High-performance liquid chromatography of selenium in biological samples.
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Chromatography, High Pressure Liquid↗
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Serum selenium levels in distinct manifestations of coronary artery disease.
The trace element selenium plays an important role in the oxidation of lipids and is therefore closely associated with atherosclerosis. In a series of 49 unselected male patients having undergone coronary angiography, the serum selenium level was determined using flameless atomic absorption spectrometry (Zeeman technique), and compared to a standard (Seronorm; Nycomed). In the whole series the serum selenium levels were markedly decreased with no significant difference between patients with or without coronary artery disease. The severity of the coronary artery disease (CAD) did not correlate with the selenium level. However, patients with prior myocardial infarction had a significant higher selenium level than those without. Thus, the level of selenium does not appear to be a marker or a risk factor for coronary artery disease.
Aged↗
Is the selenium drinking water standard justified?
Four cases are presented which suggest that the present U.S.E.P.A. drinking water standard for selenium of 10 micrograms/L in inappropriate. The rationale upon which this standard is based is that selenium is carcinogenic, induces dental caries formation, and is highly toxic to animals. However, a critical assessment of this literature can not support these claims. Case no. 1 demonstrates that there is insufficient evidence to classify selenium as a carcinogen. Data derived from the three respective groups of researchers claiming a carcinogenic effect induced by selenium are obscure due to 1) the inability to accurately identify malignancies, 2) the apparent opposite effects of different selenium compounds, and 3) the lack of proper controls. Case no. 2 reviews recent evidence that selenium reduces the incidence of cancer in laboratory animals and in man, an effect which can probably be attributed to the antioxidant properties of selenium compounds. Case no. 3 provides evidence which does not permit the classification of selenium as a cariogenic element. Epidemiological studies supporting such a claim are inadequate since they lack properly matched control groups. Animal data do not support this link as well. Case no. 4 is a review of studies which clearly demonstrate the essentiality of selenium, an aspect of selenium metabolism that was not considered when the 10 micrograms/L standard was promulgated. In light of the four cases presented and an assessment of selenium toxicity in man, it is concluded that the 10 micrograms/L standard can not be justified. Instead, it is suggested that 50 micrograms/L selenium should provide sufficient protection from the toxic effects of this element. This is consistent with the current state of knowledge with respect to the potential adverse health effects associated with selenium.
9,10-Dimethyl-1,2-benzanthracene↗
Encephalopathy in megacystis-microcolon-intestinal hypoperistalsis syndrome patients on long-term total parenteral nutrition possibly due to selenium deficiency.
This report concerns two patients (female, 9 and 6 years) who were diagnosed with megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS). Although they exceeded the usual life expectancy of patients diagnosed with MMIHS because of total parenteral nutrition (TPN), they demonstrated progressive neurological deficits and showed histopathological features in the brain. Both patients were diagnosed with MMIHS in the neonatal period and were fed by TPN. The first patient developed visual and gait disturbances at the age of 7 years. Two months later, she developed dysarthria and muscular weakness, and could not maintain her posture. The level of serum selenium was extremely low. The second patient developed flexion and spasticity of the extremities followed by decorticate posture at the age of 3 years. Both patients died of sepsis. The brain weights of the two cases were 880 g and 715 g. In both cases, severe neuronal loss and gliosis were present in the medial convolutions of the occipital lobe, including the visual cortex. The postcentral gyrus and temporal transverse gyrus were also involved. In addition, extensive loss of Purkinje cells and granular neurons, and gliosis were observed in the cerebellum. We measured the selenium content of the brains and livers using the graphite furnace atomic absorption spectrometry method. Selenium was not detected in either brain, although the livers of both cases contained a low level of selenium. On immunohistochemical examination of the anti-oxidative enzymes, histiocyte-macrophage lineage cells in MMIHS cases, including microglia and Kupffer cells, showed only a weak reaction for glutathione peroxidase, of which selenium is an essential component. However, the cells in the control cases were strongly positive. In cases of MMIHS and methylmercury intoxication, the brain features similar lesions, in both their topographical and histopathological aspects. We considered that the brain lesions of the MMIHS patients mainly resulted from oxidative damage of the brain related to the low levels of glutathione peroxidase and other selenoproteins due to selenium deficiency.
