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PubMed1981

Selenocystine-resistant mutants of Histoplasma capsulatum.

Cysteine metabolism has been thought to be important to the phenomenon of dimorphism in Histoplasma capsulatum. We sought mutants with genetic blocks in the metabolism of cysteine by selection of colonies resistant to the toxic analogue, selenocystine. The 22 resistant strains thus obtained were all deficient in uptake of cystine from the surrounding medium but were normally able to convert from mycelium to yeast and back again. Furthermore, they had normal quantities of NADH-dependent cystine reductase when this enzyme was measured. We conclude that mutants defective in cystine uptake can be readily obtained by selection of colonies resistant to selenocystine, and that a lesion in cystine-uptake does not appear to affect the phenomenon of dimorphism in this organism.

Cystine↗
PubMed1993

Accumulation of unsulphated precursors in Dictyostelium discoideum during selenate inhibition of growth.

Incubation of Dictyostelium discoideum cells with selenate is known to inhibit vegetative growth. In this paper we show that in the presence of selenate macromolecules accumulate which can be converted to sulphated products once the selenate is removed. The presence of cycloheximide, an inhibitor of protein synthesis, during the subsequent incubation does not prevent this conversion but tunicamycin, an inhibitor of glycosylation does. It is concluded that, in the presence of selenate, precursors accumulate as unglycosylated proteins, suggesting that feedback inhibition of glycosylation may be operated.

Animals↗
PubMedDate not supplied

The toxicity and bioaccumulation of selenate, selenite and seleno-L-methionine in the cyanobacterium Anabaena flos-aquae.

A laboratory investigation was conducted to study the toxicity and bioaccumulation of seleno-L-methionine, selenate and selenite in the cyanobacterium Anabaena flos-aquae. The first sub-lethal effects of seleno-L-methionine, selenite and selenate occurred at 0.1, 3.0, and 3.0 mg/L, respectively with a decrease in chlorophyll a concentration (P less than 0.0001). Selenium bioconcentration factors (BCF) were in the order of seleno-L-methionine, selenite, and selenate. Significant decreases in intracellular selenium concentration were observed at both the no effect (NOEL) and low effect levels (LOEL) at each oxidation state tested in the given experiment (p less than 0.0001). Mechanisms for the assimilation, toxicity and regulation of selenium are presented.

Cyanobacteria↗
PubMed1987

A study of selenate efflux from human placental microvillus membrane vesicles.

Selenate efflux from human placental brush border membrane vesicles was studied using an ion-exchange column assay. Selenate efflux was found to be mediated almost exclusively by a temperature dependent DIDS-sensitive pathway. Chromate markedly inhibited selenate efflux: in contrast medium selenate had no effect. It is concluded that selenate and sulphate share a common pathway for transport across the human placental microvillus membrane.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1985

Limits on asymmetric orthopositronium formation in high Z optically active molecules.

The proposed connection between the parity violating handedness of beta particles in radioactive decay and the sign (L) of biological chirality (the Vester-Ulbricht [V-U] hypothesis) is experimentally tested. The theoretically predicted asymmetry in triplet positronium formation (Aps) is measured in several high Z optically active molecules using low energy positrons with a net helicity. We find Aps less than 3 X 10(-4) in selenocystine (Z = 34) and thyroxine (Z = 53), excluding part of the theoretically predicted range of 4 X 10(-3) greater than Aps greater than 2 X 10(-6) in these molecules. The connection between these limits and limits on asymmetric radiolysis (AR) is made, with a new limit of AR greater than 10(-9) being placed. This limit on AR, which is thirty times lower than a previous measurement in the amino acid leucine (Z = 6), is still not small enough to rule out the V-U hypothesis. rule out the V-U hypothesis.

Cystine↗
PubMed1991

Mitogenic activity of selenoorganic compounds in human peripheral blood leukocytes.

