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PubMed1991

Inhibition of rat brain prostaglandin D synthase by inorganic selenocompounds.

Various inorganic selenocompounds dose-dependently inhibited the rat brain prostaglandin (PG) D synthase, both in the purified enzyme preparation and in the crude brain supernatant. All of the quadrivalent selenium compounds tested had a very limited range of IC50 values in the purified enzyme (11-12 microM) and in the brain supernatant (9-15 microM). A divalent selenium compound was also inhibitory, but a hexavalent selenium compound was ineffective. In contrast, organic selenocompounds such as selenomethionine and selenourea had no effect on the PGD synthase activity. Furthermore, sodium sulfate and sodium sulfite up to 10 mM did not inhibit the activity. The inhibition by selenium required the preincubation of the metal with sulfhydryl compounds such as dithiothreitol (DTT), indicating that the formation of selenotrisulfide or some other adduct(s) is essential for the inhibition. Furthermore, the inhibition was reversed by an excess amount of dithiothreitol, suggesting that the selenotrisulfide derivative of DTT binds to the SH group of the PGD synthase. The kinetic analysis revealed the inhibition by selenite to be noncompetitive with a Ki value of 10.1 microM. On the other hand, glutathione-dependent PGD synthase from rat spleen was much less inhibited, and PGF synthase and PGD2 11-ketoreductase activities were not inhibited by the selenium compound.

Animals↗
PubMed1986

Selenium content and glutathione peroxidase activity in the testis of the maturing rat.

In rats fed a diet with 0.25 mg Se/kg the testis selenium content rose during maturation. The value in 4-mo-old animals (7.0 mg Se/kg dry mass; 0.9 mg Se/kg wet mass) was six times higher than that in 20-d-old weanling rats. By comparison, the selenium content in the main selenium pools, muscle and liver, remained unchanged and rose by half, respectively. Due to the increased selenium requirement of the testis during its pubertal maturation the amount of selenium taken up by the male gonads was 50% of the amount deposited in muscle and liver, whereas before and after that period it was about 10%. Feeding animals a low vitamin E diet had no effect on the rise in testis selenium. Glutathione peroxidase activity was twice as high in 4-mo-old animals as in weanling rats. Because only a small percentage of the element in the male gonads was bound to the enzyme, the rise in testis selenium must have been due to other selenium compounds. The selenium content of the spermatozoa was about 21 mg Se/kg dry mass, which by far exceeded the level of this element in other compartments of the rat. The increase in testis selenium content coincided with the beginning of spermatogenesis, and it may therefore ensure the supply of adequate amounts of the element for the spermatozoa.

Animals↗
PubMed2002

Comparative study on the bioactivation mechanisms and cytotoxicity of Te-phenyl-L-tellurocysteine, Se-phenyl-L-selenocysteine, and S-phenyl-L-cysteine.

Tellurium compounds are effective antioxidants and chemoprotectors, even more active than their selenium and sulfur analogues. In addition to these properties, some selenium compounds, such as selenocysteine Se-conjugates, possess significant chemopreventive and antitumor activities, and selenol metabolites are considered as active species. In the present study, we have synthesized Te-phenyl-L-tellurocysteine and evaluated its bioactivation and cytotoxicity. The activities of this compound were compared with those of the corresponding selenium and sulfur analogues. Te-Phenyl-L-tellurocysteine is bioactivated into its corresponding tellurol, as detected by GC-MS, by cysteine conjugate beta-lyase and amino acid oxidase, analogously to what has been shown previously for Se-phenyl-L-selenocysteine. The rate of beta-elimination may reflect the bond strength of the corresponding C-S, C-Se, and C-Te bond. Bioactivation of Te-phenyl-L-tellurocysteine and its selenium and sulfur analogues by oxidative enzymes was evaluated by measuring NADPH-dependent activation of hepatic mGST and inhibition of EROD. Te-Phenyl-L-tellurocysteine and Se-phenyl-L-selenocysteine displayed strong and time-dependent mGST activation, while S-phenyl-L-cysteine resulted in no significant activation. Te-Phenyl-L-tellurocysteine was also a strong inhibitor of EROD activity. In addition to EROD inhibition, Te-phenyl-L-tellurocysteine was the strongest inhibitor of several human cytochrome P450 isoenzymes followed by Se-phenyl-L-selenocysteine, while S-phenyl-L-cysteine was the weakest inhibitor. Interestingly, Te-phenyl-L-tellurocysteine selectively inhibited cytochrome P450 1A1 directly, which is, for example, responsible for the activation of several procarcinogens. Preliminary cytotoxicity studies with Te-phenyl-L-tellurocysteine in freshly isolated rat hepatocytes showed a time-dependent depletion of GSH and LDH leakage comparable with the relatively nontoxic drug paracetamol, while the selenium and sulfur analogues were nontoxic toward rat hepatocytes. In conclusion, because the chemopreventive and antitumor activities of selenium compounds are thought to be mediated via their selenol metabolites and tellurium compounds might be even more active than selenium compounds, tellurocysteine Te-conjugates might be an interesting novel class of prodrugs for the formation of biologically active tellurols.