Abnormalities, Multiple↗
Vitamin E, selenium, and the membrane-associated drug-metabolizing enzyme system of rat liver.
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Aminopyrine N-Demethylase↗
Selenium supplementation decreases nuclear factor-kappa B activity in peripheral blood mononuclear cells from type 2 diabetic patients.
OBJECTIVE: The role of selenium in preventing cardiovascular diseases has been largely described. Oxidative stress and the subsequent activation of nuclear factor-kappa B (NF-kappaB) have been linked to the development of vascular complications. We investigated the effects of selenium supplementation in type 2 diabetic patients on several oxidative stress parameters and NF-kappaB activity. METHODS: We enrolled 56 type 2 diabetic patients with similar glycaemic control: 21 were supplemented by selenium (960 micro g d(-1), 3 months) and 27 received a placebo, and 10 nondiabetic subjects formed the control group. To determine NF-kappaB activation, we used an electrophoretic mobility shift assay followed by a semi-quantitative determination of NF-kappaB in peripheral blood mononuclear cells. RESULTS: Selenium treatment resulted in a significant increase in plasma selenium and red-cell Se GSH px activity. It had no effect on lipid peroxidation measured by malone-dialdehyde (MDA) or on red-cell Cu/Zn SOD. NF-kappaB activity was increased by 80% in diabetic patients. In patients receiving selenium supplementation, selenium NF-kappaB activity was significantly reduced, reaching the same level as the nondiabetic control group. CONCLUSION: In type 2 diabetic patients, activation of NF-kappaB measured in peripheral blood monocytes can be reduced by selenium supplementation, confirming its importance in the prevention of cardiovascular diseases.
Diabetes Mellitus, Type 2↗
Antioxidant enzyme systems in rat liver and skeletal muscle. Influences of selenium deficiency, chronic training, and acute exercise.
The influences of selenium deficiency (Se-D), chronic training, and an acute bout of exercise on hepatic and skeletal muscle antioxidant enzymes, i.e., superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPX), as well as glutathione S-transferase (GST) and tissue lipid peroxidation, were investigated in post-weaning male Sprague-Dawley rats. Se-D per se depleted GPX in both liver and skeletal muscle but had no effect on SOD or catalase activity. One hour of treadmill running (20 m/min, 0% grade and 27 m/min, 15% grade for untrained and trained rats, respectively) significantly elevated hepatic catalase and cytosolic SOD activity; more prominent activations were found in the Se-D or untrained rats, whereas skeletal muscle antioxidant enzymes were little affected. Ten weeks of training (1 h/day, 5 days/week at 27 m/min, 15% grade) increased hepatic mitochondrial SOD by 23% (P less than 0.05) in Se-D rats. Both hepatic mitochondrial and cytosolic GPX were decreased by training whereas GPX was increased twofold in skeletal muscle mitochondria. Se-independent GPX was elevated by training only in the skeletal muscle mitochondria of Se-D rats. Lipid peroxidation (malondialdehyde formation) was increased by an acute bout of exercise in hepatic mitochondria of the untrained rats and in skeletal muscle mitochondria of the Se-D rats. These data indicate that antioxidant enzymes in liver and skeletal muscle are capable of adapting to selenium deficiency and exercise to minimize oxidative injury caused by free radicals.
Animals↗
The possible role of selenium in antioxidation in marine waders; a preliminary study.
In a marine wader, the oystercatcher (Haematopus ostralegus), the activity of the selenium-dependent enzyme glutathione peroxidase (GSH-Px) in the red blood cells (RBC) was measured. The average activity, 97 +/- 19 units/g Hb, is within the range reported for mammals. No correlation was observed between the selenium concentration and GSH-Px activity in the erythrocytes and it is calculated that only a small percentage of the selenium present in the RBC is bound to the enzyme. Therefore, it is concluded that the high selenium concentrations in the avian red cells cannot be ascribed to GSH-Px. It is argued that a function of selenium in antioxidation is still possible. The positive relationship found between selenium and iron concentrations in the tissues of the oystercatcher directs to such a role. A pitfall in the measurement of GSH-Px activity is outlined.
