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PubMed2001

Studies on unimolecular and bimolecular photoprocesses of a newly synthesized selenium compound, 7-chloro-2-phenyl-9H-[1]-benzopyrano[3,2-b]-selenophene-9-one (SeP).

Using steady state/time resolved spectroscopic and electrochemical techniques the spectroscopic and photophysical studies were made on a novel synthesized selenophene compound SeP in nonpolar methylcyclohexane (MCH), polar aprotic acetonitrile (ACN) and polar protic ethanol (EtOH) solvents at the ambient temperature as well as at 77 K. Both from the studies on unimolecular and bimolecular photoprocesses this selenophene compound was found to possess several electronic levels, 1Bb, 1La, 1Lb (all are of pi pi* nature and 1Lb is hidden within 1La band envelop like the characteristics of most of the acenes) and 1(nO pi*) state arising due to carbonyl oxygen atom. In polar ACN environment this nO pi* state disappears because it moves within the envelop of intense 1La band due to large destabilization. Large overlapping of different band systems within the 1La band of SeP was confirmed from the observed depolarization effect. The lack of phosphorescence of SeP both in MCH and EtOH rigid glassy matrix at 77 K has been inferred due to large vibronic interactions between closely lying triplets of the corresponding 1nO pi* and 1Lb states. From the bimolecular investigations, it reveals that SeP acts as a good electron donor in presence of the well known electron acceptor 9 cyanoanthracene (9CNA). Transient absorption spectra measured by laser flash photolysis technique demonstrate the formation of ion-pair when the acceptor is excited. From the analysis of the fluorescence quenching data it seemingly indicates that the major contribution in the diminution of the fluorescence intensity of the acceptor 9CNA in presence of SeP is not only due to the photoinduced electron transfer (ET) but also originates from static type (instantaneous) quenching processes along with external heavy atom effect. The possibility of occurrence of photoinduced ET reaction in Marcus inverted region is hinted.

Acetonitriles↗
PubMed1996

Effects of chemopreventive selenium compounds on Jun N-kinase activities.

Activation of Jun-N-kinases (JNK) is stimulated by diverse agents including UV-irradiation, heat shock, tumor necrosis factor and osmotic shock. In the present study we have elucidated the effect of the organoselenium chemopreventive agent 1,4-phenylenebis(methylene)selenocyanate (p-XSC, on UV-mediated JNK activation. Using mouse fibroblasts as a model cell system we found that low concentrations (1-10 microM range) of p-XSC did not affect JNK activity, yet were capable of potentiating JNK activity when administered prior to UV-irradiation. While higher doses of p-XSC have minimal effect on JNK activation, when combined with UV, there is a dose-dependent decrease in JNK activation. Similar to its effects on JNK, p-XSC is a potent inducer of src-related tyrosine kinases. p-XSC mediated changes in JNK activation correlate with its ability to potentiate the association of JNK with p21ras, in a manner similar to that we have previously observed with GTP or sodium vanadate. That p-XSC can modulate JNK activities points to a possible mechanism by which it contributes to the cell's ability to cope with stress.

3T3 Cells↗
PubMed1992

Inhibition of the biosynthesis of N-acetylneuraminic acid by metal ions and selenium in vitro.

