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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↗
PubMed2000

Roles of selenium in endotoxin-induced lipid peroxidation in the rats liver and in nitric oxide production in J774A.1 cells.

We examined the role of selenium (Se) in the mechanism of oxidative stress caused by endotoxin by feeding rats deficient a diet in this element. In rats fed the Se-deficient diet (concentration of Se, less than 0.027 microg g(-1)) for 10 weeks, Se level and glutathione peroxidase (GSH-Px) activity in the liver were about 47 and 43% lower, respectively, than those in rats fed a Se-adequate diet (Se, 0.2 microg g(-1)). Rat fed the Se-deficient diet and given endotoxin (6 mg kg(-1), i.p.) showed a mortality rates of about 43% at 18 h. Nevertheless, no lethality was observed with endotoxin (4 mg kg(-1), i.p.) challenge. Levels of serum lactate dehydrogenase and acid phosphatase leakage were significantly higher in Se-deficient rats than those in Se-adequate diet 18 h after endotoxin (4 mg kg(-1), i. p.) challenge. Superoxide anion generation and lipid peroxide formation in the liver of Se-deficient rat were markedly increased 18 h after endotoxin (4 mg kg(-1), i.p.) injection compared with those in the endotoxin/Se-adequate diet group, whereas non-protein sulfhydryl level in the liver after administration of endotoxin to Se-deficient rats was lower than that in Se-adequate rats treated with endotoxin. We investigated whether Se can suppress nitric oxide (NO) generation and cytotoxicity in endotoxin-treated J774A.1 cells. Treatment with Se (10(-6) M) markedly inhibited endotoxin (0.1 microg ml(-1))-induced NO production in J774A.1 cells. Se induced an increased activity of GSH-Px in cells after 24 h of incubation, suggesting that the preventive effect of Se on NO production in endotoxemia is due to the induction of Se-GSH-Px activity. However, Se did not affect endotoxin-induced cytotoxicity in J774A.1 cells. These findings suggested that the oxidative stress caused by endotoxin may be due, at least in part, to changes in Se regulation during endotoxemia.

Animals↗
PubMed1999

Relationship between hypercholesterolaemia, endothelial dysfunction and hypertension.

OBJECTIVES: We have previously shown that in the rat a diet high in cholesterol and deficient in vitamin E and selenium results in hypercholesterolaemia and increased lipid oxidation. We utilized this model to determine whether rats given this diet develop impaired endothelium-dependent relaxation mediated by nitric oxide (NO) in mesenteric and in renal vessels. In addition, we tested whether the impairment is due to (i) decreased endothelial NO synthase activity, (ii) increased NO inactivation and/or (iii) increased production of the endothelium-derived constricting factors thromboxane A2/prostaglandin H2 and endothelin-1. We also investigated whether endothelial dysfunction induced by dyslipidaemia increases the sensitivity for the development of hypertension in response to high dietary salt. METHODS: Male Dahl salt-sensitive (DSS) rats were divided into three groups and received a standard diet (control group), a high (4%) cholesterol diet (HChol), or a high cholesterol diet deficient in the anti-oxidants vitamin E and selenium (HChol-Def). The NaCl content of these diets was 0.5%. After 18 weeks we studied endothelium-dependent relaxation in response to acetylcholine (ACh) in aortas and in isolated perfused preparations of mesenteric arteries and kidneys. In some experiments, ifetroban, a thromboxane A2/prostaglandin H2 receptor antagonist, was added to the organ bath or the perfusion buffer. Vascular responses to endothelin-1 as well as to BQ-123, an endothelin A receptor blocker, were studied in the isolated perfused kidneys. In addition, two extra groups of rats were fed a diet high in sodium chloride (2%): one of the groups received the normal cholesterol diet whereas the other group received the diet high in cholesterol and deficient in vitamin E and selenium. RESULTS: Compared to normocholesterolemic rats, responses to ACh were significantly impaired in aortas, mesenteric arteries and kidneys of HChol-Def rats (P < 0.01). Endothelial NO synthase activity (conversion of [14C]L-arginine to [14C]L-citrulline) was similar in aortas of control, HChol and HChol-Def rats; thus suggesting that impaired endothelium-dependent relaxation in the HChol-Def rats was not due to decreased cNOS catalytic activity. Ifetroban improved the impaired endothelium-dependent relaxation in mesenteric vessels, but not in aortas and kidneys. Endothelin-1 (ET-1: 10(-13)-10(-11) mol/l) elicited NO-mediated relaxations in kidneys of control rats but not in kidneys of HChol-Def; blockade of ET-1 with BQ-123, an ET(A) receptor blocker, did not improve NO-mediated relaxation of HChol-Def. Despite impaired endothelium-dependent relaxation in renal and mesenteric vessels, HChol-Def DSS rats failed to develop hypertension (systolic blood pressure 144 +/- 1 in control and 150 +/- 2 mmHg in HChol-Def) but manifested a significant increase in sensitivity to the pressor effects of a high (2% NaCl) dietary salt content during the initial 10 weeks of the study, although the final blood pressure at 18 weeks was similar in both groups. CONCLUSION: These studies support the notion that (i) products of lipid oxidation may reduce NO bioactivity without affecting endothelial NO synthase mass or catalytic activity, (ii) the mechanisms involved in the endothelial dysfunction induced by hypercholesterolaemia and oxidized lipids may differ among vascular beds, and (iii) decreased NO bioavailability does not necessarily result in systemic hypertension, but it may enhance the sensitivity to the hypertensinogenic effect of dietary salt.

