SEARCH · PubMed Health

Results for “SELENIUM COMPOUNDS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

PubMed1997

Differential induction of growth arrest inducible genes by selenium compounds.

The effects of two types of selenium compounds on the expression levels of growth arrest and DNA damage-inducible (gadd) genes and on selected cell death genes were examined in mouse mammary MOD cells to test the hypothesis that the diversity of selenium-induced cellular responses to these compounds could be distinguished by unique gene expression patterns. Whereas the expression patterns of known cell death-related genes (bcl-2 and bax) were not informative with respect to the cellular response patterns upon exposure to selenium compounds, time-dependent and selenium species-specific induction patterns were observed for gadd34, gadd45 and gadd153 genes. It was also observed that the MOD cells expressed a truncated p53 transcript but no detectable immunoreactive P53 protein, indicating a null p53 phenotype. The fact that selenium compounds induced growth arrest and death of these cells and that these compounds induced specific patterns of expression of gadd genes indicates that these genes may mediate some selenium-induced cellular responses. The findings further imply that selenium compounds may be effective chemopreventive agents for human breast carcinogenesis, in which p53 mutations are frequent.

Animals↗

PubMed2002

Comparison of selenium distribution in mice organs after the supplementation with inorganic and organic selenium compound selenosemicarbazide.

Studies on selenium organ content and its function in living organisms just like studies on other elements provide interesting results although their interpretation is not always clear. The aim of our study was to determine the concentration and distribution of selenium in several organs and tissues in mice after supplementation with our newly synthesized organic compound of selenium selenosemicarbazide (4-o-tolyl-selenosemicarbazide of o-chlorobenzoic acid) as compared to the effects of the supplementation with inorganic compounds. SWISS mice were fed with both types of compounds at the dose of 10(-3) g Se per kg for the period of 10 days. The concentrations of selenium in brains of mice treated with selenocarbazide and sodium selenite were higher than in controls (38.04 micrograms g-1 and 32.00 micrograms g-1 vs. 26.18 micrograms g-1). There was a statistically significant increase in the selenium contents in lungs after supplementation with selenosemicarbazide and sodium selenite (11.81 micrograms g-1 and 6.79 micrograms g-1 vs. 1.75 micrograms g-1 in controls). We found a statistically insignificant increase in selenium contents in intercostal muscles after supplementation with inorganic selenium compounds and a statistically significant increase after the supplementation with selenosemicarbazide (10.13 micrograms g-1; 14.21 micrograms g-1 and 28.84 micrograms g-1, respectively). Our investigations lead to a conclusion that 4-o-tolyl-seleno-semicarbazide of o-chlorobenzoic acid, an organic selenium compound may be more easily absorbed than inorganic sodium IV selenite.

Administration, Oral↗

PubMed1980

Dependence of the sister-chromatid exchange-inducing abilities of inorganic selenium compounds on the valence state of selenium.

Inorganic selenium (Se) compounds having Se of different valence states were tested for their abilities to induce sister-chromatid exchanges (SCEs) in human whole blood cultures. The Se compounds tested (and their Se valence states) were: sodium selenide (Se(2-)), selenium dioxide (Se(4+)), selenium (Se(0)), sodium selenate (Se(6+)), and sodium selenite (Se(4+)). Human whole blood cultures were exposed to concentrations of these compounds ranging from 1.12 X 10(-6)-8.00 X 10(-5) M for the final 18 h of the 96-h incubation period. Only sodium selenate failed to induce SCEs at high concentrations. Of the 4 SCE-inducing Se compounds studied selenium was the most potent inducer of SCEs, and sodium selenite was the least effective SCE-inducing agent. The SCE-inducing abilities of the Se compounds in decreasing order of their effectiveness were: selenium > selenium dioxide > solium selenide > sodium selenite > sodium selenate.

Blood Cells↗

PubMedDate not supplied

Selenium compounds regulate p53 by common and distinctive mechanisms.

