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PubMed1985

The genotoxicity of selenium.

Selenium at nutritional levels has been shown to have numerous anticarcinogenic or preventative effects against carcinogen-induced breast, colon, liver and skin cancer in animals. Many of these anticarcinogenic effects have been summarized. In addition, numerous mutagenic and antimutagenic effects of selenium compounds have been reported. Some of the selenium compounds frequently tested for mutagenicity are listed in Table 1. Because of the numerous reported anticarcinogenic and preventative effects of selenium, many individuals are supplementing their diets with amounts of selenium that are greater than the recommended daily requirement. Selenium is also used widely in industrial products such as selenium rectifiers, photoelectric batteries, alloys and paints. Because selenium at higher levels is known to be toxic, there should be a greater understanding about its genotoxic as well as its beneficial effect. The object of this review is to summarize experimental evidence both for the antimutagenic and the mutagenic effect of selenium.

Alkylation↗
PubMed1999

Selenium.

The 4 natural oxidation states of selenium are elemental selenium (0), selenide (-2), selenite (+4), and selenate (+6). Inorganic selenate and selenite predominate in water whereas organic selenium compounds (selenomethionine, selenocysteine) are the major selenium species in cereal and in vegetables. The principal applications of selenium include the manufacture of ceramics, glass, photoelectric cells, pigments, rectifiers, semiconductors, and steel as well as use in photography, pharmaceutical production, and rubber vulcanizing. High concentrations of selenium in surface and in ground water usually occur in farm areas where irrigation water drains from soils with high selenium content (Kesterson Reservoir, California) or in lakes receiving condenser cooling water from coal-fired electric power plants (Belews Lake, North Carolina). For the general population, the primary pathway of exposure to selenium is food, followed by water and air. Both selenite and selenate possess substantial bioavailability. However, plants preferentially absorb selenates and convert them to organic compounds. Aquatic organisms (e.g., bivalves) can accumulate and magnify selenium in the food chain. Selenium is an essential component of glutathione peroxidase, which is an important enzyme for processes that protect lipids in polyunsaturated membranes from oxidative degradation. Inadequate concentrations of selenium in the Chinese diet account, at least in part, for the illness called Keshan disease. Selenium deficiency occurs in the geographic areas where Balkan nephropathy appears, but there is no direct evidence that selenium deficiency contributes to the development of this chronic, progressive kidney disease. Several lines of scientific inquiry suggest that an increased risk of cancer occurs as a result of low concentrations of selenium in the diet; however, insufficient evidence exists at the present time to recommend the use of selenium supplements for the prevention of cancer. The toxicity of most forms of selenium is low and the toxicity depends on the chemical form of selenium. The acute ingestion of selenious acid is almost invariably fatal, preceded by stupor, hypotension, and respiratory depression. Chronic selenium poisoning has been reported in China where changes in the hair and nails resulted from excessive environmental exposures to selenium. Garlic odor on the breath is an indication of excessive selenium exposure as a result of the expiration of dimethyl selenide. The US National Toxicology Program lists selenium sulfide as an animal carcinogen, but there is no evidence that other selenium compounds are carcinogens.

Animals↗
PubMed1978

[Convulsive properties of various organoselenium compounds].

Three organo-selenium compounds have been synthetized : methyl seleno-2 benzoic acid, acetylseleno-2 benzoic acid and diselenosalicylic acid. These compounds induce convulsive seizures in the rat, the most active of them being methyl seleno 2 benzoic acid. Convulsions are stopped after anaesthesia with pentobarbitone.

Animals↗
PubMed2004

Effects of selenium-containing compounds and their metabolism in intact rats and in animals with bone fractures.