Animals↗
Solution-phase synthesis and electrochemical hydrogen storage of ultra-long single-crystal selenium submicrotubes.
Ultra-long single-crystalline trigonal selenium submicrotubes were synthesized using a facile one-step solution-phase approach with the assistance of nonionic surfactant Polyoxyethylene(20)sorbitan monolaurate (Tween-20), which turned out to be significant for the formation of ultra-long Se submicrotubes. XRD, Raman, SEM, and TEM were adopted to characterize the morphology, structure and phase composition of the as-prepared Se products. It was found that the length of the obtained Se submicrotubes was over 100 microm. By variation of the experimental parameters, the t-Se spheres, nanowires, and broken microtubes can be prepared. The possible growth mechanism of the ultra-long selenium submicrotubes was explained. In addition, we have also demonstrated that the synthesized ultra-long t-Se submicrotubes using the Tween-20-assisted approach can electrochemically charge and discharge with the high capacity of 265 mAh/g (corresponding to 0.97 wt % hydrogen in SWNTs) under normal atmosphere at room temperature. Cyclic voltammetry was adopted to investigate the adsorption-oxidation behavior of ultra-long selenium submicrotubes. It was observed that the morphology of the synthesized selenium products had a remarkable influence on their capacity of electrochemical hydrogen storage. These differences in hydrogen storage capacity are likely due to the size and density of tubes as well as the microcosmic morphology of different Se samples. The as-obtained ultra-long Se submicrotubes are expected to find wide applications in hydrogen storage, high-energy batteries, and optoelectronic, biologic, and catalytic fields as well as in the studies of structure-property relationships. This simple Tween-assisted approach might be extended to the preparations of one-dimensional nanostructures of tellurium and other anisotropic materials.
Journal Article↗
Modification of methylmercury toxicity and metabolism by selenium and vitamin E: possible mechanisms.
Selenium and vitamin E exert powerful effects in reducing acute or chronic methylmercury toxicity. Levels of selenium normally found in foods (below 1 ppm) delay the onset of toxic signs caused by much higher levels of methylmercury. Tissue levels of mercury in selenium-supplemented animals equal or exceed those found in animals given methylmercury alone. Selenium does not appear to act by simply modifying intake, absorption, excretion, or distribution of methylmercury, and direct effects of both selenium and vitamin E have been observed in vitro when methylmercury was added to cultured nervous tissue cells. The only established functions for selenium and vitamin E in animals are related to the prevention of oxidative damage in tissues. To encompass the protective effects of selenium and vitamin E and to explain other toxicological aspects of methylmercury and other alkylmetals, a new hypothesis is proposed: The toxicity of the alkylmetals is not caused soley by the intact molecule, but also involves free radicals formed by homolytic fission of the carbon-metal bond.
Animals↗
Influence of 7beta-hydroxycholesterol on glutathione status and nitric oxide production in macrophages: in vitro studies.
Incubation of murine peritoneal macrophages with 7beta-hydroxycholesterol (7beta-OH) for 24 hr led to dose-dependent reduction in cellular glutathione content as well as nitrite levels in the medium. Treatment with an inorganic form of selenium, sodium selenite which is a potent antioxidant, elevated the cellular glutathione levels and decreased nitrite levels. Our results suggest that 7beta-OH may exert its pro-atherogenic effect by inhibiting glutathione synthesis and nitric oxide production by macrophages present in the arterial wall and thus, impair the cellular antioxidant defense system.
Animals↗
Fatty acids and plasma antioxidants in HIV-positive patients: correlation with nutritional and immunological status.
