Showing papers on "Selenium published in 1981"

Exclusion of Selenium from Proteins of Selenium-Tolerant Astragalus Species

Abstract: Protein fractions from three selenium-tolerant and three selenium-sensitive Astragalus species, grown in the presence of [75Se]selenate, were analyzed for their selenium content. Though tolerant species are known to accumulate considerably more selenium than do sensitive plants, protein fractions from the three selenium accumulators were found to contain significantly less selenium (0.46 to 0.57 picomoles selenium per milligram protein) than did protein fractions from the three nonaccumulators (4.17 to 5.02 picomoles selenium per milligram protein). Under similar conditions, seedlings of Vigna radiata (L.) Wilczek had taken up selenium (6.31 picomoles selenium per milligram protein) at levels comparable to those observed in the proteins of the nonaccumulator Astragali. These results establish that the ability to tolerate and to circumvent the toxic effects of selenium, characteristic of the accumulator species of Astragalus, is associated with a reduced incorporation of this element into protein.

Prophylaxis of Mammary Neoplasia by Selenium Supplementation in the Initiation and Promotion Phases of Chemical Carcinogenesis

Abstract: The present study was designed to determine the chemopreventive effect of dietary selenium supplementation in the initiation or promotion phase of 7,12-dimethylbenz[a]anthracene-induced mammary carcinogenesis in rats fed a high-fat diet. Control animals received 0.1 ppm of selenium (as sodium selenite), while experimental groups were supplemented with 5 ppm of selenium for various periods of time: -2 to +24, -2 to +2, +2 to +24, +2 to +12, +12 to +24, and -2 to +12. The time of 7,12-dimethylbenz[a]anthracene administration (50 days of age) was taken as Time 0; minus and plus signs represent the time in weeks before and after 7,12-dimethylbenz[a]anthracene administration, respectively. The following conclusions were drawn from the results: ( a ) selenium can inhibit both the initiation and promotion phases of carcinogenesis; ( b ) a continuous intake of selenium is necessary to achieve maximal inhibition of tumorigenesis; ( c ) the inhibitory effect of selenium in the early promotion phase is probably reversible; and ( d ) the efficacy of selenium is attenuated when it is given long after carcinogenic injury. In addition, the present investigation also assessed the effectiveness of selenium in inhibiting the reappearance of mammary tumors that had regressed after ovariectomy. By supplementing tumor-bearing animals with 5 ppm of selenium in the diet immediately after endocrine ablation, it was found that tumors reappeared at a slower rate compared to the controls. The data suggested that selenium is not only effective in chemoprevention but can also be used as an adjuvant chemotherapeutic agent.

Inhibitory Effects of Selenium on the Growth of L1210 Leukemic Cells

Abstract: Selenium has been shown to inhibit L1210 cells both in vitro and in vivo. The death of L1210 cells in vitro as indicated by trypan blue exclusion was dependent upon the form and concentration of selenium tested. Incubation of L1210 cells in buffer containing selenium at 1 µg/ml for 1 hr prior to inoculation into mice significantly retarded the ability of the cells to propagate in vivo. Sodium selenite injected i.p. increased the longevity of mice inoculated with L1210 cells. Administration of 40 µg selenium as sodium selenite daily for 7 days resulted in a 65% increase in longevity of mice inoculated with 105 L1210 cells. Injections of sodium selenite at doses of 40 µg/day or less for 7 days did not significantly alter growth, liver weight, or red and white blood cell counts. The efficacy of selenium therapy was dependent upon the total number of tumor cells given in the initial inoculum. Selenium administration as sodium selenite was shown to be more effective in increasing the longevity of L1210-inoculated mice than was treatment with sodium selenate, selenocystine, or selenomethionine. Sodium selenite treatment at 20, 30, or 40 µg/day in mice inoculated with 102 cells resulted in 50, 80, and 90% cures, respectively. Supplementation of the drinking water with 3 ppm selenium as sodium selenite increased the longevity of L1210-inoculated mice by approximately 30%. Combined therapy with selenium (30 µg/day) and methotrexate resulted in a significantly longer life span of L1210-treated mice than resulted from either compound administered separately.

Mercury and selenium content and chemical form in fish muscle

Abstract: Data on the content, chemical form, and distribution of mercury and selenium in edible muscle are presented for several species of marine and freshwater fish. For most species, 60 to 95% of the total mercury content is present as methylmercury. For all species, 15 to 35% of the total selenium content is in the form of selenate (Se VI). Muscle selenium content does not correlate with the corresponding mercury content. For freshwater and processed (canned) marine samples, 60 to 90% of the total mercury content is water-extractable. On a percentage basis, methylmercury is slightly more extractable than inorganic mercury. For nonprocessed marine samples, only 25 to 45% of the total mercury is water-extractable, inorganic mercury being more extractable than methylmercury. For all species, 55 to 80% of the total selenium content is water-extractable, Se VI is more extractable on a percentage basis than selenite (Se IV) and selenide (Se-II).