Blood content of MDA in rats increased 1 and 2 weeks after mandibular bone fracture at stages of cellular fibrous and chondroid callus and decreased 4 weeks after fracture at the stage of primary bone callus. Treatment with Se (intragastrically and electrophoretically) reduced this increase by activating selenium-containing glutathione peroxidase. In order to clear out the relationship between Se and carbohydrate metabolism in different ages, the distribution of Se between the blood and mandibular bone, diaphysis and metaepiphyseal zone of the femoral bone was studied using the bone/blood relative radioactivity coefficient after intraperitoneal injection of [(75)Se]selenate. In control 1-month-old rats the radioactivity had 2 peaks corresponding to 6 and 48 h. The first peak was presumably caused by Se adsorption on hydroxyapatite, the second by chemosorption on hydroxyapatite and protein binding. Only one peak of relative radioactivity (after 12-48 h) was observed in 3-month-old control rats, and it could be increased by sucrose diet. The relative radioactivity was higher in rats receiving sucrose ration for 2 months starting from the age of 1 month in comparison with the control.

Animals↗
PubMedDate not supplied

Further investigation on the radiation induced inactivation of ribonuclease and the radioprotective effect of some selenium-containing compounds.

Steady state inactivation data on dilute aqueous solutions of RNase show that all water radicals, e-aq, OH, and H are responsible for the inactivation, but the most efficient radical is H atom, only about 4 of them being required for one inactivating event. The data are, therefore, more in agreement with the conclusions of Mee et al. (1972). In the transient absorption spectra of pulse irradiated ribonuclease different components derived by the individual radicals are observed. Organic and inorganic selenium-containing compounds offer a great protection of the enzyme activity, in agreement with the data obtained in other chemical and biological systems. In particular the effects of two new secondary radicals (CNSe)-2 and SeO-3 are in good accord with the known structure of ribonuclease.

Kinetics↗
PubMed2006

Diphenyl ditelluride- and methylmercury-induced hyperphosphorilation of the high molecular weight neurofilament subunit is prevented by organoselenium compounds in cerebral cortex of young rats.

Organotellurides are important intermediates in organic synthesis and, consequently, the occupational exposure to them is a constant risk for laboratory workers. These compounds can elicit many neurotoxic events in the central nervous system (CNS) that are associated with several neurological symptoms. In contrast, organoselenium compounds are considered to exert neuroprotective actions on such effects. Neurofilaments (NF) are important cytoskeletal proteins and phosphorylation/dephosphorylation of NF is important to stabilize the cytoskeleton. In this work we investigated the potential protective ability of the selenium compounds ebselen and diphenyl diselenide (PhSe)(2) against the effect of diphenyl ditelluride (PhTe)(2) and methylmercury (MeHg) on the total (phosphorylated plus nonphosphorylated) and phosphorylated immunocontent of the high molecular weight neurofilament subunit (NF-H) from slices of cerebral cortex of 17-day-old rats. We observed that 1muM MeHg induced hyperphosphorylation, increasing the total immunocontent of this subunit of the high-salt Triton insoluble NF-H. Otherwise, 15muM (PhTe)(2) induced hyperphosphorylation of the high-salt Triton insoluble NF-H without altering the total immunocontent of this protein into the cytoskeletal fraction. Concerning the selenium compounds, 15muM (PhSe)(2) and 5muM ebselen did not induce alteration per se on the in vitro phosphorylation of NF-H. In addition, (PhSe)(2) and ebselen at these concentrations, presented a protective effect against the action of (PhTe)(2) and MeHg, on the immunoreactivity of NF-H. Considering that hyperphosphorylation of NF-H is associated with neuronal dysfunction it is probable that the effects of (PhTe)(2) and MeHg could be related to the remarkable neurotoxicity of these organocalcogenides. Furthermore the neuroprotective action of selenium compounds against (PhTe)(2) and MeHg effects could be a promising route to be exploited for a possible treatment of calcogenides poisoning.

Animals↗
PubMed1985

Inhibition of the effects of 12-O-tetradecanoylphorbol-13-acetate on mouse epidermal glutathione peroxidase and ornithine decarboxylase activities by glutathione level-raising agents and selenium-containing compounds.

