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PubMed1991

Inhibition of sleep in rats by inorganic selenium compounds, inhibitors of prostaglandin D synthase.

Prostaglandin (PG) D2 has been postulated to be an endogenous sleep-promoting factor in rats, and SeCl4 and Na2SeO3 recently have been shown to inhibit the PGD synthase (prostaglandin-H2 D-isomerase, EC 5.3.99.2) activity of rat brain. The effect of these selenium compounds on sleep-wake activities was examined in freely moving rats along with their effects on brain temperature, food and water intake, and behavior. Test substances were administered for 6 hr into the third ventricle of rats, using a microdialysis technique. SeCl4, time- and dose-dependently, inhibited sleep at perfusion rates of 60 pmol/0.2 microliter per min and higher, and the inhibition was almost complete at rates greater than 200 pmol/0.2 microliter per min. The effect was reversible and was followed by a rebound. Na2SeO3 exhibited similar effects, but Na2SO3 did not show any effect on sleep. Simultaneous administration of dithiothreitol eliminated the sleep-inhibiting effects of these selenium compounds. These findings indicate that the decrease in sleep is due to inhibition of the PGD synthase activity in the brain by SeCl4 as well as Na2SeO3. During the inhibition of sleep, the rats in general showed an activation of behavior with moderate elevation of brain temperature and a detectable increase in food and water intake, suggesting that the sleep-inhibited state of the rats was similar to the physiological state of wakefulness and that the inhibitory effect was not due to the general toxicity of selenium.

Animals↗
PubMed2004

Retention of arsenic and selenium compounds using limestone in a coal gasification flue gas.

Volatile arsenic and selenium compounds present in coals may cause environmental problems during coal combustion and gasification. A possible way to avoid such problems may be the use of solid sorbents capable of retaining these elements from flue gases in gas cleaning systems. Lime and limestone are materials that are extensively employed for the capture of sulfur during coal processing. Moreover, they have also proven to have good retention characteristics for arsenic and selenium during combustion. The aim of this work was to ascertain whether this sorbent is also useful for retaining arsenic and selenium species in gases produced in coal gasification. The study was carried out in a laboratory-scale reactor in which the sorbent was employed as a fixed bed, using synthetic gas mixtures. In these conditions, retention capacities for arsenic may reach 17 mg g(-1) in a gasification atmosphere free of H2S, whereas the presence of H2S implies a significant decrease in arsenic retention. In the case of selenium, H2S does not influence retention which may reach 65 mg g(-1). Post-retention sorbent characterization, thermal stability, and water solubility tests have shown that chemical reaction is one of the mechanisms responsible for the capture of arsenic and selenium, with Ca(AsO2)2 and CaSe being the main compounds formed.

Air Pollution↗
PubMed2000

High-performance liquid chromatography of selenium compounds utilizing perfluorinated carboxylic acid ion-pairing agents and inductively coupled plasma and electrospray ionization mass spectrometric detection.

Increasing speciation demands in clinical chemistry, toxicology and nutrition have made the determination of the total elements in a sample inadequate; the amount of an element and the chemical forms in which it is present need to be known. Inductively coupled plasma mass spectrometry (ICP-MS) was used after high-performance liquid chromatographic (HPLC) separation, as was electrospray ionization mass spectrometry (ESI-MS). The effect of variation of the number of carbon atoms in perfluorinated carboxylic acids used as ion-pairing agents for the separation of selenium compounds was examined. Trifluoroacetic acid (0.1%), pentafluoropropanoic acid (0.1%) or heptafluorobutanoic acid (0.1%; HFBA) were alternatively used as additives to methanol-water (1:99, v/v) solutions as mobile phases. Reversed-phase HPLC-ICP-MS with 0.1% HFBA in the mobile phase allowed more than 20 selenium compounds to be separated in 70 min in an isocratic elution mode; the separation of natural selenium-enriched sample extracts was examined and explained. The pH of the 0.1% HFBA solution was modified with hydrochloric acid or ammonia and the pH of the sample extracts before injection was modified in order to overcome unwanted double peak formation in the chromatograms of sample extracts. Oxidations of standard gamma-glutamyl-Se-methylselenocysteine and Se-methylselenocysteine were carried out using 30% H2O2 solution and identifications of selenium-containing oxidation products were made using HPLC-ICP-MS and HPLC-ESI-MS. The principal organic oxidation product in both cases was methaneseleninic acid (MeSeO2H).