Selenium compounds show much promise in the prevention of prostate and other human cancers. Various selenium chemical forms have been shown to differ widely in their anticancer properties. The main dietary form is selenomethionine, which we showed modulated p53 activity by causing redox regulation of key p53 cysteine residues. In the current study we included other selenium chemical forms, sodium selenite and methyl-seleninic acid. All three forms are relevant selenium sources in human populations. All three forms can affect p53 activity defined as trans-activation of a p53-dependent reporter gene. In addition to the reduction of cysteine sulfhydryl groups, p53 phosphorylation was also affected in cells treated with selenium compounds. Methyl-seleninic acid caused phosphorylation of one or more p53 threonine residues, but did not affect any known serine phosphorylation sites. By contrast sodium selenite caused phosphorylation of p53 serines 20, 37 and 46 known to mediate apoptosis. Selenomethionine did not cause detectable phosphorylation of p53 serines or threonines. Our data show that, although p53 modulation may be a common denominator of selenium compounds, specific mechanisms of p53 activation differ among selenium chemical forms. Post-translational modifications of p53 are determinants of p53 activity and probably affect the threshold for p53-mediated functions. Different selenium chemical forms may differentially modify p53 for DNA repair or apoptosis in conjunction with a given level of endogenous or exogenous DNA damage.

Apoptosis↗

PubMed2006

An organic selenium compound attenuates apomorphine-induced stereotypy in mice.

Selenium compounds display neuroprotective activities mediated at least in part by their antioxidant actions. Oxidative damage has been implicated in psychiatric disorders including schizophrenia and bipolar disorder, and an alteration in expression of selenium-binding protein-1 (SELENBP-1) has been recently reported in both the blood and brain of schizophrenic patients. In the present study we examined the effects of the organic selenium compound 3'3-ditrifluoromethyldiphenyl diselenide [(F3CPhSe)2] on apomorphine-induced stereotypy in mice, an animal model of psychosis. Systemic administration of (F3CPhSe)2 at the highest dose used (25.0 micromol/kg in a 10.0 ml/kg injection volume) significantly reduced apomorphine-induced stereotyped behaviors. A series of control experiments showed that the same dose of (F3CPhSe)2 did not affect open-field behavior, habituation, or aversively motivated memory. The results indicate that organic selenium compounds should be further investigated as agents with possible antipsychotic properties.

Analysis of Variance↗

PubMed1983

[Selenium compounds and carcinogenesis].

Starting with a brief outline of the general toxic effects of selenium compounds, their biological importance for the organism as a trace element and with an analysis of the different hypotheses on the action mechanism of selenium and selenium compounds, a survey is provided in which way selenium compounds may influence malignant transformation and related processes in vivo and in vitro. Furthermore, observations are viewed on the effects of selenium compounds on spontaneously developing, chemically or virally induced tumors. Based on the data available so far it cannot, at present, be assessed whether selenium and its compounds can be used in the future for chemoprevention of cancer.

Animals↗

PubMed1986

Effects of selenium compounds on phospholipid/Ca2+-dependent protein kinase (protein kinase C) system from human leukemic cells.

Selenium compounds (selenium dioxide, selenious acid, and selenic acid) were found to inhibit phospholipid/Ca2+-dependent protein kinase (protein kinase C) and the phorbol ester-stimulated phosphorylation of endogenous substrate proteins from HL60 cells. Kinetic analysis indicated that selenium dioxide (SeO2) inhibited the enzyme noncompetitively with respect to phosphatidylserine (apparent Ki, 60 microM) and Ca2+ (apparent Ki, 68 microM). The inhibitory effect of SeO2 on protein kinase C was additive to that of another inhibitor of the enzyme (alkyl-lysophospholipid) when present together. SeO2 was also equally inhibitory to myosin light chain kinase, a calmodulin/Ca2+-dependent class of protein kinase. It, however, affected only very slightly cyclic adenosine 3':5'-monophosphate-dependent protein kinase. It is suggested that inhibition of Ca2+-dependent reactions might be related to the anticarcinogenic property of selenium.