Acetylcholine↗
PubMed1999

Protective effects of selenium, vitamin C and vitamin E against oxidative stress of cigarette smoke in rats.

Cataractous lenses have been found to have an altered distribution of the intracellular ionic environment: the concentrations of potassium and magnesium being decreased and the concentrations of sodium and calcium increased. These changes arise as a result of changes to lens membrane characteristics causing an increase in lens membrane permeability. In this study flame atomic absorption spectroscopy (AAS) was used for calcium, magnesium, iron and zinc determination, and flame atomic emission spectroscopy (AES) was used for sodium and potassium contents in normal and cigarette smoke-exposed rat lenses. The methods are sensitive enough to detect quantitatively all six cations in a single rat lenses. In this work, six elements, including Ca2+, K+, Na+, Zn2+, Fe2+ and Mg2+ in experimental rat eye lenses and normal transparent lenses were determined. It was found that the concentrations of Ca2+, Na+, Zn2+, and Fe2+ were increased dramatically while K+ and Mg2+ decreased in smoke-exposed rat lenses when compared to the control rat lenses. There were no significant changes between 'smoked' rats supplied with vitamin C and control groups. A positive correlation was found also in the other two groups of 'cigarette smoked' animals supplemented with selenium plus vitamin E and selenium when compared with 'cigarette smoked' without any supplements. These data provide support for the hypothesis that cigarette smoking increases the risk of cataract formation. We investigated whether vitamin C is the most important antioxidant in the body. The roles of diet with optimum amounts of antioxidant vitamins C and vitamin E and the antioxidant mineral selenium are discussed.

Animals↗
PubMed2002

Selenium supplementation acting through the induction of thioredoxin reductase and glutathione peroxidase protects the human endothelial cell line EAhy926 from damage by lipid hydroperoxides.

