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PubMedDate not supplied

Cytometric and electron microscopic studies of the direct interaction of divalent nickel with intact and chemically modified HuT-78 lymphoblasts.

Cytometric and ultrastructural studies on 24 hr cultures of intact, 1.0 mM H5IO6, and 0.1 mM SeO2-oxidized HuT-78 lymphoblasts were performed after their direct, 30 min interaction with 1.0 mM NiCl2. Except for moderately depressed cell viability, divalent nickel did not alter the progression of intact and oxidized target cells through the phases of the cell cycle. Although the plasma membrane remained structurally intact, marked distortion of mitochondria structure and increased osmiophilia were an invariable attribute of all nickel-pulsed cells. Moreover, numerous electron-opaque, intracellular depositions were detected in SeO2-oxidized, nickel-pulsed cells. It is concluded that the initial state of plasma membrane, and the interaction of nickel with other trace elements, have jointly determined the response of HuT-78 cells to brief and direct, divalent nickel pulses.

Cell Cycle↗
PubMed1983

Altered oxidative metabolism in selenium-deficient rat granulocytes.

Rats fed a selenium-deficient diet for 12 to 15 wk became selenium-depleted, measured by the selenium content of liver and granulocytes. The activity of granulocyte glutathione peroxidase, a selenoenzyme, in deficient rats was 11% of the activity in replete rat granulocytes. When stimulated with an H2O2 generating system, the HMPS activity of the deficient granulocytes was 50% of replete; however, when stimulated with methylene blue, the HMPS activity in deficient and replete granulocytes was the same. When granulocytes were incubated with PMA or OPZ, deficient granulocytes initially had the same O-2-generating activity as replete granulocytes; however, with increasing duration of stimulation, granulocytes from deficient rats generated less O-2 than replete rats. After 20 min in an H2O2-generating system, deficient granulocytes stimulated with PMA or OPZ generated less O-2 than replete granulocytes. These results indicate that deficient granulocytes did not metabolize H2O2 as well as replete granulocytes and that H2O2 caused damage to the O2-generating system. Measurement of O-2 generation in membrane-enriched particles showed the above effects were due to inactivation of the NADPH-dependent O2-generating system. Deficient granulocytes stimulated with OPZ for 20 min had 70% less membrane O-2-generating activity than controls. In addition, when membrane-enriched particles were made from cells that had been stressed with an H2O2-generating system, NADPH-dependent O-2-generating activity in deficient granulocytes was 50% of replete. In selenium-deficient granulocytes with low GSH-Px activity, prolonged incubation with stimulants and prior incubations with an H2O2-generating system caused loss of activity of the membrane-bound, NADPH-dependent, O-2-generating system.

Animals↗
PubMed2003

Selenium supplementation to prevent short-term morbidity in preterm neonates.

BACKGROUND: Selenium is an essential trace element and component of a number of selenoproteins including glutathione peroxidase, which has a role in protecting against oxidative damage. Selenium is also known to play a role in immunocompetence. Blood selenium concentrations in newborns are lower than those of their mothers and lower still in preterm infants. In experimental animals low selenium concentrations appear to increase susceptibility to oxidative lung disease. In very preterm infants low selenium concentrations have been associated with an increased risk of chronic neonatal lung disease and retinopathy of prematurity. OBJECTIVES: To assess the benefits and harms of selenium supplementation in preterm or very low birthweight infants. SEARCH STRATEGY: Searches were made of the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 2, 2003), MEDLINE (1966-May 2003), and Embase (1980-May 2003). The reference lists of recent trials were also searched and abstracts from the Society for Pediatric Research from 1990 were hand-searched. SELECTION CRITERIA: Randomised controlled trials which compared selenium supplementation either parenterally or enterally with placebo or nothing from soon after birth in preterm or very low birthweight infants and which reported clinical outcomes were considered for the review. DATA COLLECTION AND ANALYSIS: Data on selenium supplementation dose, formulation and route of administration; mortality, oxygen requirement at 28 days and 36 weeks post-menstrual age, retinopathy of prematurity, and one or more episodes of sepsis; blood selenium and glutathione peroxidase concentrations at or close to 28 days, were excerpted by both reviewers independently. Data analysis was conducted according to the standards of the Cochrane Neonatal Review Group. MAIN RESULTS: Three eligible trials were identified. Two trials, including one trial with a much larger sample size than the others combined, were from geographical areas with low population selenium concentrations. Meta-analysis of the pooled data showed a significant reduction in the proportion of infants having one or more episodes of sepsis associated with selenium supplementation [summary RR 0.73 (0.57, 0.93); RD -0.10 (-0.17, -0.02); NNT 10 (5.9, 50)]. Supplementation with selenium was not associated with improved survival, a reduction in neonatal chronic lung disease or retinopathy of prematurity. REVIEWER'S CONCLUSIONS: Supplementing very preterm infants with selenium is associated with benefit in terms of a reduction in one or more episodes of sepsis. Supplementation was not associated with improved survival, a reduction in neonatal chronic lung disease or retinopathy of prematurity. Supplemental doses of selenium for infants on parenteral nutrition higher than those currently recommended may be beneficial. The data are dominated by one large trial from a country with low selenium concentrations and may not be readily translated to other populations.

