中国成人硒需要量研究

目的 探讨使人体血浆硒蛋白P(SEPPI)达到饱和的硒摄入量,以评估硒需要量,为膳食硒参考摄入量DRIB的修订提供参考.方法 时98名低硒健康受试者(体重平均58kg)进行为期40w的双盲补硒实验.随机分为七组,补硒(以硒蛋氨酸形式)剂量分别为0、21、35、55、79、102和125 μg/d.定期检测血浆中谷胱甘肽...     

硒的生物标志物

人体必需微量元素硒具有多种生物学活性,这依赖于硒摄入的水平。相对较低的硒摄入决定含硒酶的表达,含硒酶是人体质量主要的组份。较高水平的硒摄入已被证明具有抗肿瘤的潜能,而非常高的硒摄入可对机体产生不良影响。这种生物活性的层次性要求不同水平的硒暴露有不同的生物标志物信息。一些硒的生物标志物,如硒蛋白,特别是GPX3和SEPP1,可直接提供功能相关的信息,并在识别营养性硒缺乏及追踪硒缺乏个体补硒治疗疗效方面有重要价值。它们在硒摄入情况下可有效的调节范围内硒蛋白的表达。其他硒生物标志物通过基于食品、组织、尿液或粪便中硒含量的推论间接的提供信息。它们可以提示硒缺乏或不良反应的可能性,却不能提供其直接证据。它们的价值在于提供广泛的硒摄入量的硒状态信息,特别是来自食物形式的。     

Longitudinal selenium status in healthy British adults: assessment using biochemical and molecular biomarkers

Human selenium (Se) requirements are currently based on biochemical markers of Se status. In rats, tissue glutathione peroxidase-1 (Gpx1) mRNA levels can be used effectively to determine Se requirements; blood Gpx1 mRNA levels decrease in Se-deficient rats, so molecular biology-based markers have potential for human nutrition assessment. To study the efficacy of molecular biology markers for assessing Se status in humans, we conducted a longitudinal study on 39 subjects (age 45 +/- 11) in Reading, UK. Diet diaries (5 day) and blood were obtained from each subject at 2, 8, 17 and 23 weeks, and plasma Se, glutathione peroxidase (Gpx3) enzyme activity, and selenoprotein mRNA levels were determined. There were no significant longitudinal effects on Se biomarkers. Se intake averaged 48 +/- 14 microg/d. Plasma Se concentrations averaged 1.13 +/- 0.16 micromol/l. Plasma Se v. energy-corrected Se intake (ng Se/kJ/d) was significantly correlated, but neither Gpx3 activity v. Se intake (ng Se/kJ/d) nor Gpx3 activity v. plasma Se was significantly correlated. Collectively, this indicates that subjects were on the plateaus of the response curves. Selenoprotein mRNAs were quantitated in total RNA isolated from whole blood, but mRNA levels for Gpx1, selenoprotein H, and selenoprotein W (all highly regulated by Se in rodents), as well selenoprotein P, Gpx3, and phospholipid hydroperoxide glutathione peroxidase were also not significantly correlated with plasma Se. Thus selenoprotein molecular biomarkers, as well as traditional biochemical markers, are unable to further distinguish differences in Se status in these Se replete subjects. The efficacy of molecular biomarkers to detect Se deficiency needs to be tested in Se-deficient populations.     