The human endothelial cell line EAhy926 was used to determine the importance of selenium in preventing oxidative damage induced by tert-butyl hydroperoxide (tert-BuOOH) or oxidised low density lipoprotein (LDLox). In cells grown in a low selenium medium, tert-BuOOH and LDLox killed cells in a dose-dependent manner. At 555 mg/l LDLox or 300 microM tert-BuOOH, >80% of cells were killed after 20 h. No significant cell kill was achieved by these agents if cells were pre-incubated for 48 h with 40 nM sodium selenite, a concentration that maximally induced the activities of cytoplasmic glutathione peroxidase (cyGPX; 5.1-fold), phospholipid hydroperoxide glutathione peroxidase (PHGPX;1.9-fold) and thioredoxin reductase (TR; 3.1-fold). Selenium-deficient cells pre-treated with 1 microM gold thioglucose (GTG) (a concentration that inhibited 25% of TR activity but had no inhibitory effect on cyGPX or PHGPX activity) were significantly (P<0.05) more susceptible to tert-BuOOH toxicity (LC(50) 110 microM) than selenium-deficient cells (LC(50) 175 microM). This was also the case for LDLox. In contrast, cells pre-treated with 40 nM selenite prior to exposure to GTG were significantly more resistant to damage from tert-BuOOH and LDLox than Se-deficient cells. Treatment with GTG or selenite had no significant effect on intracellular total glutathione concentrations. These results suggest that selenium supplementation, acting through induction of TR and GPX, has the potential to protect the human endothelium from oxidative damage.

Aurothioglucose↗
PubMed2003

The associations among semen quality, oxidative DNA damage in human spermatozoa and concentrations of cadmium, lead and selenium in seminal plasma.

To explore the associations among semen quality, oxidative DNA damage in human spermatozoa and concentrations of cadmium, lead and selenium in seminal plasma, 56 non-smoking subjects were asked to collect semen by masturbation into a sterile wide-mouth metal-free plastic container after 3 days of abstinence. The conventional semen parameters were analysed. The concentrations of Cd, Pb and Se in seminal plasma were detected using atomic absorption spectrophotometer. 8-OHdG levels in sperm DNA were measured using HPLC-EC. The results showed that the geometric mean concentrations of Cd, Pb and Se were 0.78, 7.8 and 51.4 microg/l, respectively. The geometric mean of 8-OHdG/10(6) dG was 51.4 (95% CI: 21.5-123.0). A significant inverse correlation exists between Cd and sperm density (r=-0.28, P<0.05), and between Cd and sperm number per ejaculum (r=-0.27, P<0.05). In contrast, there was a significantly positive correlation between Se and sperm density (r=0.50, P<0.01), between Se and sperm number (r=0.49, P<0.01), between Se and sperm motility (r=0.40, P<0.01), and between Se and sperm viability (r=0.38, P<0.01). No statistically significant correlation was observed between Pb and semen quality. A significant inverse correlation was observed between 8-OHdG and sperm density (r=-0.34, P<0.01), between 8-OHdG and sperm number per ejaculum (r=-0.30, P<0.01), and 8-OHdG and sperm viability (r=-0.24, P<0.05). 8-OHdG was significantly correlated with Cd in seminal plasma (r=0.55, P<0.01). A significant but weak positive correlation was found between 8-OHdG and Pb concentration in seminal plasma (r=0.28, P<0.05). In contract, a significant inverse correlation was observed between 8-OHdG and Se concentration in seminal plasma (r=-0.40, P<0.01). The results indicate that Cd in seminal plasma could affect semen quality and oxidative DNA damage in human spermatozoa. Se could protect against oxidative DNA damage in human sperm cells. Pb did not appear to have any association with the semen quality when concentration of Pb in seminal plasma was below 10 microg/l.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1981

Selenium-dependent and selenium-independent formate dehydrogenases of Methanococcus vannielii. Separation of the two forms and characterization of the purified selenium-independent form.

Anaerobic oxidation of formate by Methanococcus vannielii is catalyzed by two readily separable formate dehydrogenases. One of these is a 105,000-dalton protein that contains molybdenum, iron, and acid-labile sulfide, but not selenium. The other is a high molecular weight complex composed of selenoporotein and molybdo-iron sulfur protein subunits. Selenium occurs in this selenoenzyme in the chemical form of selenocysteine residues. M. vannielii cells from selenium-deficient media contain the 105,000-dalton formate dehydrogenase. Marked stimulation of growth by selenite supplementation is correlated with the simultaneous appearance in the cells of the high molecular weight selenoprotein . enzyme complex. The latter is the predominant form in cells from media additionally supplemented with tungstate. Under these conditions partial replacement of molybdenum with tungsten appears to occur. Both formate dehydrogenases are maximally active at pH 8.5 to 9.2 and at 60 degrees C and are extremely oxygen-sensitive. They utilize as electron acceptors 8-hydroxy-5-deazaflavin, FMN, FAD, and viologen and tetrazolium dyes.