Chronic Disease↗
PubMed1991

[The effect of the selenium status of goats on the resistance of erythrocytes to oxidative damage].

The effect of selenium status on the development of Heinz body anaemia was studied in 16 three months old Saanen goats which received a diet with a low selenium content. The control group (Se-, n = 8) received no supplementary selenium while the treated group (Se+, n = 8) received selenium by injection. Erythrocyte glutathione peroxidase concentration was significantly higher in the Se+ group than in the control group (105 vs 36 U/g Hgb). The animals were drenched once per day with 30 mg of dimethyl disulphide (DMDS) per kg of body weight for 14 days and with 50 mg per kg during the following 11 days. Erythrocytes with Heinz bodies appeared within one week after increasing the DMDS dose to 50 mg/kg/day and reached a peak one week later (30% and 37% of erythrocytes with Heinz bodies in group Se+ and Se- respectively). Within the next three weeks haemoglobin levels dropped from 135 g/l to 123 g/l and 114 g/l in the Se+ and the Se- group respectively. Differences between the two groups were statistically significant for the percentage of erythrocytes with Heinz bodies and for haemoglobin values (p less than 0.05). The data support the hypothesis that selenium status influences the resistance of ruminants to brassica-induced Heinz body anaemia.

Anemia↗
PubMed1994

Dietary vitamin E and selenium effects on resistance to oxidative stress in rat liver mitochondria.

Mitochondria-rich fractions isolated from livers of rats fed diets differing in their vitamin E (E) and/or selenium (Se) contents were subjected to NADPH/ADP/Fe(3+)- dependent assays of lipid peroxidation. Addition of GSH resulted in an inhibition, or lag period, of lipid peroxidation in mitochondria from rats supplemented with E. This effect was independent of the Se status of the rats. Addition of GSH + GSSG did not potentiate the lag period over that observed with GSH alone. Significant changes in mitochondrial alpha-TH during lipid peroxidation, either in the presence or absence of GSH, were not observed. Total protein thiol (PrSH) content of native mitochondria was lower in rats fed a diet deficient in both E and Se, compared to the other dietary groups. Addition of GSH or GSH + GSSG maintained mitochondrial PrSH at higher levels during lipid peroxidation than in control assays without added GSH/GSSG. Addition of GSSG alone decreased PrSH in mitochondria prepared from all rats regardless of their E or Se status. Reduced ubiquinone-9 (U-9) and the % of total U-9 and U-10 in the reduced form were significantly decreased in liver tissue from rats fed the diet deficient in both E and Se.

Animals↗
PubMed1983

The effect of selenium-deficiency on rat fat-cell glucose oxidation.

When rats are fed a selenium-deficient diet, the glutathione peroxidase activity of epididymal fat-cells decreases to 5-9% of that of control rats fed the same diet supplemented with 0.5 p.p.m. of selenium as sodium selenite. [1-14C]Glucose oxidation in fat-cells from rats fed a selenium-deficient diet is unresponsive to the action of t-butyl hydroperoxide, which stimulates 14CO2 formation from [1-14C]glucose 4-fold in control rats. Insulin enhances [1-14C]glucose oxidation and incorporation into lipids in fat-cells from both groups of rats; however, the response elicited is reduced in fat-cells prepared from selenium-deficient animals. The 'C-1/C-6 ratio' (ratio of glucose C-1 to glucose C-6 oxidized) is enhanced by insulin to a similar degree in fat-cells from both groups of animals. The stimulatory action of Zn2+ and dithiothreitol on [1-14C]glucose oxidation observed in fat-cells from selenium-supplemented rats is greatly reduced in fat-cells from selenium-deficient rats. [1-14C]Glucose oxidation in fat-cells from both groups of animals is highly sensitive to the stimulatory action of adenosine. It is concluded that the enhanced formation and glutathione-linked destruction of H2O2 plays, at the most, only a minor role in the stimulation of the flux of glucose through the pentose phosphate pathway elicited by insulin, although elimination of glutathione peroxidase activity may influence the action of insulin on glucose oxidation. Production and subsequent destruction of H2O2 may play an important role in the stimulatory action of Zn2+ and dithiothreitol on fat-cell [1-14C]glucose oxidation.

Adipose Tissue↗
PubMed2003

A simple synthesis of 7,4'-dihydroxy-6-methoxyisoflavone, glycitein, the third soybean isoflavone.