Biomarkers of Selenium Status

The essential trace element, selenium (Se), has multiple biological activities, which depend on the level of Se intake. Relatively low Se intakes determine the expression of selenoenzymes in which it serves as an essential constituent. Higher intakes have been shown to have anti-tumorigenic potential; and very high Se intakes can produce adverse effects. This hierarchy of biological activities calls for biomarkers informative at different levels of Se exposure. Some Se-biomarkers, such as the selenoproteins and particularly GPX3 and SEPP1, provide information about function directly and are of value in identifying nutritional Se deficiency and tracking responses of deficient individuals to Se-treatment. They are useful under conditions of Se intake within the range of regulated selenoprotein expression, e.g., for humans <55 μg/day and for animals <20 μg/kg diet. Other Se-biomarkers provide information indirectly through inferences based on Se levels of foods, tissues, urine or feces. They can indicate the likelihood of deficiency or adverse effects, but they do not provide direct evidence of either condition. Their value is in providing information about Se status over a wide range of Se intake, particularly from food forms. There is need for additional Se biomarkers particularly for assessing Se status in non-deficient individuals for whom the prospects of cancer risk reduction and adverse effects risk are the primary health considerations. This would include determining whether supranutritional intakes of Se may be required for maximal selenoprotein expression in immune surveillance cells. It would also include developing methods to determine low molecular weight Se-metabolites, i.e., selenoamino acids and methylated Se-metabolites, which to date have not been detectable in biological specimens. Recent analytical advances using tandem liquid chromatography-mass spectrometry suggest prospects for detecting these metabolites.     

Dietary selenium requirements based on glutathione peroxidase-1 activity and mRNA levels and other Se-dependent parameters are not increased by pregnancy and lactation in rats

The hierarchy of selenium (Se) requirements for growing rats ranges from <0.01 to 0.1 microg Se/g diet, depending on the choice of Se status parameter. To further evaluate the efficacy of molecular biology markers to determine Se requirements in later periods of the life cycle, which are less amenable to traditional approaches, we studied pregnant and lactating rats. Female weanling rats were fed a Se-deficient diet (<0.01 microg Se/g) or supplemented with graded levels of dietary Se (0-0.3 microg Se/g) for >10 wk, bred, and killed on d 1, 12, and 18 of pregnancy and d 7 and 18 of lactation; Se response curves were determined for 10 parameters including liver glutathione peroxidase (GPX). Growth, and mRNA levels for selenoprotein P, 5'-deiodinase, and GPX4 were not decreased by Se deficiency. GPX4 activity required 0.05 microg Se/g diet for maximum activity, similar to growing rats. Dietary Se requirements for plasma GPX3 activity decreased 33% in pregnancy, but returned during lactation to the requirement of growing rats. The Se requirement for GPX1 activity decreased 25% in pregnancy but not in lactation. GPX1 mRNA required 0.05 microg Se/g diet for maximum levels in both pregnancy and lactation, similar to growing rats. Clearly, Se requirements do not increase during pregnancy and lactation relative to Se requirements in growing rats. Unexpectedly, Se-adequate levels of GPX1 mRNA and activity declined to <40 and 50%, respectively, of nonpregnant Se-adequate levels during pregnancy and lactation, illustrating the need to fully understand biomarkers at all stages of the life cycle.     

Genetic variation in GPX1 is associated with GPX1 activity in a comprehensive analysis of genetic variations in selenoenzyme genes and their activity and oxidative stress in humans

Previous studies suggest some effects of selenium on risk of several chronic diseases, which may be mediated through a small number of selenoenzymes with antioxidant properties. In this cross-sectional analysis of 195 participants from the Seattle Barrett's Esophagus Study who were free of esophageal cancer at the time of blood draw, we examined whether the number of the minor alleles in 26 tagging single nucleotide polymorphisms (SNP) of five selenoenzyme genes [i.e., glutathione peroxidase 1-4 (GPX1-4) and selenoprotein P (SEPP1)] was associated with activity of GPX1 in white blood cells and GPX3 in plasma, and concentrations of SEPP1 and markers of oxidative stress [malondialdehyde (MDA) and protein carbonyl content] in plasma. At the gene level, associations were observed between overall variation in GPX1 and GPX1 activity (P = 0.02) as well as between overall variation in GPX2 and SEPP1 concentrations (P = 0.03). By individual SNP, two variants in GPX1 (rs8179164 and rs1987628) showed a suggestive association with GPX1 activity (P = 0.10 and 0.08, respectively) and two GPX2 variants (rs4902346 and rs2071566) were associated with SEPP1 concentration (P = 0.004 and 0.002, respectively). Furthermore, two SNP in the SEPP1 gene (rs230813 and rs230819) were associated with MDA concentrations (P = 0.03 and 0.02, respectively). Overall, our study supports the hypothesis that common genetic variants in selenoenzymes affect their activity.     