The present study was undertaken to determine the effect of 12-O-tetradecanoylphorbol-13-acetate (TPA), a potent tumor promoter known to inhibit superoxide dismutase (SOD) (superoxide: superoxide oxidoreductase, EC 1.15.1.1) and catalase (CAT) (H2O2: H2O2 oxidoreductase, EC 1.11.1.6) activities, on mouse epidermal glutathione (GSH) peroxidase (glutathione: H2O2 oxidoreductase, EC 1.11.1.9) activity in vivo and in vitro. TPA led to a rapid and transient increase in GSH peroxidase specific activity within 30 min followed by a decrease from 1 to 12 h. Incubation of isolated epidermal cells with GSH level-raising agents and/or selenium-containing compounds increased remarkably basal GSH peroxidase activity, and thus, abolished totally the prolonged inhibitory effects of TPA on this enzyme. The inhibitory effects of 0.2 mM cysteine (Cys) or 0.5 mM GSH and 2.5 microM Na2 SeO3 or 50 microM selenocystamine on TPA-decreased GSH peroxidase activity were additive, in relation with their additive inhibitory effects on TPA-induced ornithine decarboxylase (ODC) (L-ornithine carboxylase, EC 4.1.1.17) activity. These data support the hypothesis that the stimulators of the GSH-dependent antioxidant protective system of the epidermal cells may inhibit the oxidative challenge linked to skin tumor promotion by TPA.

Animals↗
PubMed1996

Synthesis, Characterization, and Crystal Structures of New Dications Bearing the -Se-Se- Bridge.

Starting from 1,3-dimethyl-4-imidazoline-2-selone (1), 1,2-bis(2-selenoxo-3-methyl-4-imidazolinyl-2-)ethane (3) and 1,3-dimethylimidazolidine-2-selone (4), the following six compounds, [(C(5)H(8)N(2)Se-)(2)](2+).2Br(-) (I), [(C(5)H(8)N(2)Se-)(2)](2+).2I(-) (II), [(C(5)H(8)N(2)Se-)(2)](2+).Cl(-).I(3)(-) (III) [(C(5)H(10)N(2)Se-)(2)](2+).Br(-).IBr(2)(-) (IV), [(C(5)H(7)N(2)Se-)(2)](2+).I(3)(-).(1)/(2)I(4)(-) (V) and [(C(5)H(7)N(2)Se-)(2)](2+).2I(-).CH(3)CN (VI), in which the selenium compounds are oxidized to dications bearing the uncommon -Se-Se- bridge, have been prepared, and I-V crystallographically characterized. I and III were obtained by reacting 1 with IBr and ICl respectively, while II was obtained by reduction of previously described hypervalent selenium compound of 1 (5) bearing the I-Se-I group with elemental tellurium. These three compounds contain the same [(C(5)H(8)N(2)Se-)(2)](2+) dication balanced by two bromides in I, two iodides in II, and Cl(-) and I(3)(-) in III. However, on the basis of the Se-Cl bond length of 2.778(5) Å, III can also be considered as formed by the [(C(5)H(8)N(2)Se-)(2)Cl](+) cation, with I(3)(-) as counterion. Similarly to III, compound IV, which was obtained by reacting 4 with IBr, can be considered as formed by [(C(5)H(10)N(2)Se-)(2)Br](+) cations and IBr(2)(-) anions. As in II, compound V has been prepared by reduction of the hypervalent selenium compound of 3 (6) bearing two I-Se-I groups with elemental tellurium. In V, the [(C(5)H(7)N(2)Se-)(2)](2+) cation is balanced by I(3)(-) and half I(4)(2-) anions. The structural data show that all the cations are very similar, with Se-Se bond lengths ranging from 2.409(2) to 2.440(2) Å. FT-IR and FT-Raman spectra of I-VI allow one to identify two bands around 230 +/- 10 and 193 +/- 5 cm(-1) that are common to all compounds. These bands are generally strong in the FT-Raman and weak in the FT-IR spectra and should contain a contribution of the nu(Se-Se) stretching vibration. The spectra are also in good agreement with the structural features of the polyhalide anions present in the crystals. Crystallographic data are as follows: I is monoclinic, space group P2(1), with a = 9.849(6) Å, b = 11.298(5) Å, c = 7.862(6) Å, beta = 106.44(2) degrees, Z = 2, and R = 0.0362; II is monoclinic, space group P2(1), with a = 8.063(6) Å, b = 11.535(5) Å, c = 10.280(5) Å, beta = 107.13(2) degrees, Z = 2, and R = 0.0429, III is monoclinic, space group P2(1)/n, with a = 10.431(7) Å, b = 18.073(5) Å, c = 11.223(6) Å, beta = 100.76(2) degrees, Z = 4, and R = 0.0490; IV is monoclinic, space group P2(1)/n, with a = 10.298(5) Å, b = 18.428(7) Å, c = 11.475(6) Å, beta = 104.10(4) degrees, Z = 4, and R = 0.0300; V is triclinic, space group P&onemacr;, with a = 7.456(6) Å, b = 11.988(5) Å, c = 12.508(5) Å, alpha = 79.32(2) degrees, beta = 85.49(2) degrees, gamma = 80.62(2) degrees, Z = 2, and R = 0.0340.

