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PubMed1991

Selenium: inhibition of microtubule formation and interaction with tubulin.

We have studied the interaction of Na2SeO3 with microtubule proteins and tubulin. This selenium compound inhibits the polymerization of MTP (half-inhibition occurred for Na2SeO3 10 microM), and to a lesser that of tubulin. This effect of selenite is related to the formation of disulfide bridges between tubulin sulfhydryl groups, inducing a conformational change of the protein. This is corroborated by the modified binding of colchicine and vinblastine in presence of selenium. The selenite inhibitory concentrations are similar to the toxic blood levels of selenium (40 microM).

Animals↗

PubMedDate not supplied

Selenium. Preclinical studies of anticancer therapeutic potential.

Selenium is a trace element that is essential to the human diet. Deficiency states have been described in both animals and humans. In addition, selenium compounds have demonstrated toxicity in humans, as well as in human tissues in culture. As early as 1956, one form of selenium was used as an antineoplastic agent in humans with some demonstrated activity. Recently, evidence in both tumor-bearing animals and human tumor cells in culture have confirmed an antitumor effect of potential clinical benefit. The mechanism of this cytoxic effect appears, at least in part, to relate to the property of some forms of selenium to oxidize critical sulfhydral groups in the cell. Evidence for this, and the resulting implications for the use of selenium in anticancer treatment, is presented in this manuscript.

Antineoplastic Agents↗

PubMedDate not supplied

Report on the 1986 A.S.P.E.N. Research Workshop on selenium in clinical nutrition.

Selenium in human nutrition was the theme of the 1986 Research Workshop of the American Society for Parenteral and Enteral Nutrition. At the workshop, evidence for the nutritional essentiality of selenium to humans was reviewed, and it was concluded that Keshan disease, the cardiomyopathy of children and young women described in China, is now firmly linked to selenium deficiency, although other factors may be involved. Selenium metabolism and techniques for assessing selenium status also received attention at the workshop. A measurement of blood selenium levels was accepted, in general, as a valid technique for assessing selenium status in individuals with relatively constant selenium intakes. Clinical practitioners at the workshop reported that some of their total parenteral nutrition patients not receiving selenium presented biochemical evidence of selenium deficiency, but no characteristic clinical syndrome due to selenium deficiency has yet been observed in such patients. The workshop attendees acknowledged the need for an official guideline for selenium use in total parenteral nutrition, but were unable to develop a consensus regarding such a guideline. However, the workshop agreed that any guideline established in the future should specify the type of patients to be supplemented, the dose of selenium to be administered, and the selenium compound to be used. Until that time, the physician supervising the therapy must assume responsibility both for determining the need for selenium supplementation, and for the administration of the supplemental selenium.

Adult↗

PubMed1984

Comparison of cytotoxicity of mercury-selenium and mercury compounds on cultured cells.

In vitro effects of mercury-selenium (Hg-Se) compounds, as compared with their original mercury compounds, against growth and viability of HeLa cells were studied. A water-soluble, ethanol-insoluble black complex (GX) formed from HgCl2, Na2SeO3 and GSH was less toxic than HgCl2, but the cytotoxicity of bis(methylmercuric) selenide (BMS) seemed to be similar to that of methylmercury. This may be due to the instability of BMS; i.e., there is a possibility that BMS decomposed to methylmercury and selenium under our culture conditions.

Cell Survival↗

PubMed1982

Selenocysteine lyase, a novel enzyme that specifically acts on selenocysteine. Mammalian distribution and purification and properties of pig liver enzyme.

We have found a novel enzyme that exclusively decomposes L-selenocysteine into L-alanine and H2Se in various mammalian tissues, and have named it selenocysteine lyase. The enzyme from pig liver has been purified to homogeneity. It has a molecular weight of approximately 85,000, and contains pyridoxal 5'-phosphate as a coenzyme. Its maximum reactivity is at about pH 9.0. Balance studies showed that 1 mol of selenocysteine is converted to equimolar amounts of alanine and H2Se. The following amino acids are insert: L-cysteine, L-serine, L-cysteine sulfinate, selenocysteamine, Se-ethyl-DL-selenocysteine, and L-selenohomocysteine. L-Cysteine (Ki, 1.0 mM) competes with L-selenocysteine (Km, 0.83 mM) to inhibit the enzyme reaction. The enzyme is the first proven enzyme that specifically acts on selenium compounds.

