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PubMed2003

Vitamin E and selenium supplementation to alleviate cold-stress-associated deterioration in egg quality and egg yolk mineral concentrations of Japanese quails.

The effects of vitamin E (dl-alpha-tocopheryl acetate) and selenium (Se; Na2-SeO3) on egg production, egg quality, and mineral content of egg yolk in Japanese quails reared under a low ambient temperature (6 degrees C) were evaluated. Birds (n=300; 7 wk old) were randomly assigned to 12 treatment groups, 25 birds per group. The birds in a 3 x 2 factorial design received either three levels of vitamin E (125, 250, and 500 mg/kg diet) or two levels of selenium (0.1 or 0.2 mg/kg diet). After 2 wk on feed, six groups of the birds were maintained at 18 degrees C (thermoneutral temperature [TN]), and the other half were acclimated over 3 d to a decreased environmental temperature of 6 degrees C (cold stress [CS]). The performance, egg quality, and mineral content of egg yolk were not influenced by supplemental vitamin E and selenium in quails not exposed to cold stress (p > or = 0.09). Two hundred fifty and 500 mg vitamin E/kg diet compared with 125 mg/kg diet and higher dietary selenium inclusions (0.2 vs 0.1 mg/kg) resulted in a better body weight, egg production, and feed efficiency (p = 0.01) in quails reared under CS. Similarly, egg weight, egg specific gravity, eggshell thickness, and Haugh unit were positively influenced with vitamin E (p = 0.01) and selenium (p < or = 0.05) supplementation. Egg yolk concentrations of Zn, Fe, and Mn were higher with higher dietary vitamin E (p = 0.01) and selenium (p = 0.05). There was no interaction detected for parameters measured in the present study (p > or = 0.3). The results of the present study showed that a combination of 250 or 500 mg vitamin E and 0.2 mg selenium per kilogram of diet provides the greatest effects on performance and egg quality of Japanese quails reared under cold stress and suggest that such a supplementation can be considered as a protective management practice in Japanese quail diets to reduce the detrimental effects of cold stress.

Animals↗
PubMed2003

Selective induction of liver parenchymal cell heme oxygenase-1 in selenium-deficient rats.

Liver heme oxygenase (HO) activity is higher in selenium-deficient rats than in control animals under basal conditions and is further increased in them, but not in controls, by phenobarbital treatment. In the present study we characterized liver HO induction by selenium deficiency using molecular methods. Severe selenium deficiency in rats caused a doubling of liver HO activity without affecting spleen, kidney, brain, or testis HO activities. HO-1 protein and mRNA were increased to accompany the increased HO activity, but HO-2 protein and mRNA were not increased. Fractionation of the liver into hepatocyte and Kupffer cell/endothelial cell fractions revealed that the increased HO activity resides in the hepatocyte fraction. Immunohistochemical localization of HO-1 protein confirms the induction of HO-1 taking place solely in hepatocytes and throughout the liver lobule. Phenobarbital treatment sharply increased HO-1 mRNA and protein expression in selenium-deficient liver and HO activity in hepatocytes, but had no effect in control liver or in the Kupffer cell/endothelial cell fraction of selenium-deficient liver. Electrophoretic mobility shift assays showed increased AP-1 binding activity, suggesting an involvement of this redox-sensitive transcription factor in the induction by phenobarbital of HO-1 in selenium deficiency. We speculate that selenium deficiency affects hepatic antioxidant selenoproteins, resulting in an up-regulation of HO-1.

Animals↗
PubMed2003

Association of selenium with thyroid volume and echostructure in 35- to 60-year-old French adults.