Animals↗

PubMed2003

Determination of selenium compounds in urine by high-performance liquid chromatography--inductively coupled plasma mass spectrometry.

Selenium species, selenite, selenate, selenomethionine (Semet), seneloethionine (Seet) and trimethylselenonium ion (TmSe) were separated in aqueous solution using a gel-permeation (polyvinyl alcohol-based resin) GS-220 column by eluting with 25 mM tetramethylammonium hydroxide and 25 mM malonic acid at pH 7.9. The GS-220 column coupled with inductively coupled plasma mass spectrometry was used for the separation, identification, and quantification of selenium compounds present in certified reference material (CRM) No. 18 human urine from the National Institute for Environmental Studies in Japan (NIES). Spiking of the authentic standard to the urine and use of a silica-based LC-SCX cation-exchange column validated the peak of selenium compounds. High concentrations of chloride and bromide in the urine eluted from the GS-220 column formed molecular ions 40Ar37Cl+ and 81Br1H+ in the plasma, and these molecular ions created additional peaks in the chromatograms when 77Se and 82Se isotopes were monitored respectively. Thus, both the isotopes were selected concurrently for signal monitoring to eliminate the interfering signals. On the LC-SCX column, chloride and bromide were eluted with selenate and complicated its determination, but the peak of TmSe was baseline separated from rest of the Se compounds. Two unknown Se compounds were detected in both the columns. An additional Se compound having the same retention time as that of Semet was detected on the LC-SCX column. Peaks of selenite, selenate, TmSe and unknown selenium compounds in the urine were baseline separated on the GS-220 column, and were free from interferences. Therefore, the GS-220 column was used for the determination of selenium compounds in NIES CRM No. 18. Unknown Se compounds were the predominant selenium species followed by selenite, TmSe and selenate. The estimated value of TmSe as Se, by the standard additions method using the GS-220 column, was 3.42 +/- 0.17 microg l(-1) and was in good agreement with the LC-SCX value [3.38 +/- 0.21 (n=5) microg l(-1)].

Cations↗

PubMed2004

Interaction of selenium compounds with zinc finger proteins involved in DNA repair.

As an essential element, selenium is present in enzymes from several families, including glutathione peroxidases, and is thought to exert anticarcinogenic properties. A remarkable feature of selenium consists of its ability to oxidize thiols under reducing conditions. Thus, one mode of action recently suggested is the oxidation of thiol groups of metallothionein, thereby providing zinc for essential reactions. However, tetrahedral zinc ion complexation to four thiolates, similar to that found in metallothionein, is present in one of the major classes of transcription factors and other so-called zinc finger proteins. Within this study we investigated the effect of selenium compounds on the activity of the formamidopyrimidine-DNA glycosylase (Fpg), a zinc finger protein involved in base excision repair, and on the DNA-binding capacity and integrity of xeroderma pigmentosum group A protein (XPA), a zinc finger protein essential for nucleotide excision repair. The reducible selenium compounds phenylseleninic acid, phenylselenyl chloride, selenocystine, ebselen, and 2-nitrophenylselenocyanate caused a concentration-dependent decrease of Fpg activity, while no inhibition was detected with fully reduced selenomethionine, methylselenocysteine or some sulfur-containing analogs. Furthermore, reducible selenium compounds interfered with XPA-DNA binding and released zinc from the zinc finger motif, XPAzf. Zinc release was even evident at high glutathione/oxidised glutathine ratios prevailing under cellular conditions. Finally, comparative studies with metallothionein and XPAzf revealed similar or even accelerated zinc release from XPAzf. Altogether, the results indicate that zinc finger motifs are highly reactive towards oxidizing selenium compounds. This could affect gene expression, DNA repair and, thus, genomic stability.

Animals↗

PubMed1980

Unscheduled DNA synthesis and chromosome aberrations induced by inorganic and organic selenium compounds in the presence of glutathione.

