Influence of Dietary Sodium Selenite on Tissue Selenium Levels of Growing Pigs

Twenty Norwegian Landrace pigs were divided into 5 groups and fed a basal diet consisting of a mixture of dried skim milk and whey powder together with ground barley. The diet was supplemented with 0, 0.2, 0.8, 1.2 and 2.2 μg selenium as sodium selenite and was fed for 12 weeks. The muscle selenium level was increased by a factor of about 4 and the liver selenium by a factor of about 12 when the dietary selenium supplement was increased from zero to 2.2 μg/g. There was a significant linear correlation between dietary selenium and selenium concentrations in tissues. Possible benefit for humans consuming meat from animals having received the selenium doses used in this experiment are discussed. dietary selenium; tissue levels; pigs.     

Deletion of selenoprotein P alters distribution of selenium in the mouse

Selenoprotein P (Se-P) contains most of the selenium in plasma. Its function is not known. Mice with the Se-P gene deleted (Sepp(-/-)) were generated. Two phenotypes were observed: 1) Sepp(-/-) mice lost weight and developed poor motor coordination when fed diets with selenium below 0.1 mg/kg, and 2) male Sepp(-/-) mice had sharply reduced fertility. Weanling male Sepp(+/+), Sepp(+/-), and Sepp(-/-) mice were fed diets for 8 weeks containing <0.02-2 mg selenium/kg. Sepp(+/+) and Sepp(+/-) mice had similar selenium concentrations in all tissues except plasma where a gene-dose effect on Se-P was observed. Liver selenium was unaffected by Se-P deletion except that it increased when dietary selenium was below 0.1 mg/kg. Selenium in other tissues exhibited a continuum of responses to Se-P deletion. Testis selenium was depressed to 19% in mice fed an 0.1 mg selenium/kg diet and did not rise to Sepp(+/+) levels even with a dietary selenium of 2 mg/kg. Brain selenium was depressed to 43%, but feeding 2 mg selenium/kg diet raised it to Sepp(+/+) levels. Kidney was depressed to 76% and reached Sepp(+/+) levels on an 0.25 mg selenium/kg diet. Heart selenium was not affected. These results suggest that the Sepp(-/-) phenotypes were caused by low selenium in testis and brain. They strongly suggest that Se-P from liver provides selenium to several tissues, especially testis and brain. Further, they indicate that transport forms of selenium other than Se-P exist because selenium levels of all tissues except testis responded to increases of dietary selenium in Sepp(-/-) mice.     

Selenium Deposition in Tissues and Eggs of Laying Hens Given Surplus of Selenium as Selenomethionine

Forty-eight Norwegian bred White Leghorn chickens were divided into 6 groups and fed a basal diet containing 0.30 mig Se/kg supplemented with 0, 0.1, 0.5, 1.0, 3.0 or 6.0 mg Se/ kg in the form of selenomethionine for 18 weeks. A supplement of only 0.1 mg Se/kg induced significantly higher selenium concentrations in breast muscle and eggs, particularly in the egg white. The increase of selenium in the tissue and egg was proportional to the amounts of selenomethionine added to the feed. In the group given 6.0 mg Se/kg, the selenium concentrations in all tissues and eggs analysed ranged from 4.8 to 7.3 μg Se/g. No signs of toxic effects were observed even at the highest intake of selenium. Excess supply of selenium as selenomethionine to chickens was shown to be more potent than sodium selenite in raising the selenium concentration in tissues and eggs. A supplementation up to 10 times the requirement did not increase the levels of selenium in poultry products to such a degree that they could be considered as a potential risk for human consumption.     