Aldehyde Oxidoreductases↗
PubMed2004

Prevention against oxidative stress of eukaryotic cell membranes by selenium compounds of the rat.

By a combination of trace techniques and various biochemical methods, information about the characteristics of a 15-kDa selenoprotein was obtained. After labeling of rats in vivo with [(75)Se]selenite, subcellular fractionation of the homogenates of the prostate, lung, brain, thyroid gland, and large intestine, and gel electrophoretic separation of the proteins and subcellular fractionation, 15-kDa (75)Se was found in the cytosols of the tissues prostate > brain > lung > thyroid gland > large intestine after autoradiography. After coelectrophoresis of the separated 15-kDa labeled band obtained from each cytosolic fraction, the 15-kDa (75)Se band migrated in the same way as the combined bands isolated from the five tissue cytosols. After proteolytic cleavage in the gel of the 15-kDa labeled band obtained from the cytosol of each tissue and re-electrophoresis, the same labeled peptide pattern was found in each gel slice after autoradiography. By means of reversed-phase HPLC, we characterized a selenocysteine-containing protein that has enzymatic activity like that of glutathione peroxidase.

Animals↗
PubMed1988

Has selenium a beneficial role in human exposure to inorganic mercury?

Laboratory experiments have indicated that selenium acts as a powerful antagonist to mercury intoxication. The literature is reviewed and from this it is concluded that mercury and selenium react in various ways. 1) The mercuric ion binds to selenium to form a biologically inert complex leading to increased body burden of both elements. This reaction seems to take place only when a threshold of mercury exposure is exceeded. 2) Selenium influences the oxidation rate of elemental mercury and as such the distribution pattern. This reaction is influenced by the nature of the antioxidative system. In species with low glutathione peroxidase activity, mercury oxidation seems decreased which can lead to an increased brain uptake. In this process there is no threshold. 3) Selenium can, as part of the antioxidative defence system, counteract mercury induced lipid peroxidation. Other antioxidants e.g. vitamin E might be just as effective. Based upon the literature it is hypothesised that to man selenium is of no benefit in cases of exposure to mercury either as mercuric mercury or as vapours. The only protection against mercury will still be a low exposure level.

Free Radicals↗
PubMed2006

Selenoprotein P protects endothelial cells from oxidative damage by stimulation of glutathione peroxidase expression and activity.

A major fraction of the essential trace element selenium circulating in human blood plasma is present as selenoprotein P (SeP). As SeP associates with endothelial membranes, the participation of SeP in selenium-mediated protection against oxidative damage was investigated, using the human endothelial cell line Ea.hy926 as a model system. Hepatocyte-derived SeP prevented tert-butylhydroperoxide (t-BHP)-induced oxidative cell death of Ea.hy926 cells in a similar manner as did sodium selenite, counteracting a t-BHP-induced loss of cellular membrane integrity. Protection was detected after at least 10 h of SeP supplementation and it peaked at 24 h. SeP time-dependently stimulated the expression of cytosolic glutathione peroxidase (cGPx) and increased the enzymatic activities of glutathione peroxidase (GPx) and thioredoxin reductase (TR). The cGPx inhibitor mercaptosuccinate as well as the gamma-glutamylcysteine synthetase inhibitor buthionine sulfoximine counteracted the SeP-mediated protection, while the TR inhibitors cisplatin and auranofin had no effect. The presented data suggest that selenium supplementation by SeP prevents oxidative damage of human endothelial cells by restoring expression and enzymatic activity of GPx.

Buthionine Sulfoximine↗
PubMedDate not supplied

Modification of chemical toxicity by selenium deficiency.