Animals↗

PubMed2000

A method for measuring disulfide reduction by cultured mammalian cells: relative contributions of glutathione-dependent and glutathione-independent mechanisms.

A method is described for measuring bioreduction of hydroxyethyl disulfide (HEDS) or alpha-lipoate by human A549 lung, MCF7 mammary, and DU145 prostate carcinomas as well as rodent tumor cells in vitro. Reduction of HEDS or alpha-lipoate was measured by removing aliquots of the glucose-containing media and measuring the reduced thiol with DTNB (Ellman's reagent). Addition of DTNB to cells followed by disulfide addition directly measures the formation of newly reduced thiol. A549 cells exhibit the highest capacity to reduce alpha-lipoate, while Q7 rat hepatoma cells show the highest rate of HEDS reduction. Millimolar quantities of reduced thiol are produced for both substrates. Oxidized dithiothreitol and cystamine were reduced to a lesser degree. DTNB, glutathione disulfide, and cystine were only marginally reduced by the cell cultures. Glucose-6-phosphate deficient CHO cells (E89) do not reduce alpha-lipoate and reduce HEDS at a much slower rate compared to wild-type CHO-K1 cells. Depletion of glutathione prevents the reduction of HEDS. The depletion of glutathione inhibited reduction of alpha-lipoate by 25% and HEDS by 50% in A549 cells, while GSH depletion did not inhibit alpha-lipoate reduction in Q7 cells but completely blocked HEDS reduction. These data suggest that the relative participation of the thioltransferase (glutaredoxin) and thioredoxin systems in overall cellular disulfide reduction is cell line specific. The effects of various inhibitors of the thiol-disulfide oxidoreductase enzymes (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), arsenite, and phenylarsine oxide) support this conclusion.

Animals↗

PubMed1985

Effect of ascorbic acid supplementation on selenium bioavailability in humans.

The study was designed to investigate the effect of supplemental ascorbic acid on the bioavailability of selenium (Se) in humans by using plasma Se levels and plasma glutathione peroxidase (GSH-Px) activity as indicators of the body Se status. Three groups of female university students were supplemented for 4 weeks with either 50 micrograms sodium selenate, 50 micrograms sodium selenate together with 200 mg ascorbic acid, or with 200 mg ascorbic acid three times daily during meals. Plasma Se levels increased significantly (P less than 0.01) in all three groups regardless of the type of supplementation. The increase was highest in the group having both Se and ascorbic acid and smallest in the group receiving only ascorbic acid. The changes in plasma GSH-Px activities reflected those in plasma Se, but the increases were smaller (P less than 0.05). These results suggest that supplemental ascorbic acid may have a beneficial effect on the bioavailability of the natural Se in foods. However, ascorbic acid did not seem to affect the availability of the supplemental sodium selenate. Therefore, the effect of ascorbic acid on the bioavailability of selenium may vary depending on the ingested selenium compound.

Adult↗

PubMed1984

[Dynamics of changes in the electroretinogram of isolated frog and turtle retinas during rhythmic photic stimulation in conditions of induced lipid peroxidation].

Comparative study of isolated retinas of frogs and turtles exposed to rhythmical photostimulation was conducted. It was shown that there are marked differences between the responses of isolated retinas of frogs and turtles to the rhythmical photostimulation. A considerable depression of the total amplitude of the rhythmical electroretinogram was observed under the conditions of induced lipid peroxidation. Introduction of a selenium compound to the superfusing medium increased to a certain extent both the single and rhythmical responses of isolated retinas of the animals.

Animals↗

PubMed1998

Rheumatoid arthritis and metal compounds--perspectives on the role of oxygen radical detoxification.