Animals↗
PubMedDate not supplied

The inhibitory effect of selenium on induction of tetraploidy by dimethylarsinic acid in Chinese hamster cells.

Arsenic is a human carcinogen. On the other hand, selenium supplementation can inhibit induction of carcinogenesis by chemical carcinogens. The effect of selenium compounds on the cytotoxicity of dimethylarsinic acid (DMA) and on the induction of tetraploidy by DMA were studied using Chinese hamster V79 cells. Two selenium compounds were tested, sodium selenite and trimethylselenonium iodide (TMSeI). Trimethylselenonium is a major excretory product of selenite metabolism. The cytotoxicity of sodium selenite was 1000-fold greater than that of TMSeI. The cytotoxicity of DMA was about the same as that of TMSeI. The mitotic index for DMA administration was increased by these selenium compounds at low concentrations and decreased by them at high concentrations. The tetraploid index for DMA decreased with increasing concentrations of these selenium compounds. Tetraploidy is a form of aneuploidy, and aneuploidy is known to induce carcinogenesis. The finding that selenium inhibited induction of tetraploidy by DMA may yield clues to the role of selenium in the chemoprevention of carcinogenesis by chemical carcinogens.

Aneuploidy↗
PubMed1996

Selenium-containing compounds protect DNA from single-strand breaks caused by peroxynitrite.

Peroxynitrite (ONOO-/ONOOH) is a powerful oxidant that can induce mutations and cause single-strand breaks in plasmid supercoiled DNA. The selenium-containing compound ebselen rapidly reacts with peroxynitrite. Therefore, ebselen [2-phenyl-1,2-benzisoselenazol-3(2H)-one] and other selenium-containing molecules, selenomethionine and selenocystine, were studied as agents protecting DNA from single-strand breaks induced by peroxynitrite. Selenomethionine and selenocystine protected DNA from single-strand breaks more effectively than their sulfur analogs, methionine and cystine, and they also were more effective than glutathione or the hydroxyl radical scavenger mannitol. These results suggest that selenium-containing compounds can protect DNA from damage caused by peroxynitrite.

Cystine↗
PubMed2004

Selective modulation of the therapeutic efficacy of anticancer drugs by selenium containing compounds against human tumor xenografts.

PURPOSE: Studies were carried out in athymic nude mice bearing human squamous cell carcinoma of the head and neck (FaDu and A253) and colon carcinoma (HCT-8 and HT-29) xenografts to evaluate the potential role of selenium-containing compounds as selective modulators of the toxicity and antitumor activity of selected anticancer drugs with particular emphasis on irinotecan, a topoisomerase I poison. EXPERIMENTAL DESIGN: Antitumor activity and toxicity were evaluated using nontoxic doses (0.2 mg/mouse/day) and schedule (14-28 days) of the selenium-containing compounds, 5-methylselenocysteine and seleno-L-methionine, administered orally to nude mice daily for 7 days before i.v. administration of anticancer drugs, with continued selenium treatment for 7-21 days, depending on anticancer drugs under evaluation. Several doses of anticancer drugs were used, including the maximum tolerated dose (MTD) and toxic doses. Although many chemotherapeutic agents were evaluated for toxicity protection by selenium, data on antitumor activity were primarily obtained using the MTD, 2 x MTD, and 3 x MTD of weekly x4 schedule of irinotecan. RESULTS: Selenium was highly protective against toxicity induced by a variety of chemotherapeutic agents. Furthermore, selenium increased significantly the cure rate of xenografts bearing human tumors that are sensitive (HCT-8 and FaDu) and resistant (HT-29 and A253) to irinotecan. The high cure rate (100%) was achieved in nude mice bearing HCT-8 and FaDu xenografts treated with the MTD of irinotecan (100 mg/kg/week x 4) when combined with selenium. Administration of higher doses of irinotecan (200 and 300 mg/kg/week x 4) was required to achieve high cure rate for HT-29 and A253 xenografts. Administration of these higher doses was possible due to selective protection of normal tissues by selenium. Thus, the use of selenium as selective modulator of the therapeutic efficacy of anticancer drugs is new and novel. CONCLUSIONS: We demonstrated that selenium is a highly effective modulator of the therapeutic efficacy and selectivity of anticancer drugs in nude mice bearing human tumor xenografts of colon carcinoma and squamous cell carcinoma of the head and neck. The observed in vivo synergic interaction is highly dependent on the schedule of selenium.

