed a significantly lower (p < 0.05) tendency in Na(+)K(+)-ATPase activity, Ca(++)-ATPase activity, and Ca(++)Mg(++)-ATPase activity. There were strong correlations between antioxidant indexes and Ca(++)-ATPase activity. Thus, these results indicate that antioxidant indexes and ATPases may have special roles in broiler artery and vein injuries under Se deficiency.

Selenium Deficiency Mainly Influences Antioxidant Selenoproteins Expression in Broiler Immune Organs.

Selenoprotein has many functions in chicken, and the expression of selenoproteins is closely associated with the selenium (Se) level. However, little is known about the expression patterns of selenoproteins in chicken immune organs. Here, we investigated the effect of dietary Se deficiency on the expressions of 23 selenoproteins in broiler immune organs. In this study, 150 broilers were randomly divided into two groups (75 chickens per group). The chickens were maintained either on a diet supplemented with Se through the addition of 0.2mg/kg of Se (C group) via sodium selenite or on a Se-deficient granulated diet (L group) until the broilers exhibited an onset of exudative diathesis (ED). Following euthanasia, the samples from the immune tissues (including the spleen, thymus, and bursa of Fabricius) were quickly collected, and the messenger RNA (mRNA) expression levels of 23 selenoproteins were examined by real-time quantitative PCR and analyzed using principal component analysis. The results showed that Se deficiency decreased the mRNA levels of 23 selenoproteins in the thymus, spleen, and bursa of the Fabricius tissues of broiler chickens. Furthermore, we found that among 23 selenoproteins, the mRNA levels of Dio1 in the thymus, Txnrd2 in the spleen, and Txnrd3 in the bursa of Fabricius decreased significantly (90.9%, 83.3%, and 96.8%, respectively). In addition, the principal component analysis (PCA) results suggested that Se deficiency mainly influenced the expression of antioxidative selenoproteins, especially glutathione peroxidases (Gpxs), thioredoxin reductases (Txnrds), and iodothyronine deiodinases (Dios) in chicken immune organs. The results of this study are valuable for understanding the relevance of selenoprotein activity in vivo.

Dietary mineral supplies in Malawi: spatial and socioeconomic assessment

Dietary mineral deficiencies are widespread globally causing a large disease burden. However, estimates of deficiency prevalence are often only available at national scales or for small population sub-groups with limited relevance for policy makers. This study combines food supply data from the Third Integrated Household Survey of Malawi with locally-generated food crop composition data to derive estimates of dietary mineral supplies and prevalence of inadequate intakes in Malawi. We estimate that >50 % of households in Malawi are at risk of energy, calcium (Ca), selenium (Se) and/or zinc (Zn) deficiencies due to inadequate dietary supplies, but supplies of iron (Fe), copper (Cu) and magnesium (Mg) are adequate for >80 % of households. Adequacy of iodine (I) is contingent on the use of iodised salt with 80 % of rural households living on low-pH soils had inadequate dietary Se supplies compared to 55 % on calcareous soils; concurrent inadequate supplies of Ca, Se and Zn were observed in >80 % of the poorest rural households living in areas with non-calcareous soils. Prevalence of inadequate dietary supplies was greater in rural than urban households for all nutrients except Fe. Interventions to address dietary mineral deficiencies were assessed. For example, an agronomic biofortification strategy could reduce the prevalence of inadequate dietary Se supplies from 82 to 14 % of households living in areas with low-pH soils, including from 95 to 21 % for the poorest subset of those households. If currently-used fertiliser alone were enriched with Se then the prevalence of inadequate supplies would fall from 82 to 57 % with a cost per alleviated case of dietary Se deficiency of ~ US$ 0.36 year−1. Household surveys can provide useful insights into the prevalence and underlying causes of dietary mineral deficiencies, allowing disaggregation by spatial and socioeconomic criteria. Furthermore, impacts of potential interventions can be modelled.

Competition between the Brain and Testes under Selenium-Compromised Conditions: Insight into Sex Differences in Selenium Metabolism and Risk of Neurodevelopmental Disease.

Selenium is an essential trace element that promotes male fertility and brain function. Herein, we report that prepubescent castration provides neuroprotection by increasing selenium-dependent antioxidant activity in the brain, revealing a competition between the brain and testes for selenium utilization. These findings provide novel insight into the interaction of sex and oxidative stress upon the developing brain and have potentially significant implications for the prevention of neurodevelopmental disorders characterized by aberrant excitatory/inhibitory balance, such as schizophrenia and epilepsy.

Effect of Dietary Selenium Deficiency on the Cell Apoptosis and the Level of Thyroid Hormones in Chicken.