Effect of selenium deficiency on the antioxidative status and muscle damage in growing turkeys

An experiment investigated the effect of different selenium supplementations on the antioxidant defence system and on the occurrence of muscle dystrophy in growing turkeys. Newly hatched male turkeys (B.U.T. Big 6) were divided into eight groups of 18 turkeys each and fed either a basal diet (selenium <0.010 mg/kg diet), or the basal diet supplemented with 0.10; 0.15; 0.20; 0.25; 0.30; 0.35 or 0.40 mg selenium/kg diet in the form of sodium selenate. Vitamin E was adequately supplemented in all diets. After 35 days, muscle damage parameters including aspartate aminotransferase, creatine kinase, creatine kinase M and B were significantly increased in the selenium deficient Group I. A significant reduction of weight gain, feed consumption and selenium dependent glutathione peroxidase activity was also observed in the liver of selenium deficient birds. The ratio of oxidised glutathione (GSSG) to total glutathione (tGSH) was substantially altered in the selenium deficient Group I as well as in Group II (0.10 mg selenium/kg feed). The activity of glutathione reductase (GR) and glutathione-S-transferase (GST) was not affected by selenium deficiency.     

Tissue-specific accumulation and speciation of selenium in rainbow trout (Oncorhynchus mykiss) exposed to elevated dietary selenomethionine

The toxicity of selenium in fish is influenced by its chemical speciation and the exposure route. In the natural environment, selenium exposure to fish occurs primarily in the form of selenomethionine in diet. Thus, the main objective of this study was to examine the tissue-specific selenium burden and speciation in fish exposed to elevated dietary selenomethionine. Rainbow trout (Oncorhynchus mykiss) were treated with dietary selenomethionine (40 μg g(-1) dry mass) for 2 weeks, and at the end of the exposure different tissue samples were collected to assess the tissue-specific distribution and speciation of selenium. We used synchrotron-based X-ray absorption near edge spectroscopy (XANES) to determine the selenium speciation profile. Selenomethionine, selenocysteine and selenocystine were found to be the predominant form of selenium in all of the tissues; however their relative proportion varied across different tissues. In general, the organs primarily involved in selenium handling in fish (e.g., liver, kidney) accumulated a higher percentage of selenocystine. We also found that dietary selenomethionine exposure resulted into a marked increase in selenium burden of all major tissues in fish including the brain. Collectively, our findings provide new insights into the tissue-specific distribution and speciation of selenium in fish exposed to selenomethionine via diet.     

Effects of long-term selenium yeast supplementation on selenium status studied in the rat

To investigate the selenium status during long-term dietary supply of selenium yeast, 30-day-old male rats were fed for 379 days a methionine-adequate low-selenium diet supplemented with 0.2 mg Se/kg (selenium-adequate diet) or 1.5 mg Se/kg (high-selenium diet) in the form of selenium yeast that contained 60% of the element as l-selenomethionine. Their selenium load was determined at several intervals by neutron activation analysis of the selenium concentrations in the main selenium body pools, skeletal muscle and liver. After 64 days the tissue selenium concentrations plateaued in both groups and then stayed at that level. Compared with the selenium-adequate group, elevated tissue selenium concentrations were found in the high-selenium group, but the increase by a factor of 3.5 in the muscle and by a factor of 2.3 in the liver was smaller than the 7.5-fold increase in the selenium intake. In the selenium-adequate group about 50% of the muscle selenium and 30% of the liver selenium and in the high-selenium group about 85% of the muscle selenium and 70% of the liver selenium were estimated to be present in non-selenoprotein forms. During selenium depletion the liver glutathione peroxidase activity in the high-selenium group remained unaffected for 4 weeks and then decreased more slowly than that in the selenium-adequate group. From these results it can be concluded that selenium incorporated from the selenium yeast diet into non-selenoprotein forms can serve as an endogenous selenium source to maintain selenoprotein levels in periods of insufficient selenium supply.     