Enhancement of Mammary Tumorigenesis by Dietary Selenium Deficiency in Rats with a High Polyunsaturated Fat Intake

Abstract: The effect of selenium depletion on mammary tumorigenesis following dimethylbenz[a]anthracene administration was examined in female Sprague-Dawley rats that were fed different levels and types of fats. Four basal diets deficient in selenium were used: (a) 1% corn oil; (b) 5% corn oil; (c) 25% corn oil; and (d) a high saturated fat diet containing 1% corn oil and 24% hydrogenated coconut oil. The comparable selenium-adequate diets were obtained by adding 0.1 ppm of selenium to each of the basal diets. In animals that received an adequate supplement of selenium, an increase in fat intake was accompanied by an increased tumor incidence when corn oil was used in the diets. A high saturated fat ration, on the other hand, was much less effective in this respect. Only in those rats that were maintained on a high polyunsaturated fat diet (25% corn oil) did selenium depletion result in a further increase in tumor incidence and tumor yield. Such an augmentation was not observed in animals given either a 1 or a 5% corn oil ration or a diet rich in saturated fat. Regardless of selenium status, almost all of the tumors formed were adenocarcinomas. An enhancement of tumorigenesis as a result of selenium deficiency in rats fed the 1% corn oil regimen was detected provided a high dose of dimethylbenz[a]anthracene was used, suggesting that alterations in dimethylbenz[a]anthracene metabolism might be involved under this condition. The antioxidant property of selenium is discussed as a possible mechanism by which selenium protects against tumorigenesis, especially in animals with a high polyunsaturated fat intake.

Oxidation of elemental selenium to selenite by Bacillus megaterium

Abstract: A strain of Bacillus megaterium isolated from soil has been found to oxidize elemental selenium in laboratory cultures to selenite and a trace of selenate (

Adsorption and desorption of selenite and selenate selenium on different soils

Abstract: In the laboratory, we studied the adsorption of selenite and selenate selenium and desorption by sulfate and phosphate in normal, calcareous, high organic carbon saline, and alkali soils. Initial selenium solutions contained 5 to 150 μmole Se/g soil, and desorbing solutions contained 500 μmo

Factors influencing the anticarcinogenic efficacy of selenium in dimethylbenz[a]anthracene-induced mammary tumorigenesis in rats.

Abstract: The present study was designed to investigate the effect of selenium supplementation on dimethylbenz[a]anthracene-induced mammary tumorigenesis in female Sprague-Dawley rats fed either a 5 or 25% corn oil diet, denoted as low fat (LF) or high fat (HF), respectively. Selenium supplementation of LF and HF diets were begun at 21 days of age. In Experiment 1, rats (50 days of age) were given 5 mg of dimethylbenz[a]-anthracene p.o. and were supplemented with 0.1 (adequate level), 0.5, 1.5, and 2.5 ppm of selenium (as sodium selenite) in the diet. The total number of tumors found were as follows (30 rats/group): 26, 23, 19, and 10, respectively, in the LF group; and 65, 66, 41, and 21, respectively, in the HF group. In Experiment 2, rats (50 days of age) were given 10 mg of dimethylbenz[a]anthracene, and selenium was added to the diets at 0.1, 2.5, and 5.0 ppm. Tumor yields were found to be 71, 32, and 15, respectively, in the LF group and 135, 85, and 46, respectively, in the HF group. There was also a trend towards a longer latency period of tumor appearance with selenium supplementation. In conclusion, high dietary selenium levels are able to protect against mammary tumorigenesis, but rats on a HF diet still develop more tumors than those on a LF diet at comparable selenium supplementation.