In liver homogenate the biosynthesis of N-acetylneuraminic acid using N-acetylglucosamine as precursor can be followed stepwise by applying different chromatographic procedures. In this cell-free system 16 metal ions (Zn2+, Mn2+, La3+, Co2+, Cu2+, Hg2+, VO3-, Pb2+, Ce3+, Cd2+, Fe2+, Fe3+, Al3+, Sn2+, Cs+ and Li+) and the selenium compounds, selenium(IV) oxide and sodium selenite, have been checked with respect to their ability to influence a single or possibly several steps of the biosynthesis of N-acetylneuraminic acid. It could be shown that the following enzymes are sensitive to these metal ions (usually applied at a concentration of 1 mmol l-1): N-acetylglucosamine kinase (inhibited by Zn2+ and vandate), UDP-N-acetylglucosamine-2'-epimerase (inhibited by Zn2+, Co2+, Cu2+, Hg2+, VO3-, Pb2+, Cd2+, Fe3+, Cs+, Li+, selenium(IV) oxide and selenite), and N-acetylmannosamine kinase (inhibited by Zn2+, Cu2+, Cd2+ and Co2+). Dose dependent measurements have shown that Zn2+, Cu2+ and selenite are more efficient inhibitors of UDP-N-acetylglucosamine-2'-epimerase than vanadate. As for the N-acetylmannosamine kinase inhibition, a decreasing inhibitory effect exists in the following order Zn2+, Cd2+, Co2+ and Cu2+. In contrast, La3+, Al3+ and Mn2+ (1 mmol l-1) did not interfere with the biosynthesis of N-acetylneuraminic acid. Thus, the conclusion that the inhibitory effect of the metal ions investigated cannot be regarded as simply unspecific is justified.

Acetylglucosamine↗
PubMed1993

Carcinogenicity of trace elements with reference to evaluations made by the International Agency for Research on Cancer.

The monograph program of the International Agency for Research of on Cancer has evaluated many trace elements for their carcinogenicity to humans. Five groups of compounds were considered human carcinogens: arsenic and arsenic compounds, beryllium and beryllium compounds, cadmium and cadmium compounds, hexavalent chromium compounds, and nickel compounds. Antimony trioxide, cobalt and cobalt compounds, lead and inorganic lead compounds, methylmercury compounds, and metallic nickel were considered possibly carcinogenic to humans. Antimony trisulfide, trivalent chromium compounds, metallic chromium, ferric oxide, organolead compounds, metallic mercury, inorganic mercury compounds, selenium and selenium compounds, and titanium dioxide were not classifiable. Trace elements studied to a limited extent include copper, manganese, tin, vanadium, and zinc. Among the problems are the lack of relevant data, the definition of active species, the extrapolation of the results of experimental studies to humans, the methodological problems of epidemiologic studies, and the possible anticarcinogenic activity of some trace elements.

Humans↗
PubMed1999

Immunomodulatory effect of selenosemicarbazides and selenium inorganic compounds, distribution in organs after selenium supplementation.

Antioxidant properties of selenium producing a protective barrier against free radicals play an important role in numerous metabolic and immunologic processes associated with oxidation-reduction reactions which take place during intracellular digestion of phagocyted bacteria. The aim of our study was to examine the properties of an organic compound of selenium, 4-(o-tolilo)-selenosemicarbazide of p-chlorobenzoic acid in terms of its retention in organs, effect on erythropoesis and phagocytic abilities of neutrophiles as well as antioxidant properties in neutrophiles tested with NBT test. This compound as well as inorganic sodium selenate was given to Swiss mice at the dose of 10(-3) g Se/kg for the period of 10 days. The concentrations of selenium in livers of mice treated with sodium selenate and selenosemicarbazide were found to be higher than in controls (18.7 micrograms lg-1 and 23.2 micrograms lg-1 vs. 12 micrograms lg-1, respectively). Analysis of blood cells count has shown a significant decrease in neutrophile levels in both groups treated with selenium. The influence of selenium compounds on phagocytosis and especially NBT test has been determined (3.8% of positive cells in the controls vs. 2.2% and 0.9% in the groups treated with sodium selenate and selenosemicarbazide, respectively). Our preliminary investigations suggest that selenosemicarbazides are biologically active compounds and can modify neutrophile functions.

Animals↗
PubMed1985

[Cytotoxic action of selenium-containing compounds on cultured cells of human ovarian carcinoma].

The effect of different inorganic and organic selenium compounds on the nucleic acid synthesis in culture of human carcinoma ovary cells was studied. The rate of synthesis was determined by the incorporation of 3H-thymidine in the DNA and 3H-uridine in the RNA. Selenium compounds in the concentration to 1 mg/ml inhibited the nucleic acid synthesis in human tumour cells. The level of nucleic acid inhibition depends on the concentration of examined compounds. The tetravalent selenium compounds possessed the most pronounced cytotoxic effect.