Carboxylic Acids↗
PubMed2000

Selenium compounds prevent the induction of drug resistance by cisplatin in human ovarian tumor xenografts in vivo.

PURPOSE: The development of drug resistance is a major cause for the failure of chemotherapy, particularly in ovarian cancer. Most previous research has focused on approaches to reverse drug resistance once it has arisen, that is, on the use of agents which can make drug-resistant tumors more sensitive to chemotherapy. We have suggested the feasibility of an alternative approach: the use of specific agents to prevent the development of resistance. METHODS: We designed an in vivo system to assay for the ability of compounds to prevent the induction of resistance by cisplatin. In this system, mice bearing tumors (which originated from A2780 human ovarian tumor cells) were treated with a low dose (2.6 mg/kg) of cisplatin and the tumors rapidly developed resistance to subsequent cisplatin treatment. Cell lines initiated from these tumors retained the resistant phenotype even after several months in culture. RESULTS: When either selenite or selenomethionine were administered (i.p., 1.5 mg/kg) close to the time of the initial cisplatin treatment, the induction of resistance was prevented. Similar treatments with sulfite or methionine had no effect on the induction of resistance by cisplatin. Studies in cells from treated tumors have indicated that the selenium compounds may prevent the induction of resistance by preventing a cisplatin-induced increase in glutathione level. CONCLUSIONS: Selenium compounds specifically prevent the induction by cisplatin of drug resistance in human ovarian tumors in vivo.

Animals↗
PubMed1972

Effects of molybdate, tungstate, and selenium compounds on formate dehydrogenase and other enzyme systems in Escherichia coli.

The role of selenium and molybdenum in the metabolism of Escherichia coli was explored by growing cells in a simple salts medium and examining the metabolic consequences of altering the concentration of molybdenum and selenium compounds in the medium. The addition of tungstate increased the molybdate deficiency of this medium, as reflected by lowered levels of enzyme systems previously recognized to require compounds of molybdenum and selenium for their formation [formate-dependent oxygen reduction, formate dehydrogenase (FDH) (EC 1.2.2.1), and nitrate reductase (EC 1.9.6.1)]. The requirement for selenium and molybdenum appears to be unique to the enzymes of formate and nitrate metabolism since molybdate- and selenite-deficient medium had no effect on the level of several dehydrogenase and oxidase systems, for which the electron donors were reduced nicotinamide adenine dinucleotide, succinate, d- or l-lactate, and glycerol. In addition, no effect was observed on the growth rate or cell yield with any carbon source tested (glucose, glycerol, dl-lactate, acetate, succinate, and l-malate) when the medium was deficient in molybdenum and selenium. dl-Selenocystine was about as effective as selenite in stimulating the formation of formate dehydrogenase, whereas dl-selenomethionine was only 1% as effective. In aerobic cells, an amount of FDH was formed such that 3,200 or 3,800 moles of formate were oxidized per min per mole of added selenium (added as dl-selenocystine or selenite, respectively).

Aerobiosis↗
PubMed2002

Study of the stability of selenium compounds in human urine and determination by mixed ion-pair reversed-phase chromatography with ICP-MS detection.

The stability of five selenium compounds, selenate, Se(VI), selenourea, SeUr, trimethylselenonium ion, TMSe(+), selenomethionine, SeMet, and selenoethionine, SeEt, at concentrations from 30-60 micro g L(-1) in a pooled human urine, stored in dark at -20 degrees C, 4 degrees C, or ambient temperature (ca. 25 degrees C), without addition of any stabilizing reagent was evaluated. The investigated Se species were determined independently by mixed ion-pair reversed-phase liquid chromatography with inductively coupled plasma mass spectrometric (ICP-MS) detection. The general trend is the lower the temperature used for storage, the higher the stability of Se species, when other conditions such as light, acidity, and container material are kept constant. On the basis of these results it is considered that the storage of urine samples at -20 degrees C for a short-term (within one month) is safe for Se speciation analysis. Long-term storage of urine samples for speciation analysis should, however, be undertaken with caution.