Glutathione strongly enhanced the induction of unscheduled DNA synthesis (UDS) in cultured human cells by inorganic selenium compounds: sodium selenate, sodium selenite and sodium selenide. In the presence of 10(-3) M glutathione, high levels of UDS (74-114 grains per nucleus) were observed in cells treated with (i) selenate at 10(-3) M, (ii) selenite at 10(-5)-3 X 10(-4) 7, and (iii) selenide at 10(-5)-10(-3) M. Glutathione at 10(-3) M also enhanced the clastogenic and cytotoxic effects of selenite and selenate in Chinese hamster ovary (CHO) cells. Glutathione at 10(-4) M or 10(-2) M caused less enhancement of DNA damage and toxicity in both the UDS and chromosome aberration assays. In the absence of glutathione, these inorganic selenium compounds induced low levels of UDS (up to 13 grains per nucleus) and moderate frequencies of chromosome aberrations (up to 11%). 3 organic selenium compounds (selenocystine, selenocystamine and selenomethionine) were also examined for the induction of UDS. No unscheduled DNA synthesis was detected in cells treated with selenocystamine or selenomethione, with or without added glutathione. However, selenocystine alone at 10(-4)-10(-3) M induced a low level of UDS; glutathione enhanced the DNA-damaging effect of selenocystine. The maximum amount of UDS (22 grains/nucleus) occurred in the presence of 10(-2) M glutathione. This was about one-fifth of that detected in cells treated with inorganic selenium compounds and 10-fold lower concentrations of glutathione (10(-3) M). The results suggest that recution is involved in the conversion of selenium compounds to mutagenic forms. The active mutagens may be selenols, GS-Se- from inorganic selenium and R-Se- from organic selenium compounds.

Animals↗

PubMed2003

Induction of the mitochondrial permeability transition by selenium compounds mediated by oxidation of the protein thiol groups and generation of the superoxide.

The cancer chemopreventive effect of selenium compounds cannot be fully explained by the role of selenium as a component of antioxidant enzymes, suggesting that other mechanisms, such as thiol oxidation or free radical generation, also underlie this effect. The toxicities of six different selenium compounds (selenite, selenate, selenocystine, selenocystamine, selenodioxide, and selenomethionine) have now been compared in HepG2 human hepatoma cells and isolated rat liver mitochondria. Selenite, selenocystine, and selenodioxide induced apoptosis in HepG2 cells and mediated oxidation of protein thiol groups in both HepG2 cells and isolated mitochondria. Selenocystamine oxidized protein thiol groups in isolated mitochondria and crude extracts of HepG2 cells but not in intact HepG2 cells, suggesting that this compound is not able to cross the cell membrane. The selenium compounds capable of oxidizing thiol groups also induced the mitochondrial permeability transition (MPT) in isolated mitochondria. Furthermore, they generated the superoxide (O(2) .-) on reaction with glutathione in the presence of mitochondria, and an O(2) .-) scavenger inhibited their induction of the MPT. These results suggest that the pro-apoptotic action of selenium compounds is mediated by both thiol oxidation and the generation of O(2) .-), both of which contribute to opening of the MPT pore.

Cystamine↗

PubMed1991

Multiple use of plants: studies on selenium incorporation in some agricultural species for the production of organic selenium compounds.

The technique of spraying plants with inorganic forms of selenium can be employed for phytochemical production of organic selenium compounds. Fractionation of the plant material makes it possible to produce a highly concentrated and well defined selenium supplement with potential use in animal and human nutrition. The fractionation also gives opportunities to combine production of organic selenium compounds with other products, for example plant fibres. Multiple use of plants can contribute to a more efficient utilization of land area (in comparison to monocultures solely adapted to food production). It also gives the opportunity to develop systems suitable for long term fixation of carbon, as long as the plant material is not reoxidised to carbon dioxide. Plant fibres could provide raw material for the production of paper or building materials in combination with the production of organic selenium compounds preferentially accumulated in another fraction of the processed plant.