A variety of organoselenium compounds were originally described as antiinflammatory, antioxidant or glutathione-peroxidase-like agents, and as inhibitors of prostaglandin and leukotriene synthesis. Recently, the compounds have also been found to be inducers of interferon gamma and tumor necrosis factor in human peripheral blood leukocytes (PBL). We evaluated the effects of bis [2-(N-phenylcarboxamido)phenyl] diselenide and Ebselen; 2-phenyl-1,2-benzisoselenazol-3(2H)one, on the incorporation of tritiated thymidine into the DNA of PBL cultured in vitro. Both compounds were mitogenic and this effect was correlated with the expression of interleukin 2 receptor in T-lymphocytes. Therefore, we suggest that the selenoorganic compounds may induce mitogenic cytokines.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Sex-linked, androgen-dependent differences in renal retention of trimethylselenonium ions.

The metabolism of trimethylselenonium ions (TMSe) was studied in male and female rats during maturation. Selenium (Se) retention in the whole body as well as in organs was found to be significantly higher in male rats than in female a few hours after parenteral administration of TMSe. The pronounced Se accumulation was observed in male kidneys. This sex-linked difference was dependent on the presence of gonads and started to be manifested with sexual maturation during the third decade of postnatal life. The effects of steroid hormones on the retention of Se from TMSe were examined in female and castrated male rats. The results indicate that TMSe metabolism in rat kidneys may be influenced by androgen steroids.

Animals↗
PubMedDate not supplied

Nuclear all-trans retinoic acid receptors: in vitro effects of selenium.

The present study was undertaken to investigate the effects of selenite (SeIV) and selenate (SeVI) on the all-trans retinoic acid (RA)-nuclear retinoic acid receptor (RAR) complex formation in rat liver. We also present the data on the in vitro effects of SeIV on the RARalpha and the type I iodothyronine 5'-deiodinase gene expression in the GH4C1 rat pituitary tumor cells. SeIV at 1.0 micromol/L was found to reduce (p < 0.05) the RA specific binding to RAR in rat liver. Dithiothreitol (DTT), a protective agent for sulfhydryl groups, was found to be slightly effective in protecting the RAR binding properties when affected by SeIV. SeVI at 0.1 micromol/L reduced (p < 0.05) the RA specific binding to RAR in liver, as well. Seleno-L-methionine (Se-II) when compared to L-methionine did not exert any inhibitory effect on the formation of the RA-RAR complex. SeIV (up to 2.5 micromol/L) has no inhibitory effect on GH4C1 cell proliferation as well as the prolactin secretion. SeIV at 1.0 micromol/L significantly decreases the rate of mRNA synthesis and/or degradation of the alpha form of the RAR and causes the enhancement of the type I iodothyronine 5'-deiodinase gene expression in GH4C1 cells. The results based on in vitro experiments suggest that inorganic selenium may affect the RA specific binding to their cognate receptor molecules, and it may reduce expression of the gene encoding the RARalpha, with the cell vitality and the cell growth remaining unchanged.

Animals↗
PubMed1990

An interaction between selenate and a sulfate transporter in the lactating rat mammary gland.

The efficacy of selenate and other divalent anions to stimulate the efflux of radiolabeled sulfate from lactating rat mammary tissue slices has been examined. Both selenate and sulfate markedly increased the fractional release of sulfate via a system that is temperature-sensitive and sensitive to the anion-exchange inhibitor DIDS. The effect of selenate on sulfate efflux was saturable with an apparent affinity constant of approximately 0.27 mM. In addition, molybdate and thiosulfate were also found to increase sulfate efflux from the trans-aspect. It is concluded that sulfate and selenate share a pathway for transport in the lactating rat mammary gland.

Animals↗
PubMedDate not supplied

Effect of selenite and selenate on rat liver nuclear 3,5,3'-triiodothyronine (T3) receptor.