Chromatography, Liquid↗
PubMed2006

Inhibition by selenium compounds of catecholamine secretion due to inhibition of Ca2+ influx in cultured bovine adrenal chromaffin cells.

Selenium is an essential trace metal element, whereas large doses of selenium exert adverse effects to the human body. We examined the effects of selenium compounds, sodium selenite (Na2SeO3) and sodium selenate (Na2SeO4), on catecholamine secretion from cultured bovine adrenal chromaffin cells. Treatment of chromaffin cells with sodium selenite for 72, 48, and 24 h caused decreases in protein and catecholamine contents, in association with cell damage, at concentrations over 30, 300, and 300 microM, respectively. The cells treated with subtoxic conditions (<100 microM, 48 h) of sodium selenite were used for further experiments. Sodium selenite treatment for 48 h inhibited carbachol (CCh)-induced catecholamine secretion in a concentration-dependent and non-competitive manner, while it did not affect high K+- and veratridine-induced catecholamine secretion. Sodium selenite (100 microM) did not affect CCh- and veratridine-induced 22Na+ influx, while the compound inhibited 45Ca2+ influx induced only by CCh, but not high K+ and veratridine. Sodium selenate even at higher concentrations (1000 microM) did not affect any stimulus-induced catecholamine secretion and 45Ca2+ influx. Thus, sodium selenite may specifically exert adverse effects, such as inhibition of physiological stimulus-induced catecholamine secretion from adrenal chromaffin cells due to inhibition of Ca2+ influx.

Adrenal Medulla↗
PubMed2001

Catalytic oxidation of zinc/sulfur coordination sites in proteins by selenium compounds.

Zinc/thiolate (cysteine) coordination occurs in a very large number of proteins. These coordination sites are thermodynamically quite stable. Yet the redox chemistry of thiolate ligands confers extraordinary reactivities on these sites. The significance of such ligand-centered reactions is that they affect the binding and release of zinc, thus helping to distribute zinc, and perhaps controlling zinc-dependent cellular events. One new aspect focuses on the thiolate ligands of zinc as targets for the redox action of selenium compounds. A distinctive feature of this chemistry is the capacity of selenols to catalyze the oxidation of zinc/thiolate sites. We here use a chromophoric compound, 2-nitrophenylselenocyanate, to investigate its reaction mechanism with the zinc/thiolate clusters of metallothionein, a protein that is a cellular reservoir for zinc and together with its apoprotein, thionein, is involved in zinc distribution as a zinc donor/acceptor pair. The reaction is particularly revealing as it occurs in two steps. A selenenylsulfide intermediate is formed in the fast oxidative step, followed by the generation of 2-nitrophenylselenol that initiates the second, catalytic step. The findings demonstrate the high reactivity of selenium compounds with zinc/thiolate coordination sites and the potent catalytic roles that selenoproteins and selenium redox drugs may have in affecting gene expression via modulation of the zinc content of zinc finger proteins.

Anticarcinogenic Agents↗
PubMed2006

The antitumor effects of selenium compound Na5SeV5O18.3H20 in K562 cell.