Biomonitoring of selenoprotein P in human serum by fast affinity chromatography coupled to ICP-MS

Most of the Se in human serum is bound to selenoprotein P (SEPP1) in which Se is present in form of selenocysteine. The SEPP1 is a new possible biomarker for the Se status and for this reason we developed a fast, simple and reliable method for the quantitative determination of SEPP1 in serum by affinity chromatography coupled to ICP-MS. It is possible to separate SEPP1 from other selenoproteins in serum in only 5?min, which allows high sample throughput in clinical laboratories. Measured and certified concentrations of total Se and Se(SEPP1) are in good agreement for the reference material SRM 1950. The SEPP1 concentration was stable in serum samples of 3 persons for a minimum of 2 weeks. Further results of method validation were described including internal and external quality assurance.The analytical method was applied for a biomonitoring study of the SEPP1 and total Se concentration in human serum of 50 occupationally non-exposed persons living in northern Germany. Concentration ranges and mean concentrations for Se(SEPP1) are 31.1–59.7 and 46.2?μg/L, respectively. The corresponding values for total Se are 62–120 and 83.5?μg/L. The mean percentage of total Se in serum present as SEPP1 is 58%.     

Metabolism of selenite and selenomethionine in the rhesus monkey

Female rhesus monkeys were fed a commercial monkey diet and given selenium (Se) as either selenite or selenomethionine (SeMet) in the drinking water for 11 mo. Muscle and liver biopsies were taken initially and at the end of the experiment for determination of Se levels and glutathione peroxidase (GPX) activity. Blood was collected at monthly to bimonthly intervals, and the plasma and erythrocytes were subjected to gel filtration to determine the distribution of Se among proteins of various molecular weights. At the end of the experiment, there was significantly more Se in liver, muscle and hair from the monkeys given SeMet than in tissues from those given selenite, but there were no differences in liver or muscle GPX activity between the two treatment groups. The erythrocyte and plasma Se levels were significantly higher in the monkeys given SeMet than in those receiving selenite, but there were no differences in the GPX levels between these groups. About 68% of erythrocyte Se was associated with GPX in monkeys given selenite whereas only 34% was associated with GPX in those administered SeMet. The correlation coefficient for blood Se level and erythrocyte GPX activity was 0.92 in monkeys given selenite but only 0.37 in those given SeMet. Gel filtration of plasma revealed only one Se peak for plasma from the monkeys given selenite but at least two major Se peaks for plasma from monkeys receiving SeMet. The possible implications of these results for humans are discussed, including the reasons for poor correlations of GPX activity and blood Se levels.     

Selenoprotein mRNA is expressed in blood at levels comparable to major tissues in rats

Liver glutathione peroxidase-1 (GPX1) mRNA is highly regulated by Se status relative to other parameters, but is of limited use for determining Se requirements in humans. To examine the efficacy of using blood for Se status assessment using molecular biology markers, we used a ribonuclease protection assay (RPA) to study mRNA levels in whole blood relative to 16 other rat tissues. Significant amounts of total RNA (>50 microg) were obtained from 1 mL of whole blood. Total RNA from 28-d postweaning Se-adequate (0.2 microg Se/g diet) male rats was analyzed for GPX1, GPX4, GPX3, thioredoxin reductase-1 (TRR1), and selenoprotein-P (SelP). RPA detected significant mRNA expression for at least 1 selenoprotein in all tissues except pancreas. GPX1 mRNA expression using this mix of RPA probes yielded the highest signal for GPX1 relative to the other selenoprotein signals in all tissues except testis; GPX1 expression was 4th highest in blood and similar to the major organs (liver, 1st; heart, 5th; kidney, 6th). Kidney was highest for GPX3, and testes was highest for GPX4, TRR1, and SelP. This study is the first to report the gene expression pattern for a number of selenoproteins and across a comprehensive set of tissues. The mRNA levels for all selenoproteins in blood were comparable to levels in the major organs, and decreases in blood and liver GPX1 mRNA levels in Se deficiency were similar, supporting potential use of whole blood for assessing Se status using molecular biology markers.     