OBJECTIVE: To investigate red blood cell (RBC) and plasma fatty acids (FA) in HIV-positive patients in relation to oxidative stress and nutritional or immunological status. DESIGN AND METHODS: FA, plasma selenium, vitamins A and E were measured in 95 patients divided into four groups according to CD4 cells. RESULTS: Poly- and di-unsaturated FA (PUFA, DUFA) decreased and saturated FA (SFA) increased in RBC in the patients below 400/mm3 and in plasma in the patients below 50/mm3. RBC SFA correlated to CD4 cells, PUFA to MDA. Unlike vitamin E, plasma vitamin A and selenium decreased in most groups. Plasma SFA and MUFA correlated negatively to selenium and PUFA and DUFA to vitamin E. No correlation was found between PUFA and nutritional markers. CONCLUSION: FA seem to be modified during HIV infection by oxidative stress and disease evolution, but not by denutrition.
Adult↗
Do vitamin E and selenium have beneficial effects on trinitrobenzenesulfonic acid-induced experimental colitis.
The balance between oxidant and antioxidant systems may be important in the pathogenesis and/or maintenance of tissue injury in ulcerative colitis. This study was designed to evaluate the effects of vitamin E and selenium supplementations on tissue injury and oxidative stress in trinitrobenzenesulfonic acid-induced ulcerative colitis in rats. Trinitrobenzenesulfonic acid administration severely changed the normal architecture of the colon and significantly increased the levels of malondialdehyde, protein carbonyl, and xantine oxidase (P < 0.001) in the colon homogenates of these rats. Supplementation of selenium to the trinitrobenzenesulfonic acid-treated rats neither improved the histopathological findings nor decreased the levels of malondialdehyde and protein carbonyl. Vitamin E supplementation reduced the levels of malondialdehyde and protein carbonyl but did not improve the colonic lesions. Supplementation of vitamin E + selenium significantly reduced both the severity of colonic lesions and the levels of malondialdehyde and protein carbonyl. In conclusion, we suggest that antioxidants and specific micronutrients may have beneficial effects in the treatment of ulcerative colitis.
Animals↗
Reduction of inorganic compounds with molecular hydrogen by Micrococcus lactilyticus. I. Stoichiometry with compounds of arsenic, selenium, tellurium, transition and other elements.
Woolfolk, C. A. (University of Washington, Seattle) and H. R. Whiteley. Reduction of inorganic compounds with molecular hydrogen by Micrococcus lactilyticus. I. Stoichiometry with compounds of arsenic, selenium, tellurium, transition and other elements. J. Bacteriol. 84:647-658. 1962.-Extracts of Micrococcus lactilyticus (Veillonella alcalescens) oxidize molecular hydrogen at the expense of certain compounds of arsenic, bismuth, selenium, tellurium, lead, thallium, vanadium, manganese, iron, copper, molybdenum, tungsten, osmium, ruthenium, gold, silver, and uranium, as well as molecular oxygen. Chemical and manometric data indicate that the following reductions are essentially quantitative: arsenate to arsenite, pentavalent and trivalent bismuth to the free element, selenite via elemental selenium to selenide, tellurate and tellurite to tellurium, lead dioxide and manganese dioxide to the divalent state, ferric to ferrous iron, osmium tetroxide to osmate ion, osmium dioxide and trivalent osmium to the metal, uranyl uranium to the tetravalent state, vanadate to the level of vanadyl, and polymolybdate ions to molybdenum blues with an average valence for molybdenum of +5. The results of a study of certain other hydrogenase-containing bacteria with respect to their ability to carry out some of the same reactions are also presented.
Arsenic↗
Toxicity of nutritionally available selenium compounds in primary and transformed hepatocytes.
The essential trace element selenium is also toxic at low doses. Since supplementation of selenium is discussed as cancer prophylaxis, we investigated whether or not bioavailable selenium compounds are selectively toxic on malignant cells by comparing primary and transformed liver cells as to the extent and mode of cell death. Sodium selenite and selenate exclusively induced necrosis in a concentration-dependent manner in all cell types investigated. In primary murine hepatocytes, the EC50 was 20 microM for selenite, 270 microM for selenate, and 30 microM for Se-methionine. In the human carcinoma cell line HepG2, the EC50 for selenite was 40 microM, and for selenate 1.1 mM, whereas Se-methionine was essentially non-toxic up to 10 mM. Similar results were found in murine Hepa1-6 cells. Exposure of primary murine cells to selenate or selenite resulted in increased lipid peroxidation. Toxicity was inhibited by superoxide dismutase plus catalase, indicating an important role for reactive oxygen intermediates. In primary hepatocytes, metabolical depletion of intracellular ATP by the ketohexose tagatose, significantly decreased the cytotoxicity of Se-methionine, while the one of selenite was increased. These data do not provide any in vitro evidence that bioavailable selenium compounds induce preferentially apoptotic cell death or selectively kill transformed hepatocytes.
