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PubMed1983

Induction of retrovirus gene expression by selenium compounds.

Sodium selenite, sodium selenate, selenium oxide, selenophypoxanthine, selenopurine, selenocysteine, selenoethionine and selenomethionine were tested for their ability to induce endogenous retrovirus expression in cultured AKR mouse embryo fibroblasts. All except selenoethionine were highly toxic to the cells. Only selenomethionine however, had the ability to induce virus expression under the conditions used. The level of virus induction (plaque-forming-units/10(5) cells) was roughly proportional to dose over the range of concentrations from 0.25 mM to 5.0 mM. Induction was best observed when a treatment duration of 48 h was used and required the treatment of actively dividing cells. The induction and the cytotoxic effects of selenomethionine could be abrogated by simultaneous treatment with methionine. A ratio of methionine to selenomethionine of 1:10 inhibited induction by approx. 60% while equivalent amounts of methionine inhibited selenomethionine-mediated induction by greater than 96%, indicating that methionine was more efficiently recognized by the cells than was selenomethionine. A possible mechanism for selenomethionine induction involving the production of undermethylated DNA is presented.

Animals↗
PubMed1995

Effects of organic and inorganic selenium compounds on rat mammary tumor cells.

To explore cellular effects of potent organoselenium chemopreventive agents we have used a rat mammary tumor cell line. We demonstrate that 1,4-phenylenebis(methylene) selenocyanate (p-XSC) at a dose of 5 microM is a more potent inhibitor of DNA, RNA and protein synthesis as well as of mitochondrial transmembrane potential than its chemopreventive counterparts benzyl selenocyanate (BSC) and sodium selenite. These differences were also reflected in reduced growth rate by 24 and 48 hr. Cell-cycle and cell-morphology analysis revealed that higher doses of p-XSC (10 microM) caused DNA fragmentation which was accompanied with partial loss of nuclear stainability, whereas BSC caused a noticeable change in cell-cycle distribution and extensive micronucleation. Overall, our results point to cellular targets of selenium compounds which may mediate their chemopreventive activities in mammary tissues.

Animals↗
PubMedDate not supplied

Glutathione peroxidase-like activity of simple selenium compounds. Peroxides and the heterocyclic N-oxide resazurin acting as O-atom donors.

Selenite and selenocystamine [(CyaSe)2] efficiently activate the decomposition of H2O2 by GSH and by other thiols, as demonstrated using a leuco crystal violet POD-based H2O2 assay which is applicable (unlike other assays) also in presence of thiols. The GPx-like activities were estimated to be 3.6 and 2.7 mumol H2O2/min per mumol SeO3(2-) and (CyaSe)2, respectively. Both selenium compounds also activate reduction of the heterocyclic N-oxide resazurin (RN-->O) to resorufin (RN) by GSH; H2O2 competes with reduction of this dye. GSSeH and CyaSeH, formed by interaction of GSH with SeO3(2-) and (CyaSe)2, respectively, are likely to be the active reductants. CyaSeH, generated gamma-radiolytically from (CyaSe)2, exhibits an absorption peak at 243 nm and is removed by H2O2 with a rate constant of 9.7 x 10(2) M-1 s-1, and slightly slower by hydroperoxides. We have no evidence for one-electron interactions between GSSeH or CyaSeH and H2O2, with formation of free radical intermediates, as previously proposed in the case of selenium-activated reduction of cytochrome c by GSH (Levander et al., Biochemistry 23, 4591-4595 (1973)). Our results can be explained by O-atom transfer from the substrate to the active selenol group, RSeH + H2O2 (RN-->O)-->RSeOH + H2O (RN), and recycling of RSeOH to RSeH (+ H2O) by GSH, analogous to the selenenic acid pathway of GPx. The substrate specificity appears to be different, however, in that GPx is unable to catalyse RN-->O reduction, and GSSeH hardly catalyses the decomposition of cumene- or t-butyl-hydroperoxide; CyaSeH, on the other hand, is active also with the hydroperoxides. RN-->O is reduced to RN also by certain oxidizing free radicals, e.g. by the thiyl CyaS.., O-atom transfer may in this case lead to the generation of reactive oxyl radicals.

Catalysis↗
PubMedDate not supplied

Effects of dietary selenium compounds on benzo (a)-pyrene-induced forestomach tumours and whole-blood glutathione peroxidase activities in C3H mice.

Selenium (Se) compounds have shown an inhibitory effect on chemically induced tumours in several laboratory models and there is an inverse epidemiological relationship between Se status and certain types of cancer. Little is known about the influence of Se on the development of stomach cancer. Three different forms of dietary Se, selenomethionine, sodium selenite, and high-selenium yeast were investigated as possible inhibitors of benzo(a)pyrene-induced forestomach tumours in mice. The effects of sodium selenite in combination with vitamin E, and of Se-deficiency were also studied. None of the dietary modifications had any effect on tumour incidence or number. Marked elevations of whole-blood glutathione peroxidase (GSH-Px) activities were observed in animals supplemented with all Se-compounds. High-selenium yeast caused the largest increase of GSH-Px activity followed by sodium selenite and selenomethionine. The results indicate that the inhibitory effect of Se on carcinogenesis may be specific with respect to organ site or tumour cell examined.