克山病病区粮食中补充蛋氨酸对大鼠膳食硒生物利用的影响

为研究在克山病病区粮食中补充蛋氨酸对大鼠组织硒和谷胱甘肽过氧化物酶 (GPX)活性的影响 ,用克山病病区生产的低硒粮食为主配成低硒基础饲料 ,其硒含量为 0 .0 0 7mg/kg。在此基础上添加不同量的硒蛋氨酸 ,使饲料硒水平分别达到 0 .0 0 7、0 .0 6和 0 .5 0 mg/kg。每一硒水平又分别补充或不补充 4g/kg DL -蛋氨酸 ,配制成含不同硒和蛋氨酸的 6种饲料 ,分别喂养雄性 Wistar断乳大鼠 8周。结果在饲料硒水平为0 .0 0 7mg/kg时 ,补充蛋氨酸组动物除肌肉硒含量低于未补充组外 ,其它组织硒含量和各组织 GPX活力与不补充蛋氨酸动物无显著差异 ;在饲料硒水平为 0 .0 6 mg/kg时 ,补充蛋氨酸组动物组织中的硒含量出现了重新分布 ,最明显的是补充蛋氨酸组动物肌肉的硒含量减少 ,而肝脏和血硒含量增加 ,且各组织中 GPX活力显著大于未补充蛋氨酸组的动物 ;在饲料硒水平为 0 .5 0 mg/kg时 ,补充蛋氨酸组动物组织中硒含量有不同程度下降 ,但 GPX活力仍保持不变。研究结果认为病区粮食中蛋氨酸不足时 ,机体首先利用膳食中的硒蛋氨酸(谷类食物中硒的主要形式 )以替代蛋氨酸参与组织蛋白质的合成。补充蛋氨酸后 ,硒蛋氨酸即可发挥其应有生理功能。进一步提示病区粮食中蛋氨酸不足可能是与克山病发病有关的另一因素。     

Selenium Status and Supplementation Effects in Pregnancy—A Study on Mother–Child Pairs from a Single-Center Cohort

The demand for selenium (Se) increases during pregnancy since this element supports child growth, proper neuronal development and maternal thyroid function. The issue is particularly relevant for populations living in areas with a limited selenium supply, where many pregnant women opt for Se supplementation. The efficiency of this measure is unknown, although it seems vital in the prevention of severe Se deficiency. In order to evaluate this hypothesis, an observational study was conducted in Poland, where Se deficiency is prevalent. Pregnant women were invited to participate in the study and provided serum samples at the end of pregnancy (n = 115). Information on the supplemental intake of micronutrients was recorded in a face-to-face interview. In addition, serum samples were isolated from the cord blood of newborns at delivery (n = 112) and included in the analyses. Thyroid hormone status was evaluated by routine laboratory tests, and Se status was determined by total Se and selenoprotein P (SELENOP) concentrations and extracellular glutathione peroxidase (GPX3) activity. The three parameters of Se status correlated strongly within the group of mothers and within the group of newborns, with an additional significant correlation found among mother–child pairs. One-third of mothers reported additional Se intake, mainly as a component of multi-micronutrient supplements, at a mean (±SD) dosage of 42 ± 14 µg Se/day. Despite this regime, most of the women presented an insufficient Se status, with 79% of mothers displaying serum Se concentrations below 70 µg/L (indicating Se deficiency) and 22% showing levels below 45.9 µg/L (severe Se deficiency). The inadequate Se supply was also reflected in relatively low SELENOP concentrations and GPX3 activity. Neither total Se nor SELENOP or GPX3 levels were significantly higher in the group of mothers reporting the intake of supplements than in the non-supplementing group. Nevertheless, elevated SELENOP concentrations were observed in the subgroup receiving supplements with more than 55 µg/day. We conclude that the self-administered supplementation of small Se dosages was not sufficient to achieve replete Se status in the micronutrient scant area. However, the maternal Se deficit measured by either Se, SELENOP or GPX3 was transferred from mothers to the newborns, as the parameters correlated strongly in the mother–newborn pairs of samples. It is vital to re-evaluate the guidelines concerning pregnancy care and monitoring of micronutrient status during pregnancy, in particular in areas where deficiencies are present.     