Animals↗
Effect of extreme fish consumption on dietary and plasma antioxidant levels and fatty acid composition.
OBJECTIVE: To assess the effects of high-fish and low-fish diets on plasma concentrations of fatty acids and selected antioxidants. DESIGN AND SUBJECTS: The effects of fish consumption on dietary and plasma antioxidant levels and fatty acid composition were studied as part of a large dietary survey of Finnish adults (n = 1861). High-fish consumers were matched with low-fish consumers and 41 pairs were identified. The members of each pair were of the same sex, from the same 10 y age group, and from the same or adjacent areas. There were 21 men and 20 women in each group, with a mean age of 54.3 y. METHODS: The fish consumption of the subjects was investigated with a qualitative food questionnaire. Additionally, a 3 d food record was used to estimate the diet. Two indices were defined to describe the oxidation potential of the diets. The plasma alpha-tocopherol, gamma-tocopherol, and beta-carotene concentrations and various fatty acids were analysed. RESULTS: The mean fish intake was 103 g/d in the high-fish and 5 g/d in the low-fish group. The dietary intakes of vitamin C, protein, total n-3 polyunsaturated fatty acids (PUFA), eicosapentaenoic acid, docosahexaenoic acid, mercury, selenium, and salt and the theoretical oxidative potential were higher (P < 0.05) and the saturated fatty acid intake lower (P < 0.01) in the high-fish than in the low-fish group. The dietary vitamin E intake was similar in both groups but the ratio of dietary vitamin E/PUFA was higher (P < 0.01) in the high-fish than in the low-fish group (0.85 and 0.75, respectively). The plasma n-3 PUFAs were higher (P < 0.001) and n-6 PUFAs lower (P < 0.001) in the high-fish than in the low-fish group. There were no differences in plasma antioxidant levels between the groups. CONCLUSION: This study shows that extreme fish consumption does not affect plasma antioxidant levels.
Adult↗
Effects of sodium selenite on in vitro interactions between platelets and endothelial cells.
Selenium is an essential component of glutathione peroxidase enzymes, which protect cells against peroxidation and control concentrations of intracellular proxides. Since selenium deficiency is associated with an increased incidence of arterial thrombosis, we studied the effect of selenium on in vitro interactions between platelets and endothelial cells. Platelets from normal volunteers on a diet with (PLTSe+) or without (PLTSe-) selenium supplementation and human umbilical vein endothelial cells cultured in medium alone (ECSe-) or supplemented with Se (ECSe+) were used. The effect of in vivo administration or in vitro supplementation of selenium on platelet function was investigated in an aggregometry model designed for studying the interactions between platelets and endothelial cells using ADP and arachidonic acid as agonists. We observed that: (1) selenium-dependent glutathione peroxidase enzyme activity increased in both PLTSe+ and ECSe+, being about fivefold higher in the former; (2) platelet aggregation was inhibited by Se+ cells; (3) Se+ cells released less thromboxane B(2) (PLTSe+) and more 6-keto-prostaglandin F(1alpha) (ECSe+) than Se- cells; (4) when ECSe+ were treated with acetylsalicylic acid, the inhibitory effect of selenium on platelet aggregation disappeared; (5) the concentration of nitric oxide metabolites in Se+ culture media did not differ from that in Se- media. We suggest that an antithrombotic effect on the interactions between platelets and endothelial cells can be induced by stimulating glutathione peroxidase enzymes with selenium via a mechanism that is blocked by acetylsalicylic acid and is apparently unrelated to the biosynthesis of nitric oxide metabolites.
6-Ketoprostaglandin F1 alpha↗
Selenium catalysis of swelling of rat liver mitochondria and reduction of cytochrome c by sulfur compounds.
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Animals↗