4-Methoxyresorcinol (3) was synthesized as the precursor for glycitein (6) synthesis by the oxidation of 3-hydroxy-4-methoxybenzaldehyde (1) to the aryl formate with H2O2 and a catalytic amount of SeO2. Glycitein (6) was synthesized by cyclization of 2,4,4'-trihydroxy-5-methoxydeoxybenzoin (5) with N,N-dimethylformamide, boron trifluoride diethyl ether, and methanesulfonyl chloride in a microwave oven.

Catalysis↗
PubMedDate not supplied

[The effect of selenium on free-radical oxidation processes in the bone regenerate after a fracture].

The paper presents the results of examining the central part of the rat mandible for a month after its fracture. The rate of free radical oxidation was estimated by the levels of diene conjugates (DC), malonic dialdehyde (MDA) and by the activity of selenium-containing glutathione peroxidase (GPO). The findings suggest that there are profound injury-induced changes in free radical oxidation and antioxidative defense. The levels of DC and MDA showed the maximum upward change as a double-peaked curve and longer restoration to the level seen in control animals. These rats had the minimum enhanced GPO activity. In the animals receiving intragastric selenium methionine or selenium electrophoresis applied to the site of mandible fracture, alterations in DC and MDA were less pronounced and GPO showed a higher activity.

Animals↗
PubMed2006

Effect of physical restraint on oxidative stress in mice fed a selenium and vitamin E deficient diet.

Physical restraint has been associated with increased oxidative damage to lipid, protein, and DNA. The purpose of this experiment was to determine whether physical restraint would further exacerbate oxidative stress in mice fed a selenium (Se) and vitamin E (VE) deficient diet. Three-week- old mice were fed a Torula yeast diet containing adequate or deficient Se and VE. Menhaden oil was added to the deficient diet to impose an additional oxidative stress. After 4 wk feeding, half the mice in each group were restrained for 5 d in well-ventilated conical tubes for 8 h daily. Mice fed the Se and VE deficient diets had increased liver thiobarbituric acid-reactive substance (TBARS) levels and decreased liver glutathione peroxidase (GPX1) activity and alpha-tocopherol levels. Plasma corticosterone levels were elevated in restrained mice fed the deficient diet compared to unrestrained mice fed the adequate diet. Restraint had no effect on liver TBARS or alpha-tocopherol levels. Liver GPX1 activity, however, was lower in restrained mice fed the adequate diet. In addition, liver superoxide dismutase (SOD) activity was lower in the restrained mice fed the adequate or deficient diet. Thus, under our conditions, Se and VE deficient diet, but not restraint, increased lipid peroxidation in mice. Restraint, however, decreased antioxidant protection in mice due to decreased activities of GPX1 and SOD enzymes.

Animals↗
PubMed2004

Selenium attenuates lipopolysaccharide-induced oxidative stress responses through modulation of p38 MAPK and NF-kappaB signaling pathways.

Lipopolysaccharide (LPS) produces reactive oxygen species (ROS) and nitric oxide (NO) in macrophages. These molecules are involved in inflammation associated with endotoxic shock. Selenium (Se), a biologically essential trace element, modulates the functions of many regulatory proteins involved in signal transduction and affects a variety of cellular activities, including cell growth and survival. We demonstrate that Se attenuated LPS-induced ROS and NO production in murine macrophage cultures in vitro. This Se-decreased production of NO was demonstrated by decreases in both mRNA and protein expression for inducible NO synthase (iNOS). The preventive effects of Se on iNOS were p38 mitogen-activated protein kinase- and nuclear factor-kappaB-dependent. Se specifically blocked the LPS-induced activation of p38 but not that of c-jun-N-terminal kinase and extracellular signal-regulated kinase; the p38-specific pathway was confirmed using p38 inhibitor SB 203580. These results suggest that the mechanism by which Se may act as an anti-inflammatory agent and that Se may be considered as a possible preventive intervention for endotoxemia, particularly in Se-deficient locations. However, the efficacy and safety of Se need to be further investigated, because long-term intake > 0.4 mg Se/day in adults can produce adverse effects.

Animals↗
PubMed1995

Effect of double-blind cross-over selenium supplementation on lipid peroxidation markers in cystic fibrosis patients.

Lipid peroxidation was assessed in 27 cystic fibrosis children during a double-blind selenium supplementation study (2.8 micrograms of sodium selenite per kg per day) with a placebo control and inversion of treatment periods. Simultaneously, 17 healthy children living in the same area were also investigated as control subjects. Before any treatment whatsoever and despite a selenium status close to those of control subjects, cystic fibrosis patients showed significant increase in plasma lipid peroxidation markers. Thiobarbituric acid reactants (TBARs) were normalized after the first treatment period of 5 months in both cystic fibrosis groups receiving either selenium supplementation or placebo. In this latter group, TBARs were reduced despite a significant decrease in plasma selenium concentrations as compared with the control group. Organic hydroperoxide concentrations were also simultaneously normalized in both cystic fibrosis groups at the end of the second treatment period. These results showed that improvement of lipid peroxidation markers was not related to the selenium supplementation. Nevertheless, oxidative stress sustained by cystic fibrosis children must be taken into account so that it does not aggravate the prognosis of the disease.