OBJECTIVE: To investigate the relationship between selenium status, thyroid Volume and gland echostructure. DESIGN: Cross-sectional. METHODS: In 792 men (45-60 Years) and 1108 women (35-60 Years) from the SU.VI.MAX study, thyroid Volume and gland echostructure were determined ultrasonographically. At baseline, thyrotropin, free thyroxine, selenium, zinc, alpha-tocopherol, beta-carotene, retinol, urinary iodine and thiocyanate concentrations were measured. Alcohol consumption, smoking, and menopausal status were assessed by a questionnaire. A stepwise linear and a logistic regression model were used, adjusting for antioxidant vitamins, trace elements status and age. RESULTS: In women, there was an inverse association between selenium status and thyroid Volume (P=0.003). A protective effect of selenium against goiter (odds ratio (OR)=0.07, 95% confidence interval (CI)=0.008-0.6) and thyroid tIssue damage (OR=0.2, 95% CI=0.06-0.7) was observed. There was no evidence of an association between menopausal status and other antioxidant elements, thyroid Volume or thyroid hypoechogenicity. Smoking, but not alcohol consumption, was associated with an increased risk of thyroid enlargement in women (OR=3.94, 95% CI=1.64-9.48). No association between thyroid Volume, thyroid structure or selenium was found in men. CONCLUSION: Our findings suggest that selenium may protect against goiter. Selenium was related to thyroid echostructure, suggesting it may also protect against autoimmune thyroid disease.

Adult↗
PubMed2004

Selenium toxicity in breeding ring-necked pheasants (Phasianus colchicus).

A flock of breeding ring-necked pheasants received feed with a high selenium content. Within 4 days of eating the toxic feed, the rate of egg production began to decrease, and bird aggression increased. Approximately 12% of the hens died within a week. Necropsy of the hens revealed colorless fluid around the heart and a friable, but otherwise normal, liver. The rapid onset of the problem and signs noted at necropsy suggested toxicosis. Based on analysis, the feed contained 9.3 ppm of selenium. Selenium toxicity was consistent with the histologic diagnosis of degenerative cardiomyopathy, vacuolar degeneration of hepatocytes, and centrilobular hepatic necrosis. After 8 days, the toxic feed was removed and replaced with fresh feed. Egg production, which had dropped to 50%, returned to normal within 10 days of feed replacement. Hatchability of eggs laid from days 8 to 14 after delivery of the toxic feed was 35%. Approximately 10% of the chicks that hatched had deformed beaks and abnormal eyes. Many of the chicks that died in the shell had deformities, bringing the total to more than 50% of all embryos that developed. The selenium content of eggs that had no embryonic development was 2.05 ppm. Hatchability of eggs laid from days 21 to 28 after the toxic feed was delivered was almost 80%, which was slightly lower than normal. The selenium content of these eggs was 0.30 ppm. These results show the rapid onset and correction of selenium toxicity and suggest that specific embryologic defects are diagnostic for selenium toxicity.

Animal Feed↗
PubMed1997

Selenium and iodine deficiencies: effects on brain and brown adipose tissue selenoenzyme activity and expression.

Adequate dietary iodine supplies and thyroid hormones are needed for the development of the central nervous system (CNS) and brown adipose tissue (BAT) function. Decreases in plasma thyroxine (T4) concentrations may increase the requirement for the selenoenzymes types I and II iodothyronine deiodinase (ID-I and ID-II) in the brain and ID-II in BAT to protect against any fall in intracellular 3,3',5 tri-iodothyronine (T3) concentrations in these organs. We have therefore investigated selenoenzyme activity and expression and some developmental markers in brain and BAT of second generation selenium- and iodine-deficient rats. Despite substantial alterations in plasma thyroid hormone concentrations and thyroidal and hepatic selenoprotein expression in selenium and iodine deficiencies, ID-I, cytosolic glutathione peroxidase (cGSHPx) and phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activities and expression remained relatively constant in most brain regions studied. Additionally, brain and pituitary ID-II activities were increased in iodine deficiency regardless of selenium status. This can help maintain tissue T3 concentrations in hypothyroidism. Consistent with this, no significant effects of iodine or selenium deficiency on the development of the brain were observed, as assessed by the activities of marker enzymes. In contrast, BAT from selenium- and iodine deficient rats had impaired thyroid hormone metabolism and less uncoupling protein than in tissue from selenium- and iodine-supplemented animals. Thus, the effects of selenium and iodine deficiency on the brain are limited due to the activation of the compensatory mechanisms but these mechanisms are less effective in BAT.

Adipose Tissue, Brown↗
PubMed2001

Selenium status in an iodine deficient population of the West Ivory Coast.