This study assessed the effect of dietary selenium (Se) deficiency on male reproductive function in chicken. A total of 180 Hy-line laying cocks (1day old; Weiwei) were randomly divided into 2 groups (n=90) of Se-deficient chickens and control chickens. The control group was fed a basic diet (containing 0.15mg of Se/kg). The Se-deficient group was fed a Se-deficient corn-soy basal diet (containing 0.033mg of Se/kg). Fifteen chickens were killed in each group on days 30, 60, and 90, respectively. Then, serum and testes were collected and used in the detection of experimental index. Results indicated that GSH-Px activity and Bcl-2 mRNA level in the testes and thyroidal triiodothyronine (T3) and free triiodothyronine (FT3) levels in serum by dietary Se deficiency were significantly decreased compared to the corresponding control groups. Se deficiency-treated group showed a significant increase in MDA concent, TUNEL-positive cells, and mRNA level of Bax, Caspase3, and p53 in the testes and thyroidal thyroxine (T4), free thyroxine (FT4), and thyroid-stimulating hormone (TSH) levels in serum. Histopathologically, Se deficiency caused impairments in the testes. These results suggested that dietary Se deficiency exerts significant harmful effects on male reproductive organ and that the intrinsic and extrinsic pathways and the upstream regulators such as p53, Bax, and Bcl-2 were all involved in Se deficiency-induced testicular apoptosis.

Selenium Deficiency Influences the mRNA Expression of Selenoproteins and Cytokines in Chicken Erythrocytes.

Selenium (Se) deficiency induces hemolysis in chickens, but the molecular mechanism for this effect remains unclear. Se primarily elicits its function through the activity of selenoproteins, which contain the unique amino acid selenocysteine (Sec). In this study, we aimed to investigate the effect of Se deficiency on the expression of 24 selenoproteins and 10 cytokines. One hundred eighty chickens were randomly divided into 2 groups (90 chickens per group). During the entire experimental period, chickens were allowed ad libitum consumption of feed and water. The chickens were fed either a Se-deficient diet (0.008mgSe/kg; produced in the Se-deficient area of Heilongjiang, China) or a Se-supplemented diet (as sodium selenite) at 0.2mg/kg for 35days. At the 35th day, the messenger RNA (mRNA) levels of 24 selenoproteins and 10 cytokines were examined in erythrocytes of 5 chickens per group, and the correlation was analyzed. The results showed that the expression of 24 selenoproteins and 7 cytokines (IL-2, IL-4, IL-8, IL-10, IL-12β, TGF-β4, and IFN-γ) decreased (P<0.05), and the expression of 3 cytokines (IL-1γ, IL-6 and IL-7) was higher in the Se-deficient group. In both groups, glutathione peroxidase (GPX), thioredoxin 1 (Txnrd1), selenoprotein P1 (SELP), and selenoprotein synthetase (SPS2) were highly expressed compared to the other selenoproteins in chicken erythrocytes (P<0.05). These data suggest that GPXs, Txnrd1, SELP, and SPS2 possibly play a more important role than the other selenoproteins. The increase of pro-inflammatory cytokines (IL-1γ, IL-6, and IL-7) suggested that the immune system of chickens was damaged by the Se deficiency. Correlation analysis suggested that although the expression of 24 selenoproteins and 7 cytokines decreased and that of 3 cytokines increased, there was a close correlation between their expression levels and a Se diet. These results suggested that Se deficiency influenced the expressions of 24 selenoproteins and 10 cytokines in chicken erythrocytes, revealing a relationship between Se and the chicken immune system. This study offers information regarding the mechanism of Se deficiency-induced hemolysis.

Deficient and excess dietary selenium levels affect growth performance, blood cells apoptosis and liver HSP70 expression in juvenile yellow catfish Pelteobagrus fulvidraco.

We investigated the effects of deficient and excess dietary selenium (Se) on growth, blood cells apoptosis and liver heat shock protein 70 (HSP70) expression in juvenile yellow catfish (Pelteobagrus fulvidraco). After 8 weeks, yellow catfish (initial weight: 2.12 ± 0.01 g) fed isonitrogenous and isolipid diets containing <0.05 (deficient dietary Se) or 6.5 (excess dietary Se) mg Se/kg displayed a significantly lower weight gain ratio (WGR) than those fed a diet containing 0.23 (normal dietary Se) mg Se/kg. As dietary Se levels increased, liver Se concentration, glutathione peroxidase activity and the hepatosomatic index increased significantly. Plasma glucose concentration was highest in the normal treatment compared with the excess dietary Se treatment. Both deficient and excess dietary Se lead to increased reactive oxygen species (ROS) production and apoptosis ratio in blood cells, whereas only excess dietary Se increased their cytoplasmic free-Ca(2+) (CF-Ca(2+)) concentration. Excess dietary Se also resulted in the highest level of HSP70 expression, thereby possibly providing a protective mechanism against oxidative stress. These results indicate that both deficient and excess dietary Se restrained the growth of juvenile yellow catfish and caused oxidative stress. The overproduction of ROS may act as a signal molecule mediate apoptosis when dietary Se deficiency. Both ROS and CF-Ca(2+) were recorded when dietary Se excess, suggesting that Ca(2+) may be activated by Se and play a major role during Se-induced oxidative stress and cell apoptosis.