Selenium deficiency causes a number of hepatic metabolic alterations in the rat which could lead to changes in chemical toxicity. It causes a decrease in glutathione peroxidase activity, an increase in glutathione S-transferase activity, and an increase in the rate of glutathione synthesis. The hepatotoxicities of three compounds which bind to glutathione S-transferase; iodipamide, acetaminophen, and aflatoxin B1, are decreased by selenium deficiency. The toxicity of redox cycling compounds is generally increased by selenium deficiency and is accompanied by evidence of lipid peroxidation. Thus, nitrofurantoin (100 mg/kg) causes renal tubular necrosis in selenium-deficient rats but not in controls. Selenium-deficient rats are much more sensitive to diquat toxicity than are controls. Lethality of diquat in selenium-deficient rats appears to be causally linked to lipid peroxidation. Lethality of diquat in control rats is not linked to lipid peroxidation. The effect of selenium does not appear to be mediated by glutathione peroxidase, however, indicating that selenium has another oxidant defense function. Another interesting observation made was that increases in inspired O2 tension decreased ethane production (lipid peroxidation) in selenium-deficient and in control rats given diquat. Thus, O2 appears to prevent diquat-induced lipid peroxidation.

Acetaminophen↗
PubMed2006

U(IV) chalcogenolates synthesized via oxidation of uranium metal by dichalcogenides.

Treatment of uranium metal with dichalcogenides in the presence of a catalytic amount of iodine in pyridine affords molecular U(IV) chalcogenolates that do not require stabilizing ancillary ligands. Oxidation of U(0) by PhEEPh yields monomeric seven-coordinate U(EPh)4(py)3 (E = S(1), Se(2)). The dimeric eight-coordinate complexes [U(EPh)2(mu2-EPh)2(CH3CN)2]2 (E = S(3), Se(4)) are obtained by crystallization from solutions of 1 and 2 dissolved in acetonitrile. Oxidation of U(0) by pySSpy and crystallization from thf yields nine-coordinate U(Spy)4(thf) (5). Incorporation of elemental selenium into the oxidation of U(0) by PhSeSePh results in the isolation of [U(py)2(SePh)(mu3-Se)(mu2-SePh)]4.4py (6), a tetrameric cluster in which each U(IV) ion is eight-coordinate and the U4Se4 core forms a distorted cube. The compounds were analyzed spectroscopically and the single-crystal X-ray structures of 1 and 3-6 were determined. The isolation of 1-6 represents six new examples of actinide chalcogenolates and allows insight into the nature of "hard" actinide ion-"soft" chalcogen donor interactions.

Journal Article↗
PubMed2003

Low levels of glutathione peroxidase 1 activity in selenium-deficient mouse liver affect c-Jun N-terminal kinase activation and p53 phosphorylation on Ser-15 in pro-oxidant-induced aponecrosis.

Low levels of hepatic selenium (Se)-dependent glutathione peroxidase 1 (GPX1) activity have been shown to protect against oxidative liver injury in Se-deficient mice. The objective of the present study was to determine if the GPX1 protection was associated with phosphorylations of c-Jun N-terminal kinase (JNK) and p53 on Ser-15, two key signalling events in oxidative-stress-mediated cell death. Both Se-deficient GPX1 knockout (GPX1(-/-)) and wild-type (WT) mice ( n =64) were pretreated with an intraperitoneal injection of Se (as sodium selenite, 50 microg/kg body weight) 6 h before an intraperitoneal injection of paraquat (12.5 mg/kg). Liver aponecrosis, a mixed form of cell death sharing apoptosis and necrosis, was induced by paraquat in both groups of mice. However, its appearance was remarkably delayed and the severity was decreased by the repletion of hepatic GPX1 activity to <4% of the normal level by the Se injection in the WT mice, compared with that in the GPX1(-/-) mice. Consistently, the WT mice had lower levels of hepatic phospho-JNK, p53 and phospho-p53 (Ser-15) when compared with the GPX1(-/-) mice at 1-10 h after paraquat injection. Incubating liver homogenates with antibodies raised against JNK or phospho-JNK resulted in co-immunoprecipitation of phospho-p53 (Ser-15), and the amounts of the precipitated phospho-p53 were greater in the GPX1(-/-) mice when compared with that in the WT mice. The co-precipitated complex by the anti-phospho-JNK antibody was capable of phosphorylating intrinsic or extrinsic p53 on Ser-15. In conclusion, phospho-JNK may catalyse phosphorylation of p53 on Ser-15 in Se-deficient mouse liver under moderate oxidative stress, and attenuation of that cascade by low levels of GPX1 activity is associated with its protection against the pro-oxidant-induced liver aponecrosis.