Brassica↗

PubMed2006

Genotoxic and antigenotoxic properties of selenium compounds in the in vitro micronucleus assay with human whole blood lymphocytes and TK6 lymphoblastoid cells.

Selenium is known to possess both genotoxic and antigenotoxic properties. In the present study, we have evaluated the genotoxicity and antigenotoxicity of three selenium compounds (sodium selenate, sodium selenite and selenous acid) by measuring in vitro micronucleus induction. Assays were conducted in whole blood lymphocytes and in the TK6 lymphoblastoid cell line, with and without co-treatment with potassium dichromate, a known genotoxic compound. In general, the compounds were more active in TK6 cells than they were in blood lymphocytes. Only 1 microM selenous acid increased the frequency of binucleated cells containing micronuclei (BNMN) in blood lymphocytes, while all three selenium compounds increased BNMN in TK6 cells. In addition, combinations of selenous acid and potassium dichromate resulted in lower frequencies of BNMN than potassium dichromate alone in blood lymphocytes, while combinations of sodium selenate and potassium dichromate produced lower frequencies of BNMN than potassium dichromate alone in TK6 cells. The concentrations of selenium compounds that were used, in combination with the medium components and the biological physiology of the whole blood lymphocytes and TK6 cells, could have affected the redox potential of the compounds, switching the chemicals from a pro-oxidant to antioxidant status and vice-versa. The lower activities of the compounds in blood lymphocytes may be due to the protective effects of blood components. The results indicate that the genotoxic and antigenotoxic properties of selenium compounds are highly dependent upon the conditions under which they are evaluated.

Adult↗

PubMed2000

Speciation of selenium compounds with ion-pair reversed-phase liquid chromatography using inductively coupled plasma mass spectrometry as element-specific detection.

For selenium speciation analysis, the hyphenation of chromatographic separation with element-specific detection has proved a useful technique. A powerful separation system, which is capable of resolving several biologically and environmentally important selenium compounds in a single column, is greatly needed. However, that has been difficult to achieve. In this paper eight selenium compounds, namely, selenite [Se(IV)], selenate [Se(VI)], selenocystine (SeCys), selenourea (SeUr), selenomethionine (SeMet), selenoethionine (SeEt), selenocystamine (SeCM) and trimethylselenonium ion (TMSe+), were separated by using mixed ion-pair reagents containing 2.5 mM sodium 1-butanesulfonate and 8 mM tetramethylammonium hydroxide as a mobile phase. The separation of these anionic, cationic and neutral organic selenium compounds on a LiChrosorb RP18 reversed-phase column took only 18 min at a flow-rate of 1.0 ml/min with isocratic elution, and baseline separation among the six organic Se compounds was achieved. Inductively coupled plasma mass spectrometry (ICP-MS) was employed as element-specific detection. A comparison of ICP-MS signal intensity obtained with a Barbington-type nebulizer and with an ultrasonic nebulizer (USN) was made. Different signal enhancement factors were observed for the various selenium compounds when a USN was used. The speciation technique was successfully applied to the study on chemical forms of selenium in a selenium nutritional supplement. Selenomethionine was found to be the predominant constituent of selenium in the supplement.

Chromatography, High Pressure Liquid↗

PubMed1983

In vitro hemolysis of rat erythrocytes by selenium compounds.

Rat erythrocytes were incubated in vitro with various selenium compounds at 37 degrees. Hemolysis occurred with some selenium compounds but not with corresponding sulfur analogues. Selenite induced more rapid loss of intracellular glutathione (GSH) than did selenocystine but was less hemolytic. Cystine caused neither loss of intracellular GSH nor hemolysis. Addition of GSH to the incubation medium enhanced hemolysis by selenite and selenium dioxide but inhibited hemolysis by selenocystine. Inclusion of glucose in the incubation medium also inhibited selenocystine-induced lysis of erythrocytes from both selenium-supplemented rats and selenium-deficient rats. The results suggest a relationship between the oxidation of intracellular GSH and the hemolysis by selenocystine, selenite and selenium dioxide.