Selenium is an essential trace element which is part of the active site of seleno-dependent glutathione peroxidase and type 1 deiodinase. Therefore, it plays a key role in thyroid hormone metabolism. The present work was undertaken in order to evaluate selenium status in two Ivory Coast populations: the first with high (Glanlé) and the second with low (Abidjan) prevalence of iodine deficiency. Selenium, glutathione peroxidase, glutathione reductase, glutathione and diglutathione were determined in blood and/or urine. In plasma and erythrocytes, selenium and glutathione peroxidase were dramatically low in Glanlé. Compared to Abidjan, selenium, glutathione peroxidase, vitamin E and riboflavin status were decreased whereas diglutathione was increased in Glanlé. The results clearly demonstrate a selenium deficiency and suggest an oxidant stress in Glanlé. Causes and consequences of this selenium deficiency and oxidant stress remain to be determined.

Anthropology, Cultural↗
PubMed1985

Effects of selenium and vitamin E on incidence of retained placenta.

In a series of experiments over 3 yr, relatively low doses of selenium and vitamin E were injected intramuscularly 3 wk prepartum to pregnant Israeli-Holstein dairy cows in a high-producing herd (9000 kg milk/yr) with a history of retained placenta in 17% of the primiparous and 28% of the multiparous animals, as recorded for the 12 mo preceding the study. Selenium ranged from .035 to .109 ppm in the prepartum diet and from .160 to .200 ppm in the postpartum diet. Doses of selenium ranging from 2.3 to 23.0 mg reduced the incidence of retained placenta in 186 primiparous and in 428 multiparous to 7 and 15%, which was half of that of controls. Low doses of selenium (2.3 to 4.6 mg) tended to be more effective than higher ones. Selenium alone was at least as effective as a combination of selenium and vitamin E. Dosage, timing, mechanism, and interactions of selenium with other factors in reducing the incidence of retained placenta need clarification.

Animals↗
PubMed1976

Studies on the enteric absorption of selenium in the chick using localized coccidial infections.

Studies were conducted to determine the primary loci of gastrointestinal absorption of inorganic selenium in the chick using radiotracer techniques and Eimeria sp. infections of known site specificity for the gastrointestinal tract. Results showed that coccidial infections in the anterior regions of the small intestine reduced selenium absorption and potentiated selenium deficiency among chicks fed critical levels of the mineral. Absorption experiments showed that selenium absorption was greatest in the duodenum and anterior ileum, although selenium was bound at least transiently to tissues in the gizzard and crop. It is concluded from these experiments that dietary inorganic selenium is absorbed primarily in the duodenum and anterior ileum. Factors such as enteric disease which disrupt the integrity of the anterior intestinal mucosa can, therefore, reduce the absorption of selenium and other nutrients absorbed in that region, resulting in a potentiation of nutritional deficiencies.

Animals↗
PubMed1979

Reduction of hepatic lipid deposition in laying hens by dietary selenium-yeast interaction.

Experiments were conducted to study the effect of chromiun and selenium on liver lipid deposition and incidence of liver hemorrhage in caged layers. Commercial strains of layers were fed ad libitum equicaloric and isonitrogenous diets. Corn-torula dried yeast diets containing added selenium (.1 microgram/g) with or without supplementary chromium (10 microgram/g) significantly reduced total liver lipid and liver hemorrhage. The effects of protein source (soybean meal vs. yeast) and selenium were separated in a factorial experiment which showed that the hepatic lipid response to selenium results from an interaction of selenium with an unidentified factor in torula yeast. The addition of selenium to diets with each protein source significantly elevated glutathione peroxidase (GSHPx) activity. Inclusion of 5% brewers yeast in the corn-soy diet or vitamin E (50 IU/kg) to the corn-torula dried yeast reduced liver lipid similar to that seen in birds fed the torula-yeast diet containing .1 microgram Se/g. Comparison of oral glucose tolerance of birds fed corn-soy and corn-soy brewers yeast diets showed no significant difference. None of the dietary treatments significantly altered body weight, egg production, egg weight, or feed consumption. The results indicate that the metabolic role of selenium in relation to its role in hepatic lipid metabolism is mediated through an interaction with a dietary factor(s) present in yeast.