Effects of Selenium on Liver and Muscle Contents and Urinary Excretion of Zinc,Copper, Iron and Manganese

Selenium is a main component of glutathione peroxidase (GPX), a key antioxidant enzyme. Other elements, such as zinc, copper, manganese and iron, are also involved in the pathogenesis of oxidative damage as well as in other important metabolic pathways. The effects of selenium supplementation on the metabolism of these elements have yield controversial results .The aim of this study is to analyse the effects of selenium supplementation on liver, muscle and urinary excretion of zinc, copper, iron and manganese in a situation of oxidative stress, such as protein deficiency. The experimental design included four groups of adult male Sprague–Dawley rats, which received the Lieber–DeCarli control diet, an isocaloric 2 % protein-containing diet and another similar two groups to which selenomethionine (6 mg/l liquid diet) was added. After sacrifice (5 weeks later), muscle, liver and serum selenium were determined, as well as muscle, liver and urinary zinc, copper, manganese and iron and liver GPX activity and liver malondialdehyde. Selenium addition led to decreased liver copper, increased muscle copper, increased copper excretion and increased liver iron, whereas zinc and manganese parameters were essentially unaltered. Muscle, liver and serum selenium were all significantly correlated with liver GPX activity.     

Effects of Selenium- and Chromium-Enriched Diets on Growth Performance,Lipid Profile,and Mineral Concentration in Different Tissues of Growing Rabbits

The aim of this study was to investigate the effect of dietary supplementation with different sources of selenium and/or organic chromium on the growth performance, digestibility, lipid profile, and mineral content of hair, liver, and fore and hind limb of growing rabbits. A total of 150 weanling New Zealand White (NZW) male rabbits were randomly allotted to six dietary treatment groups: (1) basal diet (control group), (2) basal diet + 0.6 mg sodium selenite/kg diet, (3) basal diet + 0.6 mg selenium yeast/kg diet, (4) basal diet + 0.3 mg sodium selenite/kg diet + 0.3 mg selenium yeast/kg diet, (5) basal diet + 0.6 mg chromium yeast/kg diet + 0.6 mg selenium yeast/kg diet, (6) basal diet + 0.6 mg chromium yeast/kg diet. Only the combination between inorganic and organic selenium led to significant improvement in body weight, body weight gain, and feed conversion ratio. Carcass traits were not different in all groups. Selenium (Se) and chromium (Cr) were deposited in the tissues of rabbits fed diets supplemented with Se and Cr, respectively. Blood serum in both of selenium- and chromium-supplemented groups showed declined total cholesterol, triglycerides, and low-density lipoprotein (LDL). Group supplemented with organic chromium showed higher high-density lipoprotein (HDL) than the other groups. It could be concluded that using a mixture of inorganic and organic Se has a positive effect on the growth performance of growing rabbits. Both Se and Cr have hypocholesterolemic effect. Both of Se and Cr can be deposited in the meat and other tissues of rabbits and that improves meat quality which positively reflects on human acceptance. The combination between inorganic (0.3 mg sodium selenite/kg diet) and organic selenium (0.6 mg selenium yeast/kg diet) improved growth performance traits of growing rabbits.

     

The effects of selenium on oxidative stress biomarkers in the freshwater characid fish matrinxã, Brycon cephalus (Günther, 1869) exposed to organophosphate insecticide Folisuper 600 BR (methyl parathion)

Methyl parathion (MP), an organophosphate widely applied in agriculture and aquaculture, induces oxidative stress due to free radical generation and changes in the antioxidant defense system. The antioxidant roles of selenium (Se) were evaluated in Brycon cephalus exposed to 2 mg L(-1) of Folisuper 600 BR (MP commercial formulation - MPc, 600 g L(-1)) for 96 h. Catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione S-transferase (GST), reduced glutathione (GSH) and lipid peroxidation (LPO) levels in the gills, white muscle and liver were evaluated in fish fed on diets containing 0 or 1.5 mg Se kg(-1) for 8 weeks. In fish treated with a Se-free diet, the MPc exposure increased SOD and CAT activities in all tissues. However, the GPx activity decreased in white muscle and gills whereas no alterations were observed in the liver. MPc also increased GST activity in all tissues with a concurrent decrease in GSH levels. LPO values increased in white muscle and gills and did not change in liver after MPc exposure. A Se-supplemented diet reversed these findings, preventing increases in LPO levels and concurrent decreases in GPx activity in gills and white muscle. Similarly, GSH levels were maintained in all tissue after MPc exposure. These results suggest that dietary Se supplementation protects cells against MPc-induced oxidative stress.     