Animals↗
PubMed2001

Anti-oxidant ebselen causes the resolution of experimentally induced hepatic fibrosis in rats.

BACKGROUND: Hepatic fibrosis occurs because of injury to the liver parenchyma and biliary system. We have investigated the effect of an organic selenium anti-oxidant, ebselen, in the resolution of experimentally induced hepatic fibrosis, and evaluated its effect on various paradigms involved in hepatic fibrosis. METHODS: Following pretreatment with phenobarbitone, liver fibrosis was induced in male Fischer 344 rats by using carbon tetrachloride treatment for 10 weeks. Carbon tetrachloride-treated rats were randomly assigned into two groups: (i) no ebselen; and (ii) ebselen administered for 3 weeks following a 10-week carbon tetrachloride treatment period. Normal controls were: (i) neither carbon tetrachloride nor ebselen treated; or (ii) ebselen treated for 13 weeks. Liver sections were stained with hematoxylin and eosin, Masson trichrome and stained for reticulin by using silver impregnation. Reverse transcription-polymerase chain reaction was used to analyze the steady-state levels of gene(s) involved in: (i) hepatic fibrosis, namely, transforming growth factor-beta1, procollagen I and III, tissue inhibitor of metalloproteinase-1 and matrix metalloproteinase-13; (ii) oxidative stress, namely, cytochrome P4502E1; and (iii) preneoplastic liver foci, namely, the placental form of glutathione-S-transferase. RESULTS: Histological staining showed that ebselen resolves carbon tetrachloride-induced hepatic fibrosis. Treatment with ebselen reduced steady-state levels of transforming growth factor-beta1, procollagen I and III, tissue inhibitor of metalloproteinase-1, cytochrome P4502E1 and placental form glutathione-S-transferase transcripts, and increased transcripts of matrix metalloproteinase-13. CONCLUSION: These findings provide evidence that ebselen significantly causes the resolution of carbon tetrachloride-induced hepatic fibrosis in rats.

Animals↗
PubMed2002

Selenium deficiency increases the expression of inducible nitric oxide synthase in RAW 264.7 macrophages: role of nuclear factor-kappaB in up-regulation.

The inducible isoform of nitric oxide synthase (iNOS) is implicated in atherosclerosis, malignancy, rheumatoid arthritis, tissue and reperfusion injuries. A key determinant of the pro-oxidant versus protective effects of NO is the underlying redox status of the tissue. Selenoproteins, such as glutathione peroxidases (GPxs) and thioredoxin reductases, are key components of cellular defence and promote optimal antioxidant/oxidant balance. In this study, we have investigated the relationship between Se status, iNOS expression and NO production in Se-deficient and Se-supplemented RAW 264.7 macrophage cell lines. The cellular GPx activity, a measure of Se status, was 17-fold lower in Se-deficient RAW 264.7 cells and the total cellular oxidative tone, as assessed by flow cytometry with 2',7'-dichlorodihydrofluorescein diacetate, was higher in the Se-deficient cells than the Se-supplemented cells. Upon lipopolysaccharide (LPS) stimulation of these cells in culture, we found significantly higher iNOS transcript and protein expression levels with an increase in NO production in Se-deficient RAW 264.7 cells than the Se-supplemented cells. Electrophoretic mobility-shift assays, nuclear factor-kappaB (NF-kappaB)-luciferase reporter assays and Western blot analyses indicate that the increased expression of iNOS in Se deficiency could be due to an increased activation and consequent nuclear localization of the redox-sensitive transcription factor NF-kappaB. These results suggest an inverse relationship between cellular Se status and iNOS expression in LPS-stimulated RAW 264.7 cells and provide evidence for the beneficial effects of dietary Se supplementation in the prevention and/or treatment of oxidative-stress-mediated inflammatory diseases.