Journal Article↗
PubMed2002

Comparison of selenite and selenate apparent absorption and retention in infants using stable isotope methodology.

The inorganic selenium compounds selenite and selenate are used for selenium fortification of infant formulas. However, information on absorption and retention of selenium from these compounds is lacking. The purpose of this study was therefore to determine apparent absorption and retention of selenium from selenate and selenite added to a milk-based infant formula in healthy infants. Labeled test meals were prepared by addition of 10 microg Se as (76)Se-selenate or (74)Se-selenite to 500 mL formula. The two batches of labeled formulas were fed as alternate feeds during the first day of the balance period, followed by unlabeled formula. Selenium isotopes were determined in feces collected for 72h after intake and in 3 consecutive 24h collections of urine. Mean apparent absorption was 97.1% for (76)Se-selenate and 73.4% for (74)Se-selenite; mean difference 23.7% (range: 13.8%-35.7%; SD 6.8%, p < 0.001). Mean urinary excretion (% of ingested dose) was 36.4% ((76)Se-selenate) and 9.7% ((74)Se-selenite); mean difference 26.7% (range: 13.9%-36.5%; SD 5.9%, p < 0.001). Mean apparent retention of selenium from (76)Se-selenate and (74)Se-selenite was not significantly different, 60.7% ((76)Se-selenate) versus 63.7% (for (74)Se-selenite). The average difference was -3.01% (range: -14.0%-12.0%; SD 9.4%, p = 0.36). Although apparent selenium absorption and urinary excretion differed for selenite and selenate, selenium was equally well retained by infants from both selenium compounds. We therefore concluded that Se fortification of infant formulas with selenate or selenite can be expected to have similar impact on the selenium nutritional status of term infants.

Female↗
PubMed1995

Dissociation of the genotoxic and growth inhibitory effects of selenium.

The effects of forms of selenium compounds that enter the cellular selenium metabolic pathway at different points were investigated in a mouse mammary carcinoma cell line. The goal of these experiments was to determine if the genotoxicity of selenium, defined as its ability to induce DNA single-strand breaks, could be dissociated from activities proposed to account for its cancer inhibitory activity. The results demonstrated that growth inhibition, measured as inhibition of cell proliferation and induction of cell death, was induced by all the forms of selenium evaluated. However, sodium selenite and sodium selenide, which are metabolized predominantly to hydrogen selenide, caused the rapid induction of DNA single-strand breaks as an early event that preceded growth inhibition. Interestingly methylselenocyanate and Se-methylselenocysteine, which are initially metabolized predominantly to methylselenol, induced growth inhibition in the absence of DNA single-strand breakage. Differences in the time course of selenium retention, in the occurrence of membrane damage, and in the induction of morphological changes by selenite versus methylselenocyanate were noted. Collectively, these data indicate that different pathways affecting cell proliferation and cell death are induced depending on whether selenium undergoes metabolism predominantly to hydrogen selenide or to methylselenol.