Administration, Oral↗
PubMed2001

Catalytic selenols couple the redox cycles of metallothionein and glutathione.

Co-ordination of zinc to the thiol group of cysteine allows mobilization of zinc through oxidation of its ligand. This molecular property links the binding and release of zinc in metallothionein (MT) to the cellular redox state [Maret W. & Vallee B.L. (1998) Proc. Natl Acad. Sci. USA 95, 3483-3488]. Biological disulfides such as glutathione disulfide (GSSG) oxidize MT with concomitant release of zinc, while glutathione (GSH) reduces the oxidized protein to thionein, which then binds to available zinc. Neither of these two redox processes is very efficient, even at high concentrations of GSSG or GSH. However, the GSH/GSSG redox pair can efficiently couple with the MT/thionein system in the presence of a selenium compound that has the capacity to form a catalytic selenol(ate). This coupling provides a very effective means of modulating oxidation and reduction. Remarkably, selenium compounds catalyze the oxidation of MT even under overall reducing conditions such as those prevailing in the cytosol. In this manner, the binding and release of zinc from zinc-thiolate co-ordination sites is linked to redox catalysis by selenium compounds, changes in the glutathione redox state, and the availability of either a zinc donor or a zinc acceptor. The results also suggest that the pharmacological actions of selenium compounds in cancer prevention and other antiviral and anti-inflammatory therapeutic applications, as well as unknown functions of selenium-containing proteins, may relate to coupling between the thiol redox state and the zinc state.

Catalysis↗
PubMed1997

Active oxygen generation as a possible mechanism of selenium toxicity.

Selenium plays an important role in scavenging active oxygen (AO) species as an essential constituent of glutathione peroxidase. On the other hand, several reports proposed a possible induction of toxic AO by selenium compounds in vitro. However, some of these experiments including ours, were revealed to conclude on the basis of experimental artifacts, and to have problems in the interpretation of data. Methods or principles so far used for the detection of AO species generated by selenium compound were measurement of chemiluminescence from lucigenin or luminol by AO species, the spectrophotometric analysis of reduction of ferricytochrome c or nitroblue tetrazolium (NBT) by superoxide anion (O2-), electron spin resonance (ESR) spectra using dimethylpyrroline oxide (DMPO) as a spin trapping agent, the deoxyribose decomposition by hydroxyl radical (HO.), the salicylate hydroxylation by HO., and the strand breakage of DNA by AO. Many of these methods together with their principles seem to have some defects which prevent clear conclusion as stated below. (i) Lucigenin was found to mediate the formation of O2- in the presence of selenite and reduced glutathione (GSH). Therefore, lucigenin is not a suitable reagent. (ii) Luminol may also mediate O2- generation in the presence of HO.. (iii) ferricytochrome c can be reduced to ferrocytochrome c in the mixture of selenite and GSH in the absence of oxygen. Moreover, the spectrophotometric method is interfered by turbidity of elemental selenium formed under some conditions in the reaction mixture containing selenite and GSH. (iv) NBT is also reduced by selenium compounds in the absence of O2. (v) ESR signals of AO species were obtained in the reaction mixture containing selenite and GSH, or in the solution of hydrogen selenide in the presence of O2. However, selenide decomposed spin adduct of DMPO with HO. (DMPO-OH). Therefore, the intensity of the signals is not quantitative. (vi) CuZn-SOD is not necessarily a good tool to prove the involvement of O2- because it enhanced HO. generation in the reaction mixture containing selenite and GSH. Thus, we would like to emphasize that carefully designed experiments are required to further identify the molecular species of active oxygen induced by selenium compounds.

Animals↗
PubMed1991

A comparison of the effects of sodium selenite and seleno-L-methionine on disposition of orally administered mercuric chloride.