硒代蛋氨酸对肝细胞L02中硒蛋白表达的影响及丝氨酸的协同作用

目的观察硒代蛋氨酸对肝细胞L02硒蛋白表达的影响及丝氨酸的协同作用。方法培养L02细胞,分为硒代蛋氨酸组和丝氨酸+硒代蛋氨酸组。硒代蛋氨酸剂量设为0.001、0.01、0.1、1和10μmol/L,丝氨酸和硒代蛋氨酸按照2∶1摩尔比混合。作用于L02细胞48 h后,采用酶联免疫吸附试验(enzyme-linked immuno-sorbent assay,ELISA)双抗体夹心法检测细胞培养上清液中硒蛋白P和裂解液中谷胱甘肽过氧化物酶1(glutathione peroxidase 1,GPx1)浓度,采用免疫印迹法检测裂解液中硒蛋白P和GPx1表达水平。结果硒代蛋氨酸浓度为0.1和1μmol/L时,硒蛋白P和GPx1表达分别达到拐点,硒代蛋氨酸浓度为10μmol/L时,GPx1和硒蛋白P表达下降。硒代蛋氨酸剂量为0.001~10μmol/L时,丝氨酸对细胞内GPx1和硒蛋白P表达具有协同作用。结论硒代蛋氨酸作用于人正常肝细胞L02时,硒蛋白合成出现拐点,且丝氨酸对硒代蛋氨酸在肝细胞L02内表达GPx1和硒蛋白P具有协同作用。     

The influence of selenium-enriched milk proteins and selenium yeast on plasma selenium levels and rectal selenoprotein gene expression in human subjects

Certain forms of dietary Se may have advantages for improving human Se status and regulating the risk for disease, such as cancers, including colorectal cancer (CRC). The present study compared the effects of a Se-enriched milk protein (dairy-Se) with a Se-rich yeast (yeast-Se) on plasma Se levels and rectal selenoprotein gene expression since we reasoned that if these genes were not regulated, there was little potential for regulating the risk for CRC in this organ. A total of twenty-three healthy volunteers with plasma Se in the lower half of the population range were supplemented with dairy-Se (150 μg/d) or yeast-Se (150 μg/d) for 6 weeks, followed by 6 weeks of washout period. Blood was sampled every 2 weeks, and rectal biopsies were obtained before and after Se supplementation and after the washout period. Plasma Se levels and glutathione peroxidase (GPx) activity, and rectal mRNA of selenoprotein P (SeP), cytosolic GPx-1 (GPx-1), gastrointestinal GPx-2 (GPx-2) and thioredoxin reductase-1 (TrxR-1) were measured. Plasma Se levels increased rapidly in both Se groups (P < 0·001); plasma GPx activity was not significantly changed. Rectal SeP mRNA increased at 6 weeks compared with baseline in both Se groups (P < 0·05); only dairy-Se resulted in a sustained elevation of SeP after the washout period (P < 0·05). Rectal GPx-1 and GPx-2 mRNA were higher with dairy-Se (P < 0·05) than with yeast-Se at 6 weeks. In conclusion, three rectal selenoprotein mRNA were differentially regulated by dairy-Se and yeast-Se. Changes in rectal selenoproteins are not predicted by changes in plasma Se; dairy-Se effectively regulates the expression of several rectal selenoproteins of relevance to the risk for CRC.     