With an approach to study the anti-tumor effects and mechanism of selenium compound, we investigated the anti-tumor activity and mechanism of Na5SeV5O18.H20 (NaSeVO) in K562 cells. The results showed that 0.625-20 mg/L NaSeVO could significantly inhibit the proliferation of K562 cells in vitro in a time- and concentration-dependent manner as determined by microculture tetrazolium (MTT) assay, the IC50 values were 14.41 (4.45-46.60) and 3.45 (2.29-5.22) mg/L after 48 h and 72 h treatment with NaSeVO respectively. In vivo experiments demonstrated that i.p. administration of 5, 10 mg/kg NaSeVO exhibited an significant inhibitory effect on the growth of transplantation tumor sarcoma 180 (S180) and hepatoma 22 (H22) in mice, with inhibition rate 26.8% and 58.4% on S180 and 31.3% and 47.4% on H22, respectively. Cell cycle studies indicated that the proportion of G0/G1 phase was increased at 2.5 mg/ L while decreased at 10 mg/L after treatment for 24, 48 h. Whereas S phase was decreased at 2.5-5 mg/L and markedly increased at 10 mg/L after treatment for 48 h. After treatment for 24 h, 10 mg/L NaSeVO also markedly increased S and G2/M phases. Take together, the result clearly showed that NaSeVO markedly increased S and G2/M phases at 10 mg/L. The study of immunocytochemistry showed that the expression bcl-2 is significantly inhibited by 10 mg/L NaSeVO, and bax increased. Morphology observation also revealed typical apoptotic features. NaSeVO also significantly caused the accumulation of Ca2+ and Mg2+, reactive oxygen species (ROS) and the reduction of pH value and mitochondrial membrane potential in K562 cells as compared with control by confocal laser scanning microscope. These results suggest that NaSeVO has anti-tumor effects and its mechanism is attributed partially to apoptosis induced by the elevation of intracellular Ca2+, Mg2+ and ROS concentration, and a reduction of pH value and mitochondria membrane potential (MMP).

Animals↗
PubMed2002

Selenium compounds inhibit I kappa B kinase (IKK) and nuclear factor-kappa B (NF-kappa B) in prostate cancer cells.

Selenium compounds are potential chemopreventive agents for prostate cancer. There are several proposed mechanisms for their anticancer effect, including enhanced apoptosis of transformed cells. Because the transcription factor nuclear factor-kappa B (NF-kappa B) is often constitutively activated in tumors and is a key antiapoptotic factor in mammalian cells, we tested whether selenium inhibited NF-kappa B activity in prostate cancer cells. In our work, we used sodium selenite and a novel synthetic compound, methylseleninic acid (MSeA), that served as a precursor of the putative active monomethyl metabolite methylselenol. We found that both selenium forms inhibited cell growth and induced apoptosis in DU145 and JCA1 prostate carcinoma cells. Sodium selenite and MeSeA, at the concentrations that induced apoptosis, inhibited NF-kappa B DNA binding induced by tumor necrosis factor-alpha and lipopolysaccharide in DU145 and JCA1 prostate cells. Both compounds also inhibited kappa B. Luciferase reporter activity in prostate cells. A key to NF-kappa B regulation is the inhibitory kappa B (I kappa B) proteins that in response to diverse stimuli are rapidly phosphorylated by I kappa B kinase complex, ubiquitinated, and undergo degradation, releasing NF-kappa B factor. We showed that sodium selenite and MSeA inhibited I kappa B kinase activation and I kappa B-alpha phosphorylation and degradation induced by TNF-alpha and lipopolysaccharide in prostate cells. NF-kappa B blockage by I kappa B-alpha d.n. mutant resulted in the sensitization of prostate carcinoma cells to apoptosis induced by selenium compounds. These results suggest that selenium may target the NF-kappa B activation pathway to exert, at least in part, its cancer chemopreventive effect in prostate.

Active Transport, Cell Nucleus↗
PubMed2003

Preconcentration of selenium compounds on a porous graphitic carbon column in view of HPLC-ICP-AES speciation analysis.

The retention of organic selenium compounds on a porous graphitic carbon stationary phase was investigated. Different acids were studied as mobile phases to elute selenocystamine, selenoethionine, selenomethionine and selenocystine. Detection was achieved using inductively coupled plasma-atomic emission spectrometry to provide selenium-specific and sensitive detection. The separation of the four species was carried out using methanoic acid. An important on-column preconcentration was obtained when solutes were injected in nitric acid or trifluoroacetic acid (TFA) media. The large injection volume employed (2,500 micro L) allowed us to reach low relative detection limits (2-6 micro g/L). The method, employing TFA as injection solvent and methanoic acid as the eluent was found to be robust with respect to different matrices spiked with selenocompounds.