Animal Feed↗
PubMed1980

[Neutron activation analysis of selenium using a coincidence counting method (author's transl)].

Neutron activation analysis of selenium using 75Se has been investigated by means of a coincidence counting of gamma-rays in the cascade decay series by a NaI(TI) detector and a Ge(Li) detector. Using this method, the background around the photopeak of 75Se-265 keV could be reduced to one twentieth, and thus the detection limit of selenium could be improved four times higher than the usual method. For examining the accuracy of this measuring method, selenium contained in Bovine Liver (NBS) was determined and the content of selenium was found to be 1.02 micrograms/g (the certified value is 1.1 +/- 0.01 micrograms/g). Selenium content in Orchard Leaves (NBS) was determined to be 0.081 +/- 0.006 micrograms/g (the certified value is 0.08 +/- 0.01 micrograms/g), though its non-destructive determination was difficult because of its very low content. The results obtained here indicate that the accuracy, the precision and the reproducibility for selenium determination are thought to be adequate. As an example of a sample containing many interference nuclides, selenium in a soot was determined on the basis of these results.

Activation Analysis↗
PubMed1998

[Protective effect of selenium on human erythrocyte rheology].

OBJECTIVE: To assess the protective effect of selenium on RBC rheology during myocardial ischemia/reperfusion period in patients with VSD or ASD who underwent cardiopulmonary bypass. METHODS: The blood samples were taken from the coronary sinus, and ascorbyl free radical (A.), peroxidants (MDA), antiperoxidative activities (plasma SOD, erythrocyte GSH-Px), the membrane shear elastic module of RBC (mu), molecular rotational correlation times of lipids and proteins of RBC membrane (tau l, tau p) were measured and compared between control and selenium groups. RESULTS: After myocardial reperfusion only for one minute, in both groups A. was significantly increased (The increased percentage in the control group +68%, in the selenium group +66%), but the selenium group had lower MDA and GSH-Px activity. On contrary to the control group with high A. level, A. of the selenium group was dropped about half since reperfusion for 5 minutes and recovered to the pre-ischemia level. After myocardial reperfusion, the control group had specific changes in membrane mu values as well as evidently prologed tau l and tau p. Simultaneously, except tau p at 5 minutes of reperfusion was obviously prolonged, no changes in the membrane mu and tau l were observed in the selenium group during the cardiac ischemia/reperfusion periol. CONCLUSION: Selenium can at least partly protect RBC rheology from free radical damage during the myocardial ischemia/reperfusion period.

Adolescent↗
PubMedDate not supplied

[Selenium and its role in nutrition].

The review presents data available in the literature on the spread of selenium deficiency. Epidemiological surveys show that there is a potential risk for selenium deficiency in pregnant females and in 7-10-year-old children. The negative impact of radiation on serum selenium levels was evidenced by a survey of Chernobyl Atomic Power Station workers. Higher selenium levels in the hairs of the pubis, beard, celiac plexus, and axillary spaces than those in the hair of the head (by 1.41, 1.34, 1.36, and 1.14 times, respectively) confirm that there is a relationship between selenium and sexual hormones in the body. Dietary fiber concentrates that are derived from plant materials and contain a complex of structural carbohydrates and lignin may be used in combination with selenium compounds in human diets to prevent selenium deficiency.

Adult↗
PubMed2000

Selenium effects on prostate cell growth.