The present study was undertaken to investigate the effects of selenite (SeIV) or selenate (SeVI) on nuclear T3 receptors of rat liver. Selenite at 0.1 microM (p < 0.01) inhibited the T3 specific binding to rat liver nuclear receptors. The specific binding of the T3 receptor was fully restored when even 1.0 microM selenite was separated from the T3 receptor by gel filtration. No inhibitory effect of selenite (up to 100 microM) on the T3 binding to nuclear receptor was found in the presence of 1.0 mM dithiothreitol. The rate of dissociation of the T3-nuclear receptor complex was effectively increased by 0.1 microM selenite. Selenate up to 1 mM as well as sulfite or sulfate up to 0.1 mM did not exert an inhibitory effect on T3 receptors. The results based on the in vitro experiments suggest that the selenium in the form of selenite may reversibly affect the T3 binding on the receptor molecule.

Animals↗
PubMed2000

Selenium: an insulin-mimetic.

Insulin or agents that can mimic its action (insulin-mimetics) are necessary to promote the entry of glucose into tissues where the glucose can either be converted into energy or stored for later use. In recent years, selenium has been shown to mediate a number of insulin-like actions both in vivo and in vitro. These insulin-like actions include stimulating glucose uptake and regulating metabolic processes such as glycolysis, gluconeogenesis, fatty acid synthesis and the pentose phosphate pathway. The mechanism by which selenium is capable of mimicking insulin is not clear; however, reports indicate that selenium does activate key proteins involved in the insulin-signal cascade. Various proteins in the insulin-signal cascade have been shown to be necessary for different insulin-regulated events, and presumably data will be forthcoming soon that illustrate this similarly for selenium. This review compares the action of selenium to that of insulin and discusses the available evidence in support of selenium as an insulin-mimetic.

Animals↗
PubMed2004

Selenium and selenoproteins in mammals: extraordinary, essential, enigmatic.

Selenium (Se), once known only for its potential toxicity, is now well established as an essential trace element for mammals. Insufficient Se intake predisposes to and manifests in a variety of diseases. Recent studies have proven that it is the synthesis of selenocysteine (Sec)-containing proteins, designated selenoproteins, which represents an essential prerequisite for regular development and a long and healthy life. New transgenic mouse models analysing those selenoproteins with proven enzymatic functions displayed particular phenotypes and highlighted essential Se-dependent processes in development, growth or against specific challenges. While there is a growing molecular understanding of and general agreement on the importance of sufficiently high Se intake and undisturbed selenoprotein biosynthesis, many of the recently identified selenoproteins are still uncharacterised, and the effects and consequences of supra-physiological Se dosages are not biochemically understood. With the recent definition of the human and mouse selenoproteomes and a growing number of available tools, the Se field is now geared for a great leap forward. Se biology has already broadened our knowledge about the genetic code and about protein translation. It now holds great promises also for a better understanding of some key aspects of cancer, inflammation, fertility and prevention of age-associated diseases.

Animals↗
PubMed2006

Effects of selenium on radiation responses of tumor cells and tissue.

PURPOSE: This review summarizes information about modulation of radiation effects in tumor cells and tissues by selenium. RESULTS: In vitro, clonogenic survival to ionizing radiation was found to be reduced, depending on selenite concentration and duration of administration, by a factor of 1.5-4.4. In experimental animal tumors, a positive effect of selenium was observed with chemotherapy. The only available study in combination with irradiation did not show any benefit of selenium with clinically relevant radiotherapy protocols in R1H tumors. None of the investigations demonstrated a negative effect on the tumor response to therapy. CONCLUSION: The only study with fractionated irradiation was performed in a rat R1H tumor, which does not show accelerated repopulation. Therefore, interaction of selenium with such repopulation processes, potentially resulting in increased tumor tolerance, could not be detected. For local administration of normal tissues with selenium, potential tumor effects may be of less importance, but these may be relevant for systemic administration. Therefore, well-designed studies with relevant tumor models and endpoints, and with clinically relevant fractionation protocols are recommended.

Animals↗