Animals↗

PubMedDate not supplied

The bioavailability of various selenium compounds to a marine wading bird.

The uptake of dietary selenium (about 3.5 mg/kg AF dry wt) as selenomethionine, selenocystine, selenite, selenate, and fish selenium in the plasma and red blood cells (RBC) of the oystercatcher has been investigated. The birds received the various selenium compounds subsequently, for at least 9 wk. After dietary supplementation of selenocystine, selenite, and selenate, plasma selenium was about 350 micrograms/L and RBC selenium 2.1 mg/kg dry wt. After supplementation of selenomethionine, the plasma concentration increased to 630 micrograms/L, and the RBC concentration to 4.1 mg/kg dry wt. When the fodder contained 3.1 mg/kg fish Se, an average plasma and RBC concentration of 415 micrograms/L and 14.4 mg/kg dry wt, respectively, was measured. The maximal increase of the selenium concentration in the plasma was attained at first sampling, 14 d after a change in dietary selenium (selenomethionine or fish Se); the uptake seemed to be a concentration-regulated process. RBC concentrations (Y in mg/kg drug wt) increased with time (X in d) according to Y = a - b e-cX. Fifty percent of the total increase was attained within 17 d, suggesting that diffusion into the RBC played a role. The selenium concentration in the plasma was positively correlated with the (fish)Se concentration in the fodder; the RBC concentration (60 d after the change in diet) was positively correlated with the plasma concentration. When the diet contained fish Se, the blood selenium concentrations of the captive birds were similar to the concentrations measured in field birds. Fish Se is a yet undetermined selenium compound. The present experiment showed that fish Se differed from selenomethionine, selenocystine, selenite, or selenate in uptake from the food and uptake in the RBC.

Animals↗

PubMed1975

Distribution of selenium in egg white and yolk after feeding natural and synthetic selenium compounds.

Practical diets containing various selenium levels, with and without selenite supplementation, were fed to hens. Eggs were then collected over a 14-day period to determine how quickly changes in dietary selenium affected egg white and yolk selenium. Changes in egg white selenium content were rapid and essentially completed seven days after changing the selenium content of a practical diet. Changes in egg yolk were not yet completed by 14 days. When selenium from practical feedstuffs was fed, the selenium content of dried egg white was about equal to or greater than the selenium content of dried egg yolk. When selenite was fed, the selenium content of dried yolk was higher. Feeding selenomethionine resulted in more selenium in egg white than in egg yolk. Feeding selenocystine resulted in more selenium in egg yolk than egg white, a pattern similar to that from feeding selenite. The data suggest that selenocystine is not incorporated into protein but is metabolized to an inorganic selenium compound.

Animal Feed↗

PubMed2004

Selenium compounds modulate the calcium release channel/ryanodine receptor of rabbit skeletal muscle by oxidizing functional thiols.

Selenium compounds, such as sodium selenite and Ebselen were shown to increase high affinity ryanodine binding to the skeletal muscle type ryanodine receptor (RyR1) at nanomolar concentrations, and inhibit the receptor at low micromolar concentrations. This biphasic response was observed in both concentration and time-dependent assays. Extensive washing did not reverse either the stimulation or suppression of receptor binding, but both were prevented or reversed by addition of reduced glutathione, GSH. Selenium compounds were also shown to induce Ca(2+) release from the isolated sarcoplasmic reticulum vesicles. Sodium selenite and Ebselen stimulated the skeletal muscle ryanodine receptor by oxidizing 14 of 47 free thiols per monomer on RyR1 (as detected with the alkylating agent 7-diethylamino-3-(4'-maleimidylphenyl)-4-methylcoumarin) (CPM). Oxidation of the remaining thiols by these selenium compounds resulted in inhibition of the ryanodine receptor.

Animals↗