An in vivo study of the antioxidant potentials of a plant food concentrate

OBJECTIVE: A plant food concentrate (PF) is a source of antioxidants. Its influence on antioxidant status has never been studied. The present longitudinal study investigated the antioxidant and lipidemic responses in 15 moderately hypercholesterolemic (>5.2 mmol/L) male subjects to the supplemental intakes of PF. METHODS: The participants underwent a two-week period where any previous supplemental intakes were withdrawn. This was followed by a two-week baseline period at entry (control). The baseline period was followed by taking PF concentrate (8.5 g twice daily) for two weeks followed by a washout period for two weeks. All subjects completed food frequency questionnaires at pre-supplemental (baseline) and post-PF period. Fasting heparinized and EDTA blood samples were collected at the end of each period. Erythrocyte superoxide dismutase (SOD), whole blood glutathione peroxidase (GPX) and plasma concentrations of zinc and copper, along with plasma levels of lipids, were determined. RESULTS: The PF supplement contributed significantly to the daily intakes of total dietary fiber. The zinc and copper-dependent SOD but not GPX activity were significantly elevated. The total and LDL-cholesterol concentrations in the plasma were significantly decreased while the ratio of HDL/LDL cholesterol was increased post-PF intake. CONCLUSIONS: These results indicate that the antioxidant and cholesterol status of moderately hypercholesterolemic subjects can be potentially improved with the supplemental intake of PF concentrate.     

Selenium supplementation in healthy Belgian adults: response in platelet glutathione peroxidase activity and other blood indices

Selenium status was explored by investigating effects of a 60-d Se supplementation with DL-selenomethionine (100 micrograms Se/d) in a group of 10 adults (plasma Se levels, 0.76-1.33 mumol/L). Plasma, erythrocyte, and urinary Se and activities of glutathione peroxidase (GSH Px) in plasma, erythrocytes, and platelets were measured before intervention and after 5, 15, 30, 45, and 60 d. A placebo was given to six adults. Plasma and urinary Se were the most sensitive indices to Se exposure. Se in plasma increased steadily during the course of the study whereas urinary Se reached a plateau between 30 and 60 d. By contrast erythrocyte Se did only change after 45 d. Enzyme in plasma and erythrocytes did not respond whereas platelet GSH Px did. The plateau of activity that was observed after 15 d for plasma Se in the range 1.40-1.50 mumol/L could mean that the Se status is insufficient for an optimal function of GSH Px and implies that dietary intake in Belgium (less than 50-60 micrograms Se/d) is not adequate.     

Selenium and Chronic Diseases: A Nutritional Genomics Perspective

Mechanistic data have revealed a key role for selenium (Se) and selenoproteins in biological pathways known to be altered in multifactorial diseases, such as cellular maintenance, response to oxidative stress and correct protein folding. Although epidemiological studies indicate that low Se intake is linked to increased risk for various chronic diseases, supplementation trials have given confusing outcomes, suggesting that additional genetic factors could affect the relationship between Se and health. Genetic data support this hypothesis, as risk for several chronic diseases, in particular cancer, was linked to a number of single nucleotide polymorphisms (SNP) altering Se metabolism, selenoprotein synthesis or activity. Interactions between SNPs in selenoprotein genes, SNPs in related molecular pathways and biomarkers of Se status were found to further modulate the genetic risk carried by the SNPs. Taken together, nutritional genomics approaches uncovered the potential implication of some selenoproteins as well as the influence of complex interactions between genetic variants and Se status in the aetiology of several chronic diseases. This review discusses the results from these genetic associations in the context of selenoprotein functions and epidemiological investigations and emphasises the need to assess in future studies the combined contribution of Se status, environmental stress, and multiple or individual SNPs to disease risk.     

An estimation of selenium requirements for New Zealanders.