Buffers↗
PubMed2006

Differential effects of selenium compounds on glucose synthesis in rabbit kidney-cortex tubules and hepatocytes. In vitro and in vivo studies.

Although selenium is taken with diet mainly as selenoamino acids, its hypoglycaemic action on hepatic gluconeogenesis has been studied with the use of inorganic selenium derivatives. The aim of the present investigation was to compare relative efficacies of inorganic and organic selenium compounds in reducing glucose synthesis in hepatocytes and renal tubules, significantly contributing to the glucose homeostasis. In contrast to hepatocytes, both selenite and methylselenocysteine inhibited renal gluconeogenesis by about 40-45% in control rabbits. Selenate did not affect this process, whereas selenomethionine inhibited gluconeogenesis by about 20% in both hepatocytes and renal tubules. In contrast to methylselenocysteine, selenite decreased intracellular ATP content, glutathione reduced/glutathione oxidized (GSH/GSSG) ratio and pyruvate carboxylase, PEPCK and FBPase activities, while methylselenocysteine diminished PEPCK activity due to elevation of intracellular 2-oxoglutarate and GSSG, inhibitors of this enzyme. Experiments in vivo indicate that in 3 of 9 alloxan-diabetic rabbits treated for 14 days with methylselenocysteine (0.182mg/kg body weight) blood glucose level was normalized, whereas in all diabetic rabbits plasma creatinine and urea levels decreased from 2.52+/-0.18 and 87.4+/-9.7 down to 1.63+/-0.11 and 39.0+/-2.8, respectively. In view of these data selenium supplementation might be beneficial for protection against diabetes-induced nephrotoxicity despite selenium accumulation in kidneys and liver.

Alloxan↗
PubMed2006

Expression of the ubiE gene of Geobacillus stearothermophilus V in Escherichia coli K-12 mediates the evolution of selenium compounds into the headspace of selenite- and selenate-amended cultures.

The ubiE gene of Geobacillus stearothermophilus V, with its own promoter, was cloned and introduced into Escherichia coli. The cloned gene complemented the ubiE gene deficiency of E. coli AN70. In addition, the expression of this gene in E. coli JM109 resulted in the evolution of volatile selenium compounds when these cells were grown in selenite- or selenate-amended media. These compounds were dimethyl selenide and dimethyl diselenide.

Bacillaceae↗
PubMed2005

Interactions between different selenium compounds and zinc, cadmium and mercury.

In this paper, we present a polarographic study of systems containing different inorganic and organic selenium compounds (sodium selenite, sodium selenate, seleno-methionine and seleno-urea) and metal ions (Zn2+, Cd2+ Hg2+) of the 12th group of elements in the periodic table. While zinc is a trace element known to be essential for plants and animals, cadmium and mercury are exogenous elements and are harmful pollutants that accumulate during aging; selenium is also recognized as an important micronutrient and is sometimes added to the diet. Experiments investigating the interactions were carried out using polarographic techniques in unbuffered systems. The three metal cations originated complexes with different strength and solubility in the presence of selenite anions; in the presence of selenate, polarography was not able to detect formation of complexes with these metal ions, at least under the experimental conditions used: a decrease of Hg2+ ion concentration was observed. Seleno-methionine did not react with Cd2+; in the presence of Zn2+, a soluble complex with a co-ordination number 1 was formed, while, again, the concentration of Hg2+ decreased in the presence of increasing concentrations of the selenium derivative. Seleno-urea did not react with Zn2+, but formed a complex with Cd2+ with limited solubility. Finally, this ligand could not be studied with Hg2+ because of the overlapping of the reduction potentials of both the ligand and the metal cation. Overall equilibrium constants for complex formation (Kf) and the solubility product (Ksp) for poorly soluble species are also reported.