Effects of vitamin E and selenium deficiency on the fatty acid composition of rat retinal tissues.

The fatty acid composition of retinal tissues was measured in rats maintained for 26--32 weeks on each of the following diets: a purified basal diet deficient in alpha-tocopherol and selenium, an identical control diet supplemented with alpha-tocopherol and selenium, and a commerical laboratory rat chow. Dietary deficiencies of antioxidant nutrients were found to cause a large decrease in total polyunsaturated fatty acids in the retinal pigment epithelium, a small decrease in the retinal rod outer segments, but no change in the whole retina or liver when compared to tissues from animals fed the vitamin E- and selenium-supplemented control diet. The polyunsaturated fatty acid content which we have observed for the retinal pigment epithelium from rats fed commerical lab chow is similar to that which we observed for bovine retinal pigment epithelium. Our results indicate that changes in fatty acid composition are not generalized to all tissues in severely antioxidant-deficient animals, but that changes do occur in some tissues, such as the retinal pigment epithelium, which appears to be particularly sensitive to in vivo lipid peroxidation.     

Distribution of arsenic in marine animals: relationship to diet

The chemical form of arsenic in the muscle tissues of marine animals in relation to diet has been examined. Inorganic arsenic concentrations in all muscle tissues were found to be low compared to total arsenic concentrations and independent of diet. Arsenic was found to be present in all tissues predominantly as a methanol-water soluble form. The ratio of lipid soluble and unextractable arsenic to total arsenic was higher in plankton feeders than in herbivores and carnivores.     

Characterization and expression of chicken selenoprotein W

As an essential trace element, selenium (Se) deficiency results in White Muscle Disease in livestock and Keshan disease in humans. The main objectives of this study were to clone and characterize the chicken selenoprotein W (SeW) gene and investigate SeW mRNA expression in chicken tissues. The deduced amino acid (AA) sequence of chicken SeW contains 85 AAs with UAG as the stop codon. Like all SeW genes identified in different species, chicken SeW contains one well-conserved selenocysteine (Sec) at the 13th position encoded by the UGA codon. The proposed glutathione (GSH)-binding site at the Cys₃₇ of SeW is not conserved in the chicken, but Cys₉ and Sec₁₃, with possible GSH binding, are conserved in SeWs identified from all species. There are 23–59% and 50–61% homology in cDNA and deduced AA sequences of SeW, respectively, between the chicken and other species. The predicted secondary structure of chicken SeW mRNA indicates that the selenocysteine insertion sequence element is type II with invariant adenosines within the apical bulge. The SeW mRNA expression is high in skeletal muscle followed by brain, but extremely low in other tissues from chickens fed a commercial maize-based diet. The SeW gene is ubiquitously expressed in heart, skeletal muscle, brain, testis, spleen, kidney, lung, liver, stomach and pancreas in chickens fed a commercial diet supplemented with sodium selenite. These results indicate that dietary selenium supplementation regulates SeW gene expression in the chicken and skeletal muscle is the most responsive tissue when dietary Se content is low.     