Previous studies demonstrated extensive effects of the administration of selenite on the biokinetics of simultaneously injected inorganic mercury. As the results of simultaneous administration might well be of questionable value for the assessment of the interaction between mercury and selenium during the long-term exposures relevant for human beings, the present study was performed. The purpose of the present study was to compare the effects of prolonged oral exposure to sodium selenite and seleno-L-methionine (7.5, 37.5, or 75 mumol/L drinking water) on the biokinetics of a single oral dose of 203Hg-labelled mercuric chloride (5 or 25 mumol/kg b.w.) in mice. Both selenium compounds caused a dose-dependent decrease in the excretion of absorbed mercury, as indicated by a 2-7 fold increase in whole-body retention of mercury. Selenite caused a significantly higher whole-body retention of mercury at day 14 than did seleno-L-methionine. Both selenium compounds affected the relative deposition of mercury in most organs, but the effect depended on the type of selenium compound, on the dose of mercury as well as on the molar ratio between mercury and the selenium compound. The amounts of mercury deposited in the liver, kidneys and spleen increased, whereas the amounts deposited in the uteri and the brain were unaffected by the selenium supplementation. Significant differences in relative organ deposition of mercury between mice given selenite and mice given seleno-L-methionine were observed in the stomach, intestinal tract and the kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

The effect of selenium on the biliary excretion and organ distribution of mercury in the rat after exposure to methyl mercuric chloride.

The influence of selenium compounds on the biliary excretion and the organ distribution of mercury after injection of methyl mercuric chloride (4 mumol/kg) have been tested. Selenite, seleno-di-N-acetylglycine and seleno-methionine strongly inhibited the biliary excretion of mercury. Selenite even in a molar dose of 1/40 of the methyl mercury dose inhibited the biliary excretion of mercury. The less toxic seleno-di-N-acetylglycine was needed in larger molar doses and did not act as rapidly as selenite. Biliary excreted methyl mercury is known to be partly reabsorbed in the gut. Subsequently a part of it is deposited in the kidneys since drainage of the bile lowered the kidney content of mercury. Rats given selenium compounds in combination with bile drainage showed further reduction of the kidney mercury content than bile duct drainage alone. Thus the demonstrated lowering effect of selenium compounds on the kidney mercury content cannot be completely explained by an inhibition of biliary excretion of mercury. The mercury concentration in the brain was increased by the selenium compounds; the effect being dependent of the selenium dose reaching a maximum at an equimolar selenite--to methyl mercury dose ratio. The mechanisms by which selenium influences the methyl mercury kinetics are discussed.

Animals↗
PubMed2003

Selenium-containing compounds attenuate peroxynitrite-mediated NF-kappaB and AP-1 activation and interleukin-8 gene and protein expression in human leukocytes.

A growing body of evidence indicates that the powerful oxidant peroxynitrite (ONOO(-)) may function as an intracellular signal for production of proinflammatory cytokines, such as interleukin-8 (IL-8) in human leukocytes. In this study, we investigated whether selenomethionine, selenocysteine, and the synthetic organoselenium compound ebselen (2-phenyl-1,2-benzisoselenazol-3(2h)-one) could inhibit ONOO(-)-mediated IL-8 gene expression in human leukocytes in whole blood. At micromolar concentrations, ebselen, selenomethionine, and selenocysteine effectively prevented nuclear accumulation of activator protein-1 (AP-1) and nuclear factor kappaB (NF-kappaB) evoked by exogenous ONOO(-), in both polymorphonuclear and mononuclear leukocytes, and inhibited IL-8 gene and protein expression. The inhibitory actions of selenium-containing molecules were concentration-dependent (EC(50) values: 8.0-13.2 muM) and were not shared by their sulphur analogs methionine and cystine. Furthermore, ebselen, selenomethionine, and selenocysteine markedly reduced LPS-evoked intracellular ONOO(-) formation in leukocytes, resulting in 36-66% decreases in nuclear accumulation of AP-1 and NF-kappaB in both polymorphonuclear and mononuclear leukocytes and inhibition of IL-8 mRNA expression and IL-8 release. These findings indicate that selenium-containing compounds can effectively oppose ONOO(-) signaling in leukocytes and suggest a role for selenium-containing molecules as potential modifiers of inappropriate leukocyte trafficking under pathological conditions associated with enhanced ONOO(-) formation.