Animals↗
PubMed1999

Active oxygen species generation and cellular damage by additives of parenteral preparations: selenium and sulfhydryl compounds.

We investigated the relationship between active oxygen species (AOS) generation and cultured vascular endothelial cellular damage caused by simultaneous exposure to selenium compounds and sulfhydryl compounds such as cysteine (Cys) or reduced glutathione (GSH). Selenium compounds, selenite, selenate or selenomethionine (SeMet), are added to total parenteral nutrition (TPN) and intravenously administered. We confirmed by luminol dependent chemiluminescence, an indicator of AOS generation, that selenite generates AOS in the presence of clinical concentrations of sulfhydryl compounds, 0.5 mM Cys or 0.5 mM GSH, and that the amount of AOS generated reaches the maximum when their mole ratio is 1:50. However, AOS generation was not observed after simultaneous administration of various concentrations of selenate or SeMet with sulfhydryl compounds. Moreover, simultaneous exposure to 10 microM selenite and sulfhydryl compounds was found to result in significant increases in the [3H]-adenine and lactate dehydrogenase (LDH) release rates from cells, a significant decrease in the amount of cellular protein, and enhancement of cellular damage as compared with after exposure to selenite alone. However, simultaneous exposure to 10 microM selenate or 10 microM SeMet together with sulfhydryl compounds did not induce cellular damage. These findings revealed that selenite generates AOS and causes cellular damage in the presence of sulfhydryl compounds. Accordingly, it seems better to choose selenate or SeMet instead of selenite when a selenium compound is to be added to TPN.

Adenine↗
PubMed2002

Action of 1-(11-selenadodecyl)-glycerol and 1-(11-selenadodecyl)-3-trolox-glycerol against lipid peroxidation.

The antioxidant action on lipid peroxidation of the synthesized selenium compounds 1-(11-selenadodecyl)-glycerol (SeG) and 1-(11-selenadodecyl)-3-Trolox-glycerol (SeTrG, where Trolox = 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid) was investigated. We compared the reactivity of the selenium compounds toward peroxyl radicals and their inhibitory effect on lipid peroxidation, induced by several kinds of initiating species such as azo compounds, metal ions, and superoxide/nitric oxide in solution, micelles, membranes, and rat plasma. SeTrG, but not SeG, scavenged peroxyl radicals. SeG reduced methyl linoleate hydroperoxides in organic solution and in methyl linoleate micelles oxidized by ferrous ion (Fe2+)/ascorbic acid. In rat plasma SeG and SeTrG decreased the formation of lipid hydroperoxides generated by hydrophilic azo compounds. SeG and SeTrG spared alpha-tocopherol (alpha-TOH) consumption in multilamellar vesicle membranes oxidized by hydrophilic or lipophilic initiators, and only SeTrG spared alpha-TOH in superoxide/nitric oxide oxidized membranes. In rat plasma oxidized by radical initiators (either hydrophilic or lipophilic) or superoxide/nitric oxide, SeTrG suppressed alpha-TOH consumption, but SeG had no effect. The two selenium-containing compounds showed inhibitory effects on lipid peroxidation that depended on their structure, the medium where they acted, and the oxidant used.

Animals↗
PubMed2000

A biomechanical and spectroscopic study of bone from rats with selenium deficiency and toxicity.

Selenium, being an essential mineral in the mammalian diet, is important in providing protection against oxidative damage. Numerous in vitro studies of selenium compounds reveal a very high correlation between catalytic activity of selenium compounds and toxicity. The present study was designed to investigate the effects of dietary selenium on the biomechanical properties of bone. New born rats of both sexes were fed with either a control, or a selenium- and vitamin E-deficient, or a selenium-excess and vitamin E-adequate diet. We obtained the stiffness (modulus of elasticity) of bones (femur and tibia) by tensile test for all groups considered. Both the deficient and the excess groups have decreased biomechanical strength with respect to the control group. To support our biomechanical results for both experimental groups, X-ray diffraction analysis and FTIR spectroscopic study were performed on the femurs and tibiae. The X-ray diffraction analysis showed that the intensities of the peak observed at around 2theta degrees = 31.820, in the control femur and tibia are stronger than the intensities of the corresponding peak of two experimental groups. In FTIR spectroscopy, the disappearance and/or reduction of the intensities of some carbonate bands in the two experimental groups indicate that there is a decrease in crystallinity and mineral contents which, together with X-ray diffraction analysis, correlate very well with the biomechanical data.