Rheumatoid arthritis (RA) is characterised by migration of activated phagocytes and other leukocytes into synovial and periarticular tissue. Activated oxygen species and other mediating substances from triggered phagocytes appear to exacerbate and perpetuate the rheumatoid condition. Iron excesses are capable of aggravating the arthritic inflammation, probably through their pro-oxidant potentials. In contrast, therapeutically given gold salts, through a lysosomal loading of the metal, inhibit the triggered cells, thereby reducing the toxic oxygen production. Pharmacological doses of zinc also may immobilise macrophages. Furthermore, the copper-zinc-containing enzyme SOD (superoxide dismutase) can act as a scavenger of toxic oxygen in the tissues. Therapeutic remission of RA has been obtained following intraarticular administration of SOD. Intramuscular administration of copper complexes has induced remission in about 60% of RA patients in open studies. Another drug, penicillamine, that protects cellular membranes against toxic oxygen in vitro, is presumed to act as an antirheumatic via the SOD mimetic activity of its copper complex. Thiomalate and other thiols may possess similar activities. Selenium compounds also may act as oxygen radical scavengers. A significant alleviation of articular pain and morning stiffness was obtained following selenium and vitamin E supplementation in a double-blind study on RA patients. The observations reviewed here indicate that metal compounds and other antioxidants can reduce the rheumatic inflammation by reducing the cellular production and/or concentration of toxic oxygen species.

Arthritis, Rheumatoid↗

PubMed1992

Selenodiglutathione is a highly efficient oxidant of reduced thioredoxin and a substrate for mammalian thioredoxin reductase.

Selenium compounds like selenite (SeO3(2-) may form a covalent adduct with glutathione (GSH) in the form of selenodiglutathione (GS-Se-SG), which is assumed to be important in the metabolism of selenium. We have isolated GS-Se-SG and studied its reactions with NADPH and thioredoxin reductase from calf thymus or with thioredoxin reductase and thioredoxin from Escherichia coli. Incubation of 0.1 microM calf thymus thioredoxin reductase or 0.1 microM thioredoxin reductase and 1 microM thioredoxin from E. coli with 5, 10, or 20 microM GS-Se-SG resulted in a fast initial reaction, followed by a large and continued oxidation of NADPH. However, anaerobic incubation of 0.1 microM calf thymus thioredoxin reductase and 20 microM GS-Se-SG resulted only in oxidation of a stoichiometric amount of NADPH; admission of oxygen started continuous NADPH oxidation. Contrary to the mammalian enzyme, GS-Se-SG was not a substrate for thioredoxin reductase from E. coli. The rate of the oxygen-dependent reaction between calf thymus thioredoxin reductase and GS-Se-SG was increased 2-fold in the presence of 4 mM GSH, indicating that HSe- was the reactive intermediate. Glutathione reductase from rat liver reduced GS-Se-SG with a very slow continued oxidation of NADPH, and the presence of the enzyme did not affect the oxygen-dependent nonstoichiometric oxidation of NADPH by GS-Se-SG and thioredoxin reductase. Fluorescence spectroscopy showed GS-Se-SG to be a very efficient oxidant of reduced thioredoxin from E. coli and kinetically superior to insulin disulfides. Thioredoxin-dependent reduction of CDP to dCDP by ribonucleotide reductase was effectively inhibited by GS-Se-SG.

Animals↗

PubMed1977

Metabolic interrelationships between arsenic and selenium.