Animals↗
PubMed1996

Teratogenic effects of selenium compounds on cultured postimplantation rat embryos.

Embryonic susceptibility to selenium (Se) teratogenicity was examined in rats using postimplantation embryo culture. Rat embryos at day 9.5 of gestation were cultured by the roller bottle method for 48 hr in the presence of Se compounds. Sodium selenite, sodium selenate, seleno-DL-methionine, and seleno-DL-cystine were embryolethal at 20, 300, 1,000, and 1,000 microM Se, respectively. All of these compounds caused abnormalities such as deformed optic vesicle and swollen rhombencephalon in the viable embryos. These abnormalities were considered to correspond to in vivo malformations caused by Se in hamster fetuses or in bird embryos. These results indicate that rat embryos are susceptible to Se teratogenicity. It seems that there are differences in potency ranking of Se compounds between rat and bird embryos.

Abnormalities, Drug-Induced↗
PubMed1988

The influence of dissolved selenium compounds on the accumulation of inorganic and methylated mercury compounds from solution by the mussel Mytilus edulis and the plaice Pleuronectes platessa.

In laboratory experiments, the effects of dissolved selenate and selenite (2 and 200 micrograms Se l-1) on the accumulation of inorganic and methylated mercury (1 microgram l-1) from solution by mussels (Mytilus edulis) and plaice (Pleuronectes platessa) have been studied. In mussels, selenate, and to a lesser extent selenite, markedly reduced the accumulation of inorganic mercury in gills, mantle, kidney and digestive gland. Selenate at 2 micrograms Se l-1 inhibited methylmercury accumulation in most organs, but the same effect was not observed at 200 micrograms l-1. Selenite had little effect on methylmercury accumulation. In plaice, selenate (2 and 200 micrograms l-1) and selenite (200 micrograms l-1) enhanced the accumulation of inorganic mercury in muscle only, but neither compound had any effect on the accumulation of methylated mercury.

Animals↗
PubMed1991

Effect of selenium compounds and thiols on human mammary tumor cells.

The effect on cell viability and growth rate of sodium selenite, selenocystine, sodium selenate, and selenomethionine at selenium concentrations of 6.25 and 12.5 uM was studied in vitro on cells of the human mammary tumor cell line HTB123/DU4475. Selenite and selenocystine affected both cell viability and growth rate of the tumor cells at these selenium concentrations. Selenite and selenocystine decreased intracellular glutathione concentrations, but did not affect tumor cell glutathione peroxidase activity. After six days of exposure to either selenate or selenomethionine, the viability of tumor cells remained stable, but cell growth, as measured by numbers of cells, was retarded. Neither selenate nor selenomethionine produced changes in concentrations of intracellular glutathione. The toxic effect of selenite on tumor cells was enhanced by addition of 0.25 mM glutathione to the growth medium. Preincubation of the tumor cells with 62.5 uM buthionine sulfoximine decreased cellular glutathione to 15% of controls at 24 h and enhanced the toxicity of selenite toward the tumor cells. Glutathione, 2-mercaptoethanol, and L-cysteine were all toxic to the tumor cells in a dose-dependent manner.

Aged↗
PubMed1995

Toxicity studies of a new selenium compound, Selol, in rats.

Selol is a new organoselenium compound synthesized in the Department of Drug Analysis, Warsaw. The general acute and cumulative toxicities of Selol were tested in rats. The compound did not display any toxic effects after parenteral administration up to 500 mg/kg-1 s.c. and 100 mg/kg-1 i.p. However, given orally it exhibited high toxicity. LD50 value after a single oral administration amounted to 100 mg/kg-1 and after administration in an increasing-dose schedule to 80 mg/kg-1. On the basis of these results the authors conclude that Selol may be converted to a more toxic product during digestion. Therefore, Selol as a source of selenium is safer given by the parenteral route.

Administration, Oral↗
PubMed1993

Kinetics of glucose oxidase catalyzed electron transfer mediated by sulfur and selenium compounds.

Unusually high electron transfer rates in Aspergillus niger glucose oxidase catalyzed oxidation of glucose using 5,6:11,12-Bis(dithio)tetracene (TTT), 1,2-dimethyltetraselenafulvalene (DMTSF) and tetrathiafulvalene (TTF) were observed. At pH 7.0 oxidation rate constants (TN/Km) in the range from 1.0.10(7) to 8.7.10(7) M.s-1 were deduced from experimental data. One of the investigated mediators, DMTSF, has been used for electrocatalytical glucose oxidation on graphite at a potential of 0.3 V vs. a standard calomel electrode (SCE). The prepared bioelectrodes have a sensitivity of 1.3 microA/(cm2.mM), a pH optimum at 6.5-7.0, and a linear range which covers the relevant range for monitoring physiological levels of glucose. The bioelectrodes are stable for more than one month.