Animals↗
PubMed1998

[Antagonistic action of organic selenium on lead poisoning].

Ninety white rats were treated with liquid lead acetate. When the concentration of lead in urine was more than (0.81 +/- 0.26) mg/L and blood lead was more than (4.8 +/- 0.33) mg/L, the rats were divided into three groups randomly. The oxygenic damage indicators in serum showed SOD activity decreased and MDA content increased. In one group of lead rats fed with an organic selenium compound (code FCQY) the SOD activities were high and the lipid peroxidation was inhibited compared with controls without selenium supplementation. The lead contents of bone, kidney and liver were measured. The results suggested that the organic selenium compound could interfere with the absorption and accumulation of lead.

Animals↗
PubMed1986

Subcellular distribution of selenium in the liver from rats fed selenium from fish: selenocystine and inorganic selenite.

Four groups of rats of a normal selenium status were given different selenium compounds during a long-term feeding experiment (28 days). The selenium supplementations (per kg diet) were sodium selenite (1 mg), selenocystine (2 mg), and two different concentration levels of selenium from fish (0.1 and 1 mg). Differential pelleting of liver homogenates demonstrated that selenium was present in all the subcellular fractions, with a recovery of 55-60% in the cytosols. Gel permeation high-performance liquid chromatography of the cytosol fractions demonstrated the presence of protein-bound selenium at a molecular weight of 70,000 daltons. The subcellular distributions as well as the protein binding of selenium in the cytosols were identical in all dietary groups. This indicates a similar long-term liver metabolism of the four selenium compounds tested in the rat.

Animals↗
PubMed2005

Enhancement of enzymatic digestion of Antarctic krill and successive extraction of selenium organic compounds by ultrasound treatment.

In a previous work we described the isolation of selenium organic species from Antarctic krill after enzymatic hydrolysis. In this paper we present the results of the influence of ultrasonication on the enzymatic treatment and the successive isolation of selenomethionine. We showed that ultrasound-assisted enzymatic digestion leads to quantitative release of selenium in the soluble fraction and recovery of selenomethionine from the krill protein within a time 2 orders of magnitude shorter. The solubilised sample was analysed by size-exclusion chromatography and the selenomethionine content was quantified by high-performance liquid chromatography-inductively coupled plasma mass spectrometry. In total, 99% of the selenomethionine in the krill hydrolysate was recovered from the chromatographic fractions. It corresponds to 35% of the total selenium content in Antarctic krill. Monitoring by microscopy of the changes in the structure of the krill samples during ultrasonication suggested that the enhancement of the ultrasound-assisted enzymatic reaction was mainly due to decrease of mass transfer limitations. A reference experiment for ultrasound-assisted enzymatic digestion of cell-free protein in a homogeneous system does not exclude direct influence of the ultrasound energy on the enzyme-substrate interaction.

Animals↗
PubMed1995

Selenium in human lactation.

The primary factor determining selenium concentration in human milk is the maternal selenium intake. A significant correlation between selenium in human milk and maternal selenium intake has been reviewed in papers from different regions of the world. Infants fed human milk have higher selenium intake than those fed commercially available formula milk or baby foods. Selenium compounds found in breast milk seem to be more biologically available for infant nutrition than those in formulas. Increased requirements of selenium have been observed in pregnant and lactating women. Supplementation of lactating and pregnant women with different selenium compounds has been assayed, and selenium supplementation of soil and cows has been used to increase the selenium status of children fed infant formula made from cow's milk.

Biological Availability↗