Epidemiological and clinical data suggest that selenium may prevent prostate cancer, but the biological effects of selenium on normal or malignant prostate cells are not well known. We evaluated the effects of sodium selenite (Na2SeO3) or l-selenomethionine (SeMet) on monolayer and anchorage-independent growth in a series of normal primary prostate cultures (epithelial, stromal, and smooth muscle) and prostate cancer cell lines (LNCaP, PC-3, and DU145). We observed differential, dose-dependent growth inhibition and apoptosis within prostate cancer cells (compared with normal prostate cells) treated with 1-500 microM of Na2SeO3 or SeMet. Na2SeO3 more potently inhibited growth at any given concentration. The androgen-responsive LNCaP cells were the most sensitive to selenium growth suppression (IC50s at 72 h for Na2SeO3 and SeMet were 0.2 and 1.0 microM, respectively). Growth of the primary prostate cells virtually was not suppressed (IC50s at 72 h for Na2SeO3 and SeMet were 22-38 and >500 microM, respectively). We also observed that DNA condensation and DNA fragmentation (terminal deoxynucleotidyltransferase dUTP nick end labeling/fluorescence-activated cell sorting) were elevated in selenium-treated cells and that activated caspase-3 colocalized with terminal deoxynucleotidyltransferase dUTP nick end labeling-stained cells by immunofluorescence. Higher basal poly(ADP-ribose) polymerase (PARP) expression levels and PARP cleavage (a substrate for caspase-3) were observed during apoptosis in tumor cells, compared with normal cells. Selective tumor cell death was associated with an increase in sub-G0-G1 cells after propidium iodide staining and fluorescence-activated cell sorting analysis. SeMet caused an increase in arrest in the G2-M phase of the cell cycle selectively in cancer cells. Inhibition of cancer cell growth by SeMet was associated with phosphorylation of P-Tyr15-p34/cdc2, which caused growth arrest in the G2-M phase. Anchorage-independent growth of prostate cancer cells in soft agar was sensitive to selenium. Our results suggest that Na2SeO3 is the more potent inducer of apoptosis in normal and cancer prostate cells. Our SeMet results involving PARP and G2-M cell-cycle arrest (cited above) indicate that SeMet selectively induces apoptosis in cancer but not primary cells of the human prostate. Our overall findings are relevant to the molecular mechanisms of selenium actions on prostate carcinogenesis and help demonstrate the selective, dose-dependent effects of selenium (especially SeMet) on prostate cancer cell death and growth inhibition.

Apoptosis↗
PubMed1979

[Serum selenium levels in sheep from birth to 90 days of age].

The results of the study of the dynamics of selenium in the blood serum were compared in 31 piglets from birth to the age of 90 days. The analyzed selenium values in the blood serum immediately after birth (0.14--0.20 ppm) provide evidence of the intra-uterine placental passage of selenium. In the period of colostral and milk nutrition, the serum concentrations of selenium showed a statistically insignificant variation, followed by an abrupt drop of the level of the microelement in the weaning period (60th day). The individual values in this period ranged from 0.08 to 0.12 ppm. Towards the end of the study, the level of selenium in the blood serum of the piglets returned to its initial value; this indicates that although the critical period connected with weaning has a transient nature, it should be averted for preventing the occurrence of a selenium-deficit disease; this can be done by adding a supplement of 0.2% solution of sodium selenate or a combined preparation of selenium and vitamin E-Selevit.

Age Factors↗
PubMed1975

Selenium-vitamin E deficiency in swine fed peas (Pisum sativum).

An experiment was conducted to study the effects of feeding a 96.8% cull pea basal ration, low in selenium (0.061 ppm) and vitamin E (7.0 IU alpha-tocopherol/kg of ration), to growing pigs with and without supplementation of selenium, vitamin E, or both. The basal ration was high in crude protein (25.2%) and contained no supplemented fat. Nine of 10 pigs fed the unsupplemented basal ration had lesions attributed to selenium-vitamin E deficiency, and 8 of these pigs died during the 160-day experiment. The deficiency was usually characterized by sudden death (with no prior signs of illness), massive hepatic necrosis, hemoglobinuric and to a lesser extent cholemic nephrosis, degenerative myopathy of cardiac and skeletal muscles, edema, icterus, and acute terminal congestion and hemorrhage. Clinical signs, deaths, or lesions attributed to selenium-vitamin E deficiency were not observed in any of the pigs fed the basal ration supplemented with as little as 0.01 ppm selenium as sodium selenite or 100 ppm alpha-tocopherol. Pigs fed the unsupplemented basal ration gained more slowly (P less than 0.01) and less efficiently and had higher serum glutamic oxalacetic transaminase (SGOT) levels (P less than 0.01) than pigs fed the basal ration supplemented with selenium, vitamin E, or both. There was no difference (P greater than 0.05) in albumin-to-globulin (A/G) ratios among dietary treatment groups. Using the criteria of this study, the minimum selenium requirement of growing pigs fed a low tocopherol cull pea diet was determined to be between 0.06 and 0.07 ppm.