Effects of vitamin E and selenium deficiency on the fatty acid composition of rat retinal tissues

The fatty acid composition of retinal tissues was measured in rats maintained for 26–32 weeks on each of the following diets: a purified basal diet deficient in α-tocopherol and selenium, an identical control diet supplemented with α-tocopherol and selenium, and a commercial laboratory rat chow. Dietary deficiencies of antioxidant nutrients were found to cause a large decrease in total polyunsaturated fatty acids in the retinal pigment epithelium, a small decrease in the retinal rod outer segments, but no change in the whole retina or liver when compared to tissues from animals fed the vitamin E- and selenium-supplemented control diet. The polyunsaturated fatty acid content which we have observed for the retinal pigment epithelium from rats fed commercial lab chow is similar to that which we observed for bovine retinal pigment epithelium.Our results indicate that changes in fatty acid composition are not generalized to all tissues in severely antioxidant-deficient animals, but that changes do occur in some tissues, such as the retinal pigment epithelium, which appears to be particularly sensitive to in vivo lipid peroxidation.     

High affinity selenium uptake in a keratinocyte model

The distribution of selenium in mammals has been recently shown to be mediated primarily by selenoprotein P. Even in the absence of selenoprotein P, selenium is distributed from the liver into all organs and tissues when supplemented in the diet. The form of selenium that is actively taken up by mammalian cells at trace concentrations has yet to be determined. We used a human keratinocyte model to determine whether reduction of the oxyanion selenite (SeO(3)(2-)) to the more reduced form of selenide (HSe(-)) would affect uptake. Indeed a reduced form of selenium, presumably selenide, was actively transported into keratinocytes and displayed saturation kinetics with an apparent K(m) of 279 nM. ATPase inhibitors blocked the uptake of selenide, as did the competing anions molybdate and chromate, but not sulfate. These results suggest that the small molecule form of selenium that is distributed in tissues is hydrogen selenide, despite its sensitivity to oxygen and reactivity to thiols.     

饲料硒和维生素E对大鼠机体抗氧化能力的影响

 用克山病病区粮配成基础低硒饲料,补充硒和/或维生素E组成四种不同水平的饲料,饲喂雄性断乳大鼠,观察其对机体抗氧化能力的影响。评价指标是用抗坏血酸诱发的红细胞溶血率、被O~-_2(超氧阴离子)氧化的血红蛋白量和组织中的TBA值。动物饲养13周后,自尾静脉取血,测定溶血率和血红蛋白被氧化的百分率,和全血SeGSHPx(含硒谷胱甘肽过氧化物酶)活力。15周后将动物断头杀死,立即取出心脏和肝脏测定SeGSHPx活力和TBA值。结果表明在克山病病区粮的饲料中补充硒或维生素E,或者二者同时补充均明显提高组织中的SeGSHPx活力和降低组织中的TBA值。不论在硒缺乏时或硒充足时,饲料中补充维生素E显著降低抗坏血酸诱发的红细胞溶血率,对O~-_2氧化血红蛋白无保护作用。在维生素E缺乏时,仅补充硒对溶血无作用。不论饲料中维生素E缺乏或者充足,补充硒对O~-_1氧化血红蛋白均有显著保护作用。     

Selenium and Glutathione Peroxidase Levels in Lambs Receiving Feed Supplemented with Sodium Selenite or Selenomethionine

Twenty-one 6 months old female lambs were divided into 7 groups and fed a basal diet containing 0.13 mg Se/kg. The basal diet was further supplemented with 0, 0.1, 0.5 or 1.0 mg Se/kg either as sodium selenite or as selenomethionine, and was fed for 10 weeks. Both feed additives produced an increase in the selenium concentration in the tissues analysed. Significant correlations were found between the concentrations of selenomethionine or sodium selenite added to the feed and the subsequent tissue levels. However, the selenium levels seemed to plateau at approximately 0.5 mg Se/kg of supplemented sodium selenite. The total glutathione peroxidase (GSH-Px) activity of the tissues increased when the selenium supplementation increased from 0 to 0.1 mg/kg for both selenium compounds. With further increase in selenium supplementation the GSH-Px activity in the tissues plateaued except in the blood where the activity continued to rise with increasing selenomethionine supplementation. The selenium dependent GSH-Px activity in the liver rose with increasing selenomethionine supplementation, but approached a plateau when 0.1 mg Se/kg as sodium selenite was added to the feed. The selenium concentration in whole blood responded more rapidly to the selenium supplementation than did GSH-Px activity. The experiment indicates that the optimal selenium concentration in the feed is considerably higher than 0.1 mg Se/kg, and that selenium levels of 1.0 mg/kg in the feed do not result in any risk for the animals or the consumers of the products.     