Adolescent↗
PubMedDate not supplied

Selenium enrichment and anti-oxidant status in baker's yeast, saccharomyces cerevisiae at different sodium selenite concentrations.

The use of selenized yeast as enriched selenium supplements in human nutrition has become a topic of increasing interest over the last decade. The present study was designed with the aim to achieve a balance between selenium (Se) incorporation and optimal growth of yeast cells along with effect of Se enrichment on antioxidant defense status of yeast cells. Since oxidative stress has been known to play a role in the life span of all types of cells, so in the present studies anti-oxidant defense status was evaluated in the Se- enriched baker's yeast cell culture model. Upon Se supplementation as sodium selenite at various concentrations in the growth medium, a continuous increase in glutathione peroxidase (GSH-Px) activity and Se content was observed. In case of reduced glutathione (GSH) decreasing trend were observed with increasing Se concentrations. An increasing trend in total glutathione as well as glutathione-s-transferase activity was observed at increasing Se concentrations. Thus, Se supplementation significantly enhanced GSH-Px levels along with alterations in other anti-oxidant enzymes, suggesting the role of Se in the enzyme defense system of yeast against oxidative damage. Further, as Se exerts growth inhibitory effect on cells, the growth inhibition study was carried out and decrease in biomass was observed with increasing concentrations of Se. Due to nutritional benefits, Se-enriched yeast may be considered a safe source of Se supplementation.

Antioxidants↗
PubMed1993

Protection of heme proteins by vitamin E, selenium, and beta-carotene against oxidative damage in rat heart, kidney, lung and spleen.

Effects of the combination of vitamin E, selenium, and beta-carotene on oxidative damage to rat heart, kidney, lung, and spleen were studied by measurement of the production of oxidized heme proteins (OHP) during spontaneous and prooxidant-induced oxidation. Male SD rats were fed with a vitamin E and selenium deficient diet or a diet supplemented with vitamin E, selenium, and beta-carotene. Homogenates of heart, kidney, lung, and spleen were incubated at 37 degrees C with and without the presence of bromotrichloromethane (CBrCl3). The diet supplemented with antioxidants showed a strong protective effect against oxidative damage to heme proteins during the early stages of both spontaneous and CBrCl3-induced oxidation in contrast to the antioxidant deficient diet. Synergism of multiple antioxygenic nutrients against oxidative damage to various animal tissues is discussed.

Animals↗
PubMed2004

Synthesis of [75Se]5-ethoxycarbonyl-4-methyl-1,2,3-selenadiazole.

Selenium-75 (t1/2 = 120.4d; 100% EC) was prepared in no-carrier-added form by 22MeV proton-bombardment of natural arsenic(III) oxide powder held in a copper-aluminum drawer target (highest yield, 35 microCi/microAh; maximum current, 6 microA), followed by oxidation to [75Se]selenium(IV) oxide. No-carrier-added [75Se]5-ethoxycarbonyl-4-methyl-1,2,3-selenadiazole was prepared in one step from ethylacetoacetate semicarbazone with [75Se]selenium(IV) oxide in glacial acetic acid at 50 degrees C. Column chromatography of the final solution afforded the desired labeled compound in 30% yield and greater than 98% radiochemical purity.

Arsenic Trioxide↗
PubMed2004

No evidence for an impact of selenium supplementation on environment associated health disorders--a systematic review.

In addition to vitamin C (and other vitamins/antioxidants), clinical ecologists (functional medicine) recommend selenium supplementation as a fundamental therapeutic remedy for the treatment of environment associated health disorders. This recommendation is based on the postulation that the trace element selenium inhibits oxidative stress generated during endogenous detoxification of xenobiotics (phase 1) by increasing selenium-dependent glutathione peroxidase activity, and that it counteracts heavy metal toxicity by forming inert metal complexes. The objective of this review was to investigate whether there are any valid studies providing reliable evidence of the therapeutic benefits of selenium supplementation in potentially environment associated health disorders. A systematic review was conducted based on the rigorous and well-defined methods developed by the Cochrane Collaboration. To achieve the demanding standards for systematic review set by the Cochrane Collaboration, study selection, quality assessment and data abstraction were performed independently and in duplicate using a standardized protocol. Overall, 1290 studies were identified as being eligible for inclusion. Twelve of these met the inclusion criteria and their quality was evaluated individually. None of the studies included in the analysis provided evidence of the therapeutic benefits of selenium supplementation in environment associated health disorders.

Aged↗