In 1938, Moxon discovered that arsenic protected against selenium toxicity. Since that time it has been shown that this protective effect of arsenic against selenium poisoning can be demonstrated in many different animal species under a wide variety of conditions. Antagonistic effects between arsenic and selenium have also been noted in teratologic experiments. Early metabolic studies showed that arsenic inhibited the expiration of volatile selenium compounds by rats injected with acutely toxic doses of both elements. This was puzzling since pulmonary excretion had long been regarded as a means by which animals could rid themselves of excess selenium. However, later work demonstrated that arsenic increased the biliary excretion of selenium. Not only did arsenic stimulate the excretion of selenium in the bile, but selenium also stimulated the excretion of arsenic in the bile. This increased biliary excretion of selenium caused by arsenic provides a reasonable rationale for the ability of arsenic to counteract the toxicity of selenium, although the chemical mechanism by which arsenic does this is not certain. The most satisfactory explanation is that these two elements react in the liver to form a detoxication conjugate which is then excreted into the bile. This is consistent with the fact that both arsenic and selenium each increase the biliary excretion of the other. Several other metabolic interactions between arsenic and selenium have been demonstrated in vitro, but their physiological significance is not clear. Although arsenic decreased selenium toxicity under most conditions, there is a pronounced synergistic toxicity between arsenic and two methylated selenium metabolites, trimethylselenonium ion or dimethyl selenide. The ecological consequences of these synergisms are largely unexplored, although it is likely that selenium methylation occurs in the environment. All attempts to promote or prevent selenium deficiency diseases in animals by feeding arsenic have been unsuccessful. Over 30 years ago it was suggested that industrial hygienists use arsenic as a tonic to prevent or cure selenium poisoning in workers exposed to this hazard. Organic arsenical feed additives were tried as partial antidotes against selenium poisoning in livestock raised in seleniferous agricultural areas but were not found to be practical.

Animals↗

PubMed1985

Development of reflexes in neonatal mice prenatally exposed to methylmercury and selenite.

The development of reflexes in neonates exposed prenatally to methylmercury and selenite was investigated. Pregnant mice were assigned to one of 4 treatments; methylmercury (MeHg), selenite(Se), combination of 2 compounds (MeHg X Se) and saline control (NaCl). Mice were injected subcutaneously (s.c.) on day 9 of gestation. The dose of each compound was 30 mumol/kg. Mercury (Hg) concentrations in the neonatal brain and liver of the MeHg X Se group were slightly lower than in the MeHg group. The results of behavioral examination revealed that the MeHg X Se group showed significantly improved development compared with the MeHg group. These facts suggest the possibility that selenium compounds have protective effects against methylmercury neurotoxicity in fetuses and neonates.

Animals↗

PubMed1992

Selenium and sulfur in antioxidant protective systems: relationships with vitamin E and malaria.

The metabolic relationships among the antioxidant nutrients selenium, sulfur, and vitamin E are particularly close. Selenium and vitamin E have long been known to spare one another in certain nutritional diseases of animals, and selenium has been considered to have a key antioxidant defense function as a component of glutathione peroxidase. However, the antioxidant role of glutathione peroxidase has been questioned and new proteins containing selenium have been identified: phospholipid hydroperoxide glutathione peroxidase, selenoprotein P, and iodothyronine deiodinase. Glutathione peroxidase activity independent of selenium resides in the glutathione S-transferases. Glutathione participates in both enzymatic and nonenzymatic antioxidant defense systems. Some low-molecular weight selenium compounds (e.g., ebselen) exhibit glutathione peroxidase-like action. Certain low molecular weight thiols decompose peroxides nonenzymatically (e.g., the ovothiols). Murine malaria appears to be a useful experimental model for investigating interrelationships of selenium and vitamin E. Vitamin E deficiency protects against the parasite, especially when the mice are concurrently fed peroxidizable fat such as fish or linseed oils. Selenium deficiency, on the other hand, has little or no protective effect against the parasite. Any practical utility of pro-oxidant diets in combating human malaria remains to be determined.

Antioxidants↗

PubMedDate not supplied

The epidemiology of selenium and human cancer.

The relation between the trace element selenium and the etiology of cancer in humans remains elusive and intriguing, despite the number of epidemiologic studies published on the topic. We address some methodologic issues, such as misclassification of exposure, particularly to single selenium compounds, effect modification, confounding, and other sources of bias, which may explain the inconsistencies in the literature. We also review the results of cohort studies, which have yielded either inverse or null or direct associations between selenium exposure and subsequent cancer risk. To date, no beneficial effect on cancer incidence at major sites, including prostate cancer, has emerged from the Finnish program begun in 1984 to increase the average selenium intake in its population. Populations exposed to unusually high or low levels of environmental selenium might offer unique opportunities to investigate if selenium exposure is related to the etiology of human cancer.