Biochemical and Clinical Effects of Selenium on Dimethylhydrazine-induced Colon Cancer in Rats

Abstract: The biochemical and clinical effects of selenium (Na2SeO3) on 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in male Sprague-Dawley rats are presented. A 4-ppm selenium supplement to the drinking water was provided before, during, and after 20 weekly injections of 20 mg DMH per kg body weight. Immediately after the 20th DMH injection, part of the rats were sacrificed. The incidences of colon tumors in groups provided selenium before DMH, before and during DMH, and only during DMH treatment were reduced to 39, 43, and 36%, respectively. The incidence in the DMH only control was 63%. Other rats in all treated and control groups were maintained up to 5 months post-DMH treatment. At 10-week intervals throughout the study, selected blood and tissue components were analyzed. The following hematological changes correlated with DMH treatment. (a) Serum glutamic oxalacetic transaminase increased 2-fold (normal, 66 +/- 14 g/dl). (b) Serum alkaline phosphatase increased 24% (normal, 166 +/- 56 units/liter). (c) Serum protein decreased 14% (normal, 6.77 +/- 0.48 g/dl). (d) White blood count increased 2- to 3-fold (normal, 7.7 +/- 2.7 X 10(3)/cu mm). And (e) hemoglobin decreased 67% (normal, 18.1 +/- 1.3 g/dl). The magnitude of these changes varies with each selenium treatment group and with each 10-week analysis period. Provision of 4 ppm selenium doubled both liver and blood selenium levels compared to unsupplemented controls. The effects of selenium and DMH treatments on glutathione peroxidase and beta-glucuronidase activities and on sialic acid are presented. Possible mechanisms by which selenium protects against DMH-induced neoplasia are discussed.

Acute toxicity of sodium selenite and selenomethionine in mice after ICV or IV administration.

Abstract: The acute intracerebroventricular administration of sodium selenite and selenomethionine in conscious mice produced neurotoxicity manifested by hyperreflexia, convulsions and dealth Selenite was 43-fold more toxic than selenomethionine on the basis of LD50 determination The intravenous administration of the selenium compounds resulted in predominantly cardio-respiratory effects, hind limb paralysis and death Selenite was 4-fold more toxic than selenomethionine A comparison of relative toxicity after icv or iv administration revealed that selenite is more toxic than selenomethionine and greater relative toxicity was noted via the icv route This toxicity difference may be attributed to the lack or low level of biotransformation of selenite by the CNS

Chemoprevention of mammary tumorigenesis by a combined regimen of selenium and vitamin A

Abstract: Mammary tumorigenesis induced in rats by 7,12-dimethylbenz[a]anthracene was markedly suppressed by combined dietary supplementation with sodium selenite and retinyl acetate; final tumor yield was reduced to 8% of control as compared with 51% and 36%, respectively, for selenium and retinyl acetate alone. A continuous intake of both agents was necessary to sustain the chemopreventive effect.

Heat Capacity and Other Thermodynamic Properties of Linear Macromolecules. I. Selenium

Abstract: The heat capacity of selenium from 0 K to 1000 K is reviewed using measurements on 20 samples reported in the literature. A set of recommended data for trigonal, monoclinic, glassy, and molten selenium is derived. Ring‐chain equilibrium parameters are critically evaluated. Entropy, enthalpy, and Gibbs energy functions are calculated. Selenium is a model compound for a monoatomic, linear macromolecule. This paper is first in a series which will ultimately cover all heat capacity measurements on linear macromolecules.

Anticarcinogenic effect of selenium in rats treated with dimethylbenz[a]anthracene and fed different levels and types of fat.

Abstract: The present investigation reports the effect of selenium supplementation on 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis in rats fed either a 5% or a 25% corn oil diet. A reduction in tumorigenesis in both groups was observed with 2.5 p.p.m. of dietary selenium. Selenium supplementation also inhibited the development of hyperplastic alveolar nodules in the mammary gland subsequent to DMBA treatment. In addition, the appearance of mammary neoplasia was reduced by selenium in rats fed a high-saturated fat diet (coconut oil), indicating that the type of fat consumed did not influence the antitumorigenic effectiveness of selenium. The lack of a correlation between the anticarciongenic efficacy of selenium and its ability to suppress lipid peroxidation in the mammary tissue of rats fed either a high-saturated fat or a high-unsaturated fat diet suggests that the inhibitory action of selenium is probably not mediated by its antioxidant function in lipid metabolism

Raman and Infrared Spectra of Rhombohedral Selenium

Abstract: Raman and infrared spectra of rhombohedral selenium have been measured and the fundamental bands observed in these spectra are assigned by analogy to the S6 ring molecule. Calculation of the normal mode vibration for the Se6 ring using a modified Urey-Bradley force field confirms this assignment. Anomalous softening of the A1g stretching mode relative to other modes and to the corresponding A1 mode in the Se8 ring was observed. This phenomenon is explained by the idea of interference of inter-molecular interaction with the intra-molecular bonding. Comparison of the observed spectra of rhombohedral selenium with those of other allotropes (α-monoclinic, trigonal, and amorphous selenium) suggests that Se6 ring molecules may exist in amorphous selenium.

Effects of ferrous chloride and iron dextran on lipid peroxidation in vivo in vitamin E and selenium adequate and deficient rats.