Anemia↗
PubMed2000

[Levels of selenium and glutathione peroxidase in dialyzed patients].

The authors examined in 37 patients dialyzed in a dialysis centre in Brno-Bohunice, a region with selenium deficiency in the population the serum selenium and glutathione peroxidase level before and after 4-hour standard haemodialysis across a polysulphone membrane. In 78% patients selenium deficiency was found. The mean value in the whole group was 33.4 micrograms Se/l. The reference range for the Brno population is 41.3-80.7 micrograms/l. After dialysis a rise of the serum selenium level by 15.4 micrograms/l occurred due to haemoconcentration during ultrafiltration and also due to redistribution of fluids and selenium during dialysis. In anuric patients selenium does not cumulate in serum, although it is excreted in healthy subjects mainly in the urine. Due to the closer bond with selenoproteins it is not significantly separated by dialysis. Glutathione peroxidase assessed in whole blood was in 76% patients before dialysis within the reference range and did not change significantly as a result of dialysis. Selenium deficiency participates significantly in the inadequate activity of antioxidant systems in the organism and in dialyzed patients it potentiates the development of chronic complications.

Female↗
PubMed2001

Serum matrix-degrading enzymes in rats intoxicated with selenium.

The effect of poisoning doses of selenium on serum matrix-degrading enzymes activity was investigated in rats intoxicated with selenium. Fifteen animals were receiving orally sodium selenite in a daily dose of 300 microg/kg body weight. Intoxication with selenium was carried out for 10 weeks. The present study revealed significant increase in activities of enzymes involved in the connective tissue matrix metabolism i.e. beta-glucuronidase, N-acetyl-beta-glucosaminidase, elastase and collagen peptidase. There was no change in the cathepsin activity. The relative enzyme activities calculated over protein level resulted in higher values than those found in direct measurements. Serum enzyme activity was increased most for elastase (about 31%) and N-acetyl-beta-glucosaminidase (about 33%) based on activity per gram of protein. The current data indicate that lysosomes are target organelles for selenium toxicity. Generalized increase in lysosomal enzymes activity contributes to the altered metabolism of the connective tissue in selenium-intoxicated animals. The mechanisms that lead to the increase of lysosomal enzymes activity in rats receiving poisoning doses of selenium could be related to biochemical disturbances caused by selenium toxicity.

Animals↗
PubMed2001

Predictors of serum selenium in cigarette smokers and the lack of association with lung and prostate cancer risk.

Epidemiological studies have suggested that low levels of selenium are associated with a higher incidence of both lung and prostate cancer. We analyzed the selenium serum concentration in 356 Carotene and Retinol Efficacy Trial (CARET) participants who later developed lung cancer and 356 matched controls and in 235 prostate cancer cases and 456 matched controls. Serum samples were obtained a mean of 4.7 years before diagnosis for both tumor types. Controls were matched to cases by year of randomization, age, smoking status, treatment arm, exposure population (asbestos workers or cigarette smokers), and year of blood draw. In the control population (n = 820), significant predictors of low serum selenium concentration were current smoking status and East Coast locations of the study center. Overall, there was no significant difference in mean serum selenium in lung cancer cases versus controls (11.91 microg/dl versus 11.77 microg/dl) or prostate cancer cases versus controls (11.48 microg/dl versus 11.43 microg/dl). No statistically significant trend in odds ratio was seen across quartiles of serum selenium for lung cancer (P = 0.49) or prostate cancer (P = 0.69). In a subpopulation of 174 prostate cancer patients who had clinical and pathological staging material reviewed, there was no association between serum selenium and Gleason score or clinical or pathological stage. In the CARET population of current and former smokers consuming an ad libitum diet, the serum concentration of selenium was not a risk factor for either lung cancer or prostate cancer.

Age Distribution↗