Aspergillus niger↗
PubMed1993

Generation of reactive oxygen species from the reaction of selenium compounds with thiols and mammary tumor cells.

Sodium selenite, sodium selenate, selenocystine and selenomethionine were tested for their abilities to generate superoxide by the oxidation of glutathione and other thiols in the absence and presence of cells of the human mammary tumor cell line HTB123/DU4475. Free radical generation was measured by lucigenin- or luminol-amplified chemiluminescence. In the absence of tumor cells, lucigenin-dependent chemiluminescence was observed from the reaction of selenite with the thiols glutathione, 2-mercaptoethanol and L-cysteine, but not with oxidized glutathione. Superoxide dismutase, catalase, and glutathione peroxidase all suppressed the observed chemiluminescence; but when these enzymes were heat inactivated they had little suppressive inhibition on chemiluminescence. Luminol-dependent chemiluminescence from the reaction of selenite with glutathione was much less than that observed by lucigenin-amplified chemiluminescence. In the presence of the HTB123/DU4475 mammary tumor cells, lucigenin-dependent chemiluminescence was observed from the reactions of selenite and selenocystine with glutathione which were 5 and 23 times greater than their respective reactions with glutathione in the absence of tumor cells. The enhanced chemiluminescence generated by selenite and selenocystine in the presence of the tumor cells was also suppressed by superoxide dismutase, catalase and glutathione peroxidase. These data suggest that a free radical, the superoxide anion (O2-), and H2O2 are produced from the reaction of selenite and selenocystine with glutathione. These free radical reactions may account for the toxicity of selenite and selenocystine in vitro in comparison to a near absence of acute tumor cell toxicity and superoxide generation by selenate and selenomethionine with thiols. Enhanced chemiluminescence in the presence of tumor cells may be an expression of cellular selenium metabolism and the capability of cells to form selenium metabolites that more easily oxidize glutathione and other thiols producing reactive free radicals and peroxides.

Catalase↗
PubMed1986

Selenium compounds in the fathead minnow (Pimephales promelas)--I. Uptake, distribution, and elimination of orally administered selenate, selenite and l-selenomethionine.

Treatment of fathead minnows (Pimephales promelas) with either [75Se]selenate, -selenite or -l-selenomethionine by gavage at 20 ng Se/g resulted in organ uptake and early distribution patterns which differed significantly between compounds. The greatest differences in uptake between compounds was observed in liver tissue which accumulated much less [75Se]selenate than either selenite or l-selenomethionine. The 75Se burdens and relative distribution among the various organs were nearly identical during the elimination phase for [75Se]selenate and -selenite. This suggests that selenium derived from these compounds converge to a common metabolic pool. The whole body T1/2, rate of 75Se uptake and magnitude of 75Se accumulation were generally greater for [75Se]selenomethionine than the inorganic forms. Selenium-75 was present in the bile following the oral administration of each compound. The partitioning of selenate and selenite into the plasma and cellular fraction of blood differs with both the compound and time following exposure.

Animals↗
PubMed1975

Biological potency of organic selenium compounds: VI. Aliphatic seleninic acids and carboxyselenic acids.

Straight-chain aliphatic seleninic acids, CH3-(CH2)n-SeOOH, with chain lengths from C4 to C17, a few dibasic acids of moderate chain length having seleninic acid groups on both ends of the molecule, HOOSe-(CH2)n-SeOOH, and a series of carbosyseleninic acids, HOOC-R-SeOOH, comprising chain lengths from C3 to C13 and several branched chains with 5 to 7 carbon atoms were tested for potency in the prevention of dietary liver necrosis in the rat. Alkylseleninic acids showed uniformly low activities, ranging from 18% to 56% of that of selenite selenium which served as a standard. There were no discernible trends or regularities with increasing chain lengths, in c-ntrast to other series of alkylselenium compounds. It is therefore unlikely that alkylseleninic acids are normal oxidation products of dialkyl mono- or diselenides in the organism. Compounds with seleninic acid groups at both ends of the chain were practically inactive. Carboxyseleninic acids carrying a carboxyl group distal to the seleninic acid group, on the other hand, were highly effective. A maximum of potency occurred at chain lengths C3 and C4, followed by a sharp decline between C4 and C6. A second maximum of activity occurred at C8. There was no alternating effect. This structure/activity pattern is analogous to that of the diselenodicarboxylic acids. However, the lower carboxyseleninic acids were, per atom of selenium, twice as active as the corresponding diseleno-dicarboxylic acids, of which the higher members were less potent. It is inferred that carboxyseleninic acids may be metabolically related to diseleno-dicarboxylic acids and that C3 and C4 carboxyseleninic acids may play a physiological role.

Animals↗