Cell Nucleus↗
PubMed1999

Feeding preferences of spodoptera exigua in response to form and concentration of selenium

Minimal information is available on the impact of various organic and inorganic forms of the ecologically and agriculturally important pollutant, selenium (Se), on insect herbivores. We conducted bioassays with artificial diet to examine the feeding responses of a generalist herbivore, Spodoptera exigua (Hubner) (Lepidoptera: Noctuidae), to various forms and concentrations of Se. Two different-aged cohorts of larvae were examined in choice tests with control diets vs. test diets incorporating lethal concentrations (LC(10), LC(30), LC(50), and LC(70)) of sodium selenate, sodium selenite, seleno-DL-cystine, and seleno-DL-methionine. Tests initiated with neonates showed larvae significantly preferred control diet over diet with sodium selenate, sodium selenite, or selenocystine, but at most concentrations showed no preference between selenomethionine and control diet. Choice tests initiated with third instars demonstrated a preference for control diet over sodium selenate treatments, and sodium selenite treatments. In contrast, no significant responses were found in tests initiated with third instars offered the choice between selenocystine or selenomethionine and untreated controls. Additionally, comparisons of consumption demonstrated that inorganic selenium compounds were antifeedants whereas the organic selenium compounds tested have little antifeedant activity. The toxicity of all of the tested forms of selenium, in combination with the lack of antifeedant activity of some compounds, has the potential to affect both the distribution and diversity of terrestrial herbivores in both agricultural and natural systems. Arch. Copyright 1999 Wiley-Liss, Inc.

Journal Article↗
PubMed2003

Comparative action of 1,4-phenylenebis(methylene)selenocyanate and its metabolites against 7,12-dimethylbenz[a]anthracene-DNA adduct formation in the rat and cell proliferation in rat mammary tumor cells.

1,4-phenylenebis(methylene)selenocyanate (p-XSC) inhibits 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis and DMBA-DNA binding in the rat mammary gland. Tetraselenocyclophane (TSC) was identified in rat feces as a metabolite of p-XSC. This led us to postulate the metabolic pathway: p-XSC-->glutathione conjugate (p-XSeSG)-->aromatic selenol (p-XSeH)-->TSC. Whether p-XSC or one of its metabolites is responsible for cancer prevention is the focus of this study. We utilized the DMBA-DNA binding assay with p-XSC as a positive control to evaluate the chemopreventive potential of p-XSC metabolites at dietary selenium levels of 10 ppm. Rats were fed AIN-76A diet supplemented with various selenium compounds for 1 week prior to the oral administration of a single dose of [3H]DMBA (5 mg per rat, specific activity 51.3 mCi/mmol). The rats were sacrificed 24 h later and DNA was isolated from the mammary fat pads. Relative levels of total binding were: [pmol/mg DNA, mean +/- S.D., n=6]; DMBA [7.2 +/- 1.6]; DMBA+p-XSC [3.5 +/- 2.7]; DMBA+p-XSeSG [2.2 +/- 1.1]; DMBA+TSC [5.6 +/- 2.9]. All selenium compounds, except TSC, significantly inhibited DMBA-DNA adduct formation; however, the difference between p-XSC and p-XSeSG was not statistically significant. The inhibition of total binding was attributed to a reduction in the formation of the three major adducts derived from bay-region diol epoxides of DMBA. On the basis of their chromatographic characteristics, these were identified as anti-diol-epoxide:deoxyguanosine, syn-diol-epoxide:deoxyadenosine, and anti-diol-epoxide:deoxyadenosine. Our results suggest that p-XSeSG, but not TSC, is the likely inhibitor of mammary cancer. Selenium levels measured by atomic absorption spectroscopy in the target organ (mammary fat pads) and in plasma following the dietary administration of selenium compounds were in the order of p-XSeSG congruent with p-XSC>TSC. These results appear to be consistent with their order of inhibitory effects on total DMBA-DNA binding. Further in vitro studies of the effect of selenium compounds on cell proliferation suggest that, depending on the dose and time point selected, p-XSC is comparable to or better than p-XSeSG; but both are more effective than TSC. Collectively, our in vivo and in vitro results indicate that p-XSC and its conjugate are better candidates than TSC for future studies on mammary cancer chemoprevention.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2002

Selenomethionine induction of DNA repair response in human fibroblasts.