Cadmium↗
PubMed1980

Toxic effect of various selenium compounds on the rat in the early postnatal period.

The toxic effect of selenium compounds (sodium selenate, D,L-selenomethionine, D,L-selenocystine, dimethyl selenide, and trimethylselenonium ion) was tested in 10-day old male rats. Increasing doses of the compounds were administered an s.c. injection and control animals were not injected. All compounds tested were lethal. Eye lens cataract was induced by the administration of selenate, D,L-selenomethionine, and D,L-selenocystine, while dimethyl selenide and trimethylselenonium ion failed to cause cataract. The cataractogenic effect of the above compounds may be attributed to their interference with glutathione metabolism.

Animals↗
PubMed2006

Maternal organo-selenium compounds and polyunsaturated fatty acids affect progeny performance and levels of selenium and docosahexaenoic acid in the chick tissues.

The effects of supplementing broiler breeder diets with polyunsaturated fatty acids (PUFA) and organo-Se compounds on the levels of Se and PUFA in chick tissues and on chick performance were assessed. Prepeak (23 wk) and peak (27 wk) production broiler breeders were fed 1 of 4 diets: a wheat-based commercial diet with soybean oil or fish oil but no added Se, and each diet with added Se as Sel-Plex (soybean oil + Se, fish oil + Se; Alltech Inc, Nicholasville, KY). The diets were designed to contain less than 0.1 mg of Se/kg and about 0.5 mg/kg for the nonsupplemented and the supplemented diets, respectively. As-hatched chicks from the 4 parental treatments were fed a nutritionally high quality diet (ME = 12.57 MJ/kg; CP = 228.7 g/kg) or a low quality diet (ME = 10.28 MJ/kg; CP = 182.8 g/kg), resulting in 8 dietary treatments. Performance was better and mortality lower in chicks from 27-wk-old breeders compared with those from 23-wk-old breeders. Fish oil in the maternal diet increased progeny mortality and reduced chick body mass at hatch. Body mass at 7 and 14 d posthatch was lower in chicks fed the low quality diet compared with chicks fed the high quality diet. At hatch, and for up to 14 d posthatch, chicks from hens fed diets high in PUFA had higher concentrations of docosahexaenoic acid (DHA) in the brain and liver compared with chicks hatched from hens fed diets low in PUFA. The DHA content of the tissues of chicks from breeders fed diets supplemented with Se was higher than that in chicks from breeders fed unsupplemented diets. Even after 14 d of being fed a diet with identical levels of Se, chicks hatched from parents fed diets high in Se had higher tissue Se concentrations than those hatched from parents fed diets low in Se. Supplementation of the maternal diet of chicks with organo-Se appears to enhance the DHA concentration of the chick brain, which may improve brain function.

Animal Feed↗
PubMed2003

Selenium compounds modulate the activity of recombinant rat AsIII-methyltransferase and the methylation of arsenite by rat and human hepatocytes.

Formation of methylated metabolites is a critical step in the metabolism of inorganic arsenic or selenium. We have previously shown that under conditions of a concurrent exposure sodium selenite inhibits methylation of arsenite by cultured rat hepatocytes. Here, we compare the effects of sodium selenite and mono-, di-, and trimethylated selenium compounds on the methylation of arsenite by purified recombinant rat As(III)-methyltransferase (Cyt19) and by primary rat and human hepatocytes. Among these compounds, sodium selenite was the most potent inhibitor of the methylation of arsenite by the recombinant enzyme (K(i) = 1.4 microM) and by cultured cells. In both systems, methylseleninic acid was an order of magnitude less potent an inhibitor (K(i) = 19.4 microM) than was sodium selenite. Dimethylselenoxide and trimethylselenonium iodide were weak activators of recombinant As(III)-methyltransferase activity but were weak inhibitors of arsenite methylation in hepatocytes. These data suggest that selenite, rather than its methylated metabolites, is responsible for inhibition of arsenite methylation in cultured hepatocytes and that inhibition may involve direct interactions between selenite and As(III)-methyltransferase.

Animals↗