Glutathione peroxidase activity and selenoprotein W levels in different brain regions of selenium-depleted rats(1)

Previous studies in selenium (Se)-depleted sheep and rats showed that selenoprotein W (SeW) levels decreased in all tissues except brain. To further investigate this depletion in different parts of the brain, second generation Se-depleted rats were used. Dams consumed a Se-deficient basal diet during gestation and lactation, and deficient rats were obtained by continuation on the same diet. Control rats were fed a diet with 0.1-mg Se/kg diet after weaning. Glutathione peroxidase (GPX) activities were measured for comparative purposes to SeW levels. GPX activity in muscle, skin, spleen, and testis increased about 4-fold with Se repletion and reached a plateau after 6 or 10 weeks, but GPX activity decreased to almost one tenth of the original activity with continuous Se depletion. In contrast, GPX activities increased, rather than declined, in various brain regions (cortex, cerebellum, and thalamus) with time of feeding the deficient diet. An experiment with first generation rats, however, indicated that GPX activity was significantly lower in these three brain regions from rats fed the deficient diet as compared to rats fed the supplemented diet. SeW levels in skin, spleen, muscle, and testis were undetectable in weanling rats, but became detectable after 6 weeks of Se repletion. In contrast, the expression of SeW in cortex, cerebellum, and thalamus was not significantly affected by Se depletion, but increased SeW levels occurred only in thalamus with Se supplementation. The results with GPX using first and second generation rats suggest that there are "mobile" and "immobile" GPX fractions in the brain.     

Selenium Concentrations in Tissues and Eggs of Growing and Laying Chickens Fed Sodium Selenite at Different Levels

Growing and laying chickens were fed graded levels of selenium in the form of sodium selenite. One day old Norwegian bred broiler chickens and 20 weeks old Norwegian bred White Leghorn chickens were divided into 5 groups each and fed a basal diet supplemented with 0, 0.1, 1.0, 3.0 or 6.0 μg Se/g for 6 and 31 weeks, respectively. At the end of the experiments significantly higher concentrations of selenium were found in the groups fed 1.0, 3.0 and 6.0 μg Se/g diet compared to the control group. Correspondingly higher concentrations of selenium were found in egg samples. The increase in egg yolk selenium was much higher than in egg white. Significant correlations were found between the amounts of selenium added to the ration and the selenium concentrations in liver, kidney, breast muscle, egg white, yolk and homogenized egg. There were no differences in body weight gain and egg production between the groups. A possible positive contribution to animal and human health of selenium supplementation of animals’ diet above the required level is discussed.     

Dietary Selenium Influences Calcium Release and Activation of MLCK in Uterine Smooth Muscle of Rats

We sought to elucidate the effects of different concentrations of dietary selenium on calcium ion release, MLCK levels, and muscle contraction in the uterine smooth muscle of rats. The selenium (Se) content of blood and of uterine smooth muscle tissues was detected by fluorescence spectrophotometry. Ca²⁺ content was measured by atomic absorption spectroscopy. Calmodulin (CaM) and MLCK RNA and protein levels were analyzed by quantitative real-time polymerase chain reaction and Western blot, respectively. Dietary Se intake increased the Se levels in the blood and in uterine smooth muscle tissues and increased the Ca²⁺ concentration in uterine smooth muscle tissues. The addition of Se also promoted CaM expression and enhanced MLCK activation in uterine smooth muscle tissues. In conclusion, Ca²⁺, CaM, and MLCK were regulated by Se in uterine smooth muscle; Se plays a major role in regulating smooth muscle contraction in the uterus.