Selenium compounds have a long history in chemoprevention of mammary and colon cancers in rodent models. Selenium compounds are in current clinical trials, having shown promise in prevention of prostate and other human cancers. In human tissues, it has been estimated that each cell sustains approximately 10 000 potentially mutagenic (if not repaired) lesions per day due to endogenous DNA damage. Almost no studies have addressed the potential for selenium compounds to induce DNA repair, a potential mechanism for their cancer-preventive actions. We show that selenium in the form of selenomethionine induces a DNA repair response in normal human fibroblasts in vitro, and protects cells from DNA damage. We show a possible mechanism for the inducible DNA repair response, in which enhanced repair complex formation was observed in selenomethionine-treated cells.

Blotting, Western↗
PubMed2005

Organoselenium compounds prevent hyperphosphorylation of cytoskeletal proteins induced by the neurotoxic agent diphenyl ditelluride in cerebral cortex of young rats.

In this work we investigated the protective ability of the selenium compounds ebselen and diphenyl diselenide against the effect of diphenyl ditelluride on the in vitro incorporation of 32P into intermediate filament (IF) proteins from slices of cerebral cortex of 17-day-old rats. We observed that ditelluride in the concentrations of 1, 15 and 50 microM induced hyperphosphorylation of the high-salt Triton insoluble neurofilament subunits (NF-M and NF-L), glial fibrillary acidic protein (GFAP) and vimentin, without altering the immunocontent of these proteins. Concerning the selenium compounds, diselenide (1,15 and 50 microM) did not induce alteration of the in vitro phosphorylation of the IF proteins. Otherwise, ebselen induced an altered in vitro phosphorylation of the cytoskeletal proteins in a dose-dependent manner. At intermediate concentrations (15 and 30 microM) it increased the in vitro phosphorylation even though, at low (5 microM) or high (50 and 100 microM) concentrations this compound was ineffective in altering the activity of the cytoskeletal-associated phosphorylating system. In addition, 15 microM diselenide and 5 microM ebselen, presented a protective effect against the action of ditelluride, on the phosphorylation of the proteins studied. Considering that hyperphosphorylation of cytoskeletal proteins is associated with neuronal dysfunction and neurodegeneration, it is probable that the effects of ditelluride could be related to the remarkable neurotoxicity of this organic form of tellurium. Furthermore the neuroprotective action of selenium compounds against tellurium effects could be a promising route to be exploited for a possible treatment of organic tellurium poisoning.

Animals↗
PubMed2001

Qualitative detection of selenium in fortified soil and water samples by a paper chromatographic-carboxyl esterase enzyme inhibition technique.

Thevetia peruviana seed carboxyl esterase was employed as a biosensor for the detection of selenium compounds by an enzyme inhibition technique on paper chromatograms. The selenium compounds (sodium selenite and selenium dioxide) appeared as white spots on a magenta background due to the inhibition of Thevetia peruviana seed carboxyl esterase (substrate 1-naphthyl acetate, coupling reagent Fast blue B salt). The minimum detectable amounts were about 5 microg of sodium selenite and 5 microg of selenium dioxide. Many other animal and plant carboxyl esterases gave no inhibition spot under the same conditions. Soil and water samples were fortified with sodium selenite and selenium dioxide. A procedure for preparing test solutions and conditions for paper chromatography was established.

Apocynaceae↗
PubMed1986

Effects of selenium in vitro on human T-lymphocyte functions and K-562 tumor cell growth.

In vitro E-rosette formation, lymphocyte mitogenesis, and natural killer (NK) cell activity of human blood lymphocytes were strongly inhibited by high concentrations (10(-4) M) of sodium selenite, sodium selenate, and selenium dioxide. Lower concentrations (10(-5) or 10(-7) M) also inhibited E-rosette formation and natural killer cell activity against K-562 tumor cells. Lymphocyte transformation induced by concanavalin A (con A) or pokeweed mitogen (PWM) was also inhibited by all selenium compounds tested, but only at the highest concentrations (10(-5) and 10(-4) M). There was depression of the total number of viable lymphocytes following incubation with selenium dioxide only at a high concentration (10(-4) M). Interferon production was enhanced at lower levels (10(-9) to 10(-6)M) of selenium dioxide while a higher concentration (10(-5) and 10(-4)M) appeared to inhibit its production. The mechanism of inhibition by selenium compounds (10(-4) M) is due, in part, to the decrease of viable lymphocytes. It is unclear how other and lower concentrations (10(-7) or 10(-9) M) of selenium compounds inhibit E-rosette formation, NK activity, or K-562 tumor cell growth.

Adult↗