Animals↗
PubMed2005

Optimization of a chemical modifier in the determination of selenium by graphite furnace atomic absorption spectrometry and its application to wheat and wheat flour analysis.

A method for the determination of total selenium in wheat and wheat flour using graphite furnace atomic absorption spectrometry (GFAAS) with palladium/ascorbic acid as a chemical modifier was studied. The effects of nickel nitrate, palladium/ascorbic acid, and palladium/magnesium nitrate as chemical modifiers on the sensitivity in the determination of selenite, selenate and selenomethionine by GFAAS were compared. The palladium/ascorbic acid modifier was used for the determination of total selenium in wheat and wheat flour, because the oxidation states of the selenium ion are not important in the determination. The detection limit was estimated to be 1 microg L(-1) (calculated as 3sigma of the blank); the calibration curve was linear for the concentration range 5 - 50 microg L(-1) and the recovery range was 96.66 - 101.80%. The optimal ashing and atomizing temperatures were 1300 degrees C and 2250 degrees C, respectively. The proposed method was successfully applied to the determination of total selenium in wheat and wheat flour.

Ascorbic Acid↗
PubMed2003

Effect of sub-chronic selenium toxicosis on lipid peroxidation, glutathione redox cycle and antioxidant enzymes in calves.

The present investigation reports the effect of sodium selenite-induced sub-chronic toxicity in crossbred cow calves on various antioxidant enzymes. Sodium selenite (0.25 mg/kg for 16 w) resulted in characteristic signs of sub-chronic selenosis, ie alopecia, cracking and enlargement of hooves, interdigital lesions, ring formation on the coronet region, and gangrene at tip of the tail. The sodium selenite resulted in significant rise of blood selenium levels and concurrent increase in erythrocytic glutathione peroxidase (GPx) activity. Blood selenium levels and GPx activity had a high positive correlation (r = 0.97). Blood glutathione levels were lowered from 211.1 +/- 13.4 to 95.56 +/- 11.8 microg/ml. Selenosis caused oxidative stress as evidenced by a 3-fold increase in lipid peroxidation: activities of glutathione-S-transferase, glutathione reductase, superoxide dismutase and catalase were significantly increased. These findings support the hypothesis that the pro-oxidant attributes of selenium play important roles in its toxicity.

Administration, Oral↗
PubMed2005

[Photoreduction of Se (VI) by marine algae-transitional metals-light system].

Seven marine phytoplankton, including five green algae (Tetraselmis levis, Chlorella autotrophica, Dunaliella salina, Nannochloropsis sp. and Tetraselmis subcordiformis), one diatom (Phaeodactylum tricornutum), one red alga (Porphyridium purpureum), and three usual transitional metals (Fe(III), Cu(II), Mn(II)) were used to make up marine phytoplankton-light or transitional metals-light or marine phytoplankton-transitional metals-light system. In such system, Se(VI) could be transformed into Se(IV) by photoreduction. The species transformation of selenium could be photo-induced by redox reaction of transitional metals. The photochemical activity of marine phytoplankton was confirmed for the first time, because marine phytoplankton could adsorb and concentrated of selenium, transitional metals and organic substances (including the exudation of algae, as reducing agent) which redox potentials were changed. The ratios of Se(VI) to Se(IV) were dominated by the species, the concentration of marine phytoplankton and transitional metals, and it could be enhanced through increasing the concentration of marine algae or the combined effect from marine algae and transitional metals. After photoreduction by ternary system, the ratio of Se(VI) to Se(IV) ranges from 1.17 to 2.85, which is close to the actual value in euphotic layer of seawater. The photochemical process that is induced by marine algae and transitional metals dominative the leading effects on the distribution of oxidation states of selenium.

Chlorophyta↗