BACKGROUND: Current US dietary recommendations for selenium are based on maximization of plasma glutathione peroxidase (GSHPx) activity according to data from one study of Chinese men. OBJECTIVE: The effect of various amounts of supplemental selenium on GSHPx activities in blood of New Zealand adults was investigated to calculate a selenium requirement for New Zealanders. The effect on plasma selenoprotein P and thyroid hormones was also investigated. DESIGN: Fifty-two adults with low blood selenium concentrations ingested a placebo or 10, 20, 30, or 40 microgram Se as L-selenomethionine daily for 20 wk. RESULTS: Plasma and whole-blood GSHPx activities increased in all supplemented groups but reached a plateau only in the group receiving 40 microgram Se, as determined by statistical analysis. Increases in selenoprotein P were greater than those for selenium and GSHPx at all supplement intakes. Thyroxine concentrations decreased in supplemented groups but the decrease was significantly different from that in the control group only for the 10-microgram group and for all supplemented groups combined. CONCLUSIONS: An upper estimated requirement of 90 microgram Se/d was calculated as the intake necessary for maximization of plasma GSHPx activity, as used in the derivation of the US recommended daily allowance. Our lower estimated requirement of 39 microgram Se/d was the intake necessary to reach two-thirds of maximal GSHPx activity, as was used in calculating the World Health Organization normative requirement. The lower estimate is a realistic goal for New Zealand but the upper estimate could be achieved only with regular inclusion of high-selenium foods.     

The selenium deficiency disease exudative diathesis in chicks is associated with downregulation of seven common selenoprotein genes in liver and muscle

Fast-growing broiler chicks are susceptible to Se deficiency diseases including exudative diathesis (ED). Our objective was to determine if ED could be induced by feeding a current, practical diet and if the incidence was related to selenogenome expression in liver and muscle of chicks. Four groups of day-old broiler chicks (n = 60/group) were fed a corn-soy basal diet (BD; 14 μg Se/kg; produced in the Se-deficient area of Sichuan, China and not supplemented with Se or vitamin E), the BD and all-rac-α-tocopheryl acetate at 50 mg/kg and Se (as sodium selenite) at 0.3 mg/kg, or both of these nutrients for 6 wk. A high incidence of ED and mortality of chicks were induced by the BD. The incidences and mortality were completely prevented by supplemental dietary Se but were only partially decreased by supplemental α-tocopherol acetate. Dietary Se deficiency decreased (P < 0.05) mRNA levels of 7 common selenoprotein genes (Gpx1, Gpx4, Sepw1, Sepn1, Sepp1, Selo, and Selk) in muscle and liver. Whereas supplementing α-tocopherol acetate enhanced (P < 0.05) only the muscle Sepx1 mRNA level, it actually decreased (P < 0.05) hepatic Gpx1, Seli, Txnrd1, and Txnrd2 mRNA levels. In conclusion, dietary Se protected chicks from the Se deficiency disease ED, probably by upregulating selenoprotein genes coding for oxidation- and/or lesion-protective proteins. The protection by vitamin E might be mediated via selenoproteins not assayed in this study and/or Se-independent mechanisms. The inverse relationship between hepatic expression of 4 redox-related selenoprotein genes and vitamin E status revealed a novel interaction between Se and vitamin E in vivo.     

Effectiveness of selenium supplements in a low-selenium area of China

BACKGROUND: Selenium is an essential micronutrient with a recommended dietary allowance for adults of 55 mug/d. It functions as an essential constituent of selenoproteins. Although there is no evidence of selenium deficiency in the United States, people in many other areas of the world are selenium deficient, with the consequence that they are unable to express their selenoproteins fully. OBJECTIVE: We carried out a supplementation trial in a selenium-deficient population in China to assess the requirement for selenium as selenite and as selenomethionine. DESIGN: One hundred twenty subjects with an average selenium intake of 10 mug/d were randomly assigned and administered tablets containing no selenium or amounts as high as 66 mug Se/d for 20 wk. Plasma was sampled before supplementation and at 4-wk intervals during supplementation and was assayed for the 2 plasma selenoproteins, glutathione peroxidase and selenoprotein P. RESULTS: Full expression of glutathione peroxidase was achieved with 37 mug Se/d as selenomethionine and with 66 mug/d as selenite. Full expression of selenoprotein P was not achieved at the highest doses of either form. CONCLUSIONS: Full expression of selenoprotein P requires a greater selenium intake than does full expression of plasma glutathione peroxidase. This suggests that selenoprotein P is a better indicator of selenium nutritional status than is glutathione peroxidase and that the recommended dietary allowance of selenium, which was set with the use of glutathione peroxidase as the index of selenium status, should be revised. Selenium as selenomethionine had nearly twice the bioavailability of selenium as selenite.