Anticarcinogenic Agents↗

PubMed1999

Influence of sodium selenite and selenomethionine on DNA/RNA synthesis and BaP binding to spleen lymphocytes in culture.

In the present study, an attempt was made to provide some information regarding the effects of organic and inorganic selenium compounds on DNA/RNA synthesis and benzo(a)pyrene uptake in cultured lymphocytes from mice spleen. It was clear from the results that there was a significant inhibition of DNA/RNA synthesis with increasing concentration of either form of selenium from 0.1 microM to 1 mM in culture medium. However, when used at the same level as selenite with respect to selenium content, selenomethionine exerted more DNA/RNA synthesis inhibitory effect than selenite. Benzo(a)pyrene uptake by proliferating lymphocytes was also significantly reduced with increasing selenium concentration (0.1 microM to 1 mM). However, both forms of selenium at the same selenium concentration showed almost the same inhibitory effect on the cellular uptake of benzo(a)pyrene, which indicated that some factor(s) other than the DNA synthesis are also involved in the interaction between benzo(a)pyrene and cells. Involvement of the changes in the carcinogen metabolism and glutathione level has been discussed. Present studies show that organic selenium as a source of selenium is a more potent chemopreventive compared to the inorganic one. This information may have a useful therapeutic potential.

Animals↗

PubMed1994

Application of nuclear analytical methods in the investigation and identification of new selenoproteins.

Nuclear methods have been applied in the investigation of selenium-containing proteins in rat tissues. Selenium was determined in tissues, cells, and cellular compartments by instrumental neutron activation analysis via 77mSe or 75Se. For tracer studies, the selenium compounds were labeled in vivo by administering 75Se with a high specific activity to rats. Quantitative determination of very small amounts of the element in protein fractions was achieved by measurement of the tracer after replenishment of selenium-depleted animals with the labeled element. The application of the nuclear methods in the detection, characterization, and identification of new selenium-containing proteins is shown with the help of some examples.

Animals↗

PubMed1985

Selenium inhibition of chemical carcinogenesis in the upper aerodigestive tract of hamsters.

Evidence suggests that ingestion of selenium compounds may inhibit carcinogenesis. We studied this in hamsters in which squamous cell carcinoma of the tongue was induced with 0.5% dimethylbenzanthracene (DMBA). Forty-five hamsters, divided into three groups of 15 each, were fed a low-selenium diet and the left lateral border of the tongue was painted with DMBA three times a week. Control animals were given deionized water, while water for animals in groups 1 and 2 contained 3 and 6 ppm selenium, respectively. All sufficiently long-lived animals developed leukoplakia of the tongue and floor of the mouth that progressed to dysplasia and papillary or ulcerative carcinoma. Carcinomas were seen less frequently on the palate and in the pyriform sinuses. Carcinoma metastasized to neck lymph nodes in two hamsters. Data indicate a 2-week delay in leukoplakia incidence for the selenium groups; a higher survival rate was also noted, although this was not statistically significant. We conclude that this model is similar to tobacco-induced squamous cell carcinoma of the upper aerodigestive tract in humans and that ingestion of supplemental selenium produces a modest inhibitory effect on leukoplakia.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1983

Exposure of man to environmental selenium - an exposure commitment assessment.

Selenium is an element which occurs naturally in varying concentrations in soil and is released from industrial sources, particularly from fossil fuel combustion. Harmful effects in animals and man may result from both deficient or excessive amounts of intake. Representative values of selenium concentrations in the background environment and in man are selected from available data and a pathway analysis is performed utilizing the exposure commitment method. Dietary intake of selenium is of the order of 70 micrograms d-1. With fractional absorption of 80% and retention in the body of 90% for an effective retention time of 140 days, the estimated mean body content of selenium is 7 mg. The contribution to the body burden from inhalation intake is much less significant. The exposure evaluation is performed for total selenium in the environment and in man. The parameters may be adjusted for specific selenium compounds, if data are available, and for more particular environmental and exposure conditions as required.

Absorption↗