Abstract: The effects of intraperitoneally injected ferrous chloride and iron-dextran on lipid peroxidation in vivo were assessed. Peroxidation was esti mated by measuring ethane, a volatile autoxidation product of omega-3-un- saturated fatty acids. Rats supplemented with 0.1 ppm dietary selenium and rats supplemented with 0.1 ppm selenium and 200 IU vitamin E/kg diet were injected with ferrous chloride at 30 mg iron/kg, or with sodium chloride, or left uninjected. In both dietary groups ferrous chloride increased ethane production while sodium chloride did not, but the iron-caused ethane increase was 8 times greater in the low E group. Iron-dextran injected at 500 mg iron/kg was fatal to rats fed a basal diet deficient in selenium and vitamin E or a diet supplemented with 0.5 ppm selenium; supplemental vitamin E at 200 lu/kg diet prevented this mortality. Iron-dextran quadrupled ethane production in rats fed the basal diet and tripled ethane production in rats fed the selenium-supplemented diet. Vita min E supplementation prevented the iron-dextran-caused rise in ethane produc tion. A histological examination of rats killed by iron-dextran showed severe generalized necrosis of the diaphragm and severe focal necrosis of thigh muscle. Vitamin E protected more effectively than selenium against iron-dextran-caused peroxidation as well as against acute iron-dextran-caused mortality. J. Nutr. Ill: 1784-1796, 1981.

Metabolic and functional defects in selenium deficiency

Abstract: This paper is concerned with present-day knowledge of the biological role of selenium, of its interaction with other nutrients including trace elements, and with the importance of selenium in human nutrition and health. Selenium has been shown to be an integral part of glutathione peroxidase, which catalyses the reduction of a large range of lipid hydroperoxides and hydrogen peroxide. The interrelation between vitamin E, selenium and polyunsaturated fatty acids is complex. First, selenium in glutathione peroxidase may control intracellular levels of hydrogen peroxide, which affect the formation of active oxygen metabolites that may serve as initiators of lipid peroxidation; this role of selenium is closely related to that of superoxide dismutases, which control intracellular levels of the superoxide anion. Secondly, vitamin E may control the formation of lipid hydroperoxides through its antioxidant function, as well as possibly entering into a structural relation with membrane phospholipids. Thirdly, glutathione peroxidase may catalyse the reduction of lipid hydroperoxides, formed from membrane lipids, to hydroxyacids without detriment to the cellular economy. In the field of human nutrition, the lack of selenium has been shown to be the cause of a cardiomyopathy known as Keshan disease, occurring in the People's Republic of China. Blood selenium levels in patients from this area are compared with blood selenium levels in three other parts of the world and the conclusion is reached that the blood selenium level of populations in Keshan disease regions are exceptionally low and that Keshan disease is the first demonstration that selenium is an essential trace element for man.

Process for the removal of selenium from aqueous systems

Abstract: A process for reducing the concentration of selenium ions in the Se(VI) oxidation state in an aqueous solution. The aqueous solution is admixed with a quantity of metallic iron. The iron reduces the selenium ions from the Se(VI) oxidation state to a lower oxidation state and then dissolves in the aqueous solution. If the pH level of the aqueous solution is above about 2.3, the selenium ions are reduced to at least the Se(IV) oxidation state and the dissolved metallic iron hydrolyses to form an iron hydroxide that precipitates. The precipitated material is separated from the aqueous solution to provide a solution having a lower concentration of selenium ions. If the pH level of the aqueous solution is below about 2.3, no iron hydrolysis is observed to occur. At least a portion of the selenium in the Se(VI) oxidation state is believed to be reduced to the elemental state. The elemental selenium then is separated from the aqueous solution to provide a solution having a lower concentration of selenium ions.

Blood selenium levels and glutathione-peroxidase activities in university and chronic intravenous hyperalimentation subjects.

Abstract: The purpose of this study was to determine selenium concentration in erythro-cytes and plasma and to compare these values to the measured erythrocyte glutathione-peroxidase activity for a university and a long-term intravenous hyperalimentation (IVH) population. In addition, we wished to determine if these chronic IVH patients were at risk for selenium deficiency. There was a positive correlation (r = 0.67) between erythrocyte selenium levels and erythrocyte glutathione-peroxidase activities in the university population. The patients receiving IVH had significantly lower mean selenium levels in erythro-cytes and plasma and mean glutathione-peroxidase activities than the values from the university population. No correlation existed between erythrocyte selenium levels and erythrocyte glutathione-peroxidase activities in this IVH patient population. These chronic IVH patients when compared with the university population appear to be at risk for selenium deficiency.