Carcinoma↗
PubMed1993

Monoselenophosphate: synthesis, characterization, and identity with the prokaryotic biological selenium donor, compound SePX.

A labile, selenium donor compound required for synthesis of selenium-dependent enzymes and seleno-tRNAs is formed from ATP and selenide by the SELD enzyme. This compound, tentatively identified as a selenophosphate [Veres, Z., Tsai, L., Scholz, T. D., Politino, M., Balaban, R. S., & Stadtman, T. C. (1992) Proc. Natl. Acad. Sci. U.S.A. 89, 2975-2979], is indistinguishable from chemically prepared monoselenophosphate by 31P NMR spectroscopy and ion pairing HPLC. Furthermore, addition of chemically prepared monoselenophosphate caused a dose-dependent decrease in the amount of 75Se incorporated into tRNAs from 75SePX generated in situ by SELD enzyme. A procedure is described for the chemical synthesis of monoselenophosphate in which the readily prepared (MeO)3PSe is converted in quantitative yield to (TMSO)3PSe followed by complete cleavage of the latter to monoselenophosphate in oxygen-free aqueous buffer. The chemical properties of chemically synthesized monoselenophosphate are described.

Adenosine Triphosphate↗
PubMed1976

Studies on selenium-related compounds. V. Cytogenetic effect and reactivity with DNA.

Five selenium compounds, Na2Se04, H2Se04, Na2Se03, H2Se03 and Se02, were tested for their capacity to induce chromosome aberrations in cultured human leukocytes and for their reactivity with DNA by a rec-assay system and inactivation of transforming activity in Bacillus subtilis. Chromosome-breaking activity was significantly higher for the compounds with four-valent than with six-valent selenium, the efficiency being in the decreasing order H2S03 greater than Na2Se03 greater than Se02 greater than H2Se04 greater than Na2Se04. Rec assay using B. subtilis with different recombination capacities suggested that damage to DNA was produced by selenites but not by selenates. The reactivity of selenites with DNA was also indicated by a significant loss of transformation of the tryptophan marker of B. subtilis DNA treated with H2Se03 and Se02.

Adult↗
PubMed2001

Se-methylselenocysteine: a new compound for chemoprevention of breast cancer.

Selenium compounds have attracted renewed interest as chemopreventive agents for human cancer on the basis of the pioneering intervention study by Clark and co-workers. The rodent mammary gland has been used extensively as a model for examining the chemopreventive activities of inorganic and organic selenium compounds. This review summarizes the rationale and results for use of a new organic selenium compound, Se-methylselenocysteine, which exhibits greater efficacy as a chemopreventive agent than several previously used selenium compounds in experimental models of breast cancer and has potential for use in human populations.

Animals↗
PubMed1994

On the nature of selenium toxicity and carcinostatic activity.

Selenium toxicity was first confirmed in 1933 to occur in livestock that consumed plants of the genus Astragalus, Xylorrhiza, Oonopsis, and Stanleya in the western regions of the United States. In 1957 selenium was identified as an essential nutrient for laboratory rats and soon thereafter for chickens and sheep. Essentiality for mammalian species was established in 1973 with the discovery that the enzyme glutathione peroxidase contained selenium. During this same period of time, human epidemiological evidence suggested that selenium possessed anticarcinogenic effects. Since the 1970s, many animal studies have confirmed the human epidemiologic evidence that selenium compounds possess carcinostatic activity. Less progress has been made in explaining why many of these compounds of selenium are toxic and why these same compounds are carcinostatic. In 1988 the observation was made that oxidation of glutathione by selenite produced superoxide, opening a new area for selenium research. This present paper, drawing information from the literature on selenium metabolism in plants and animals, selenium toxicology, selenium cytotoxicity, and selenium carcinostatic activity in animals over the last sixty years, sets forth a probable biochemical catalytic mechanism that encompasses both selenium toxicity and selenium carcinostatic activity. The thesis presented here for scrutiny is that compounds of selenium are toxic owing to their prooxidant catalytic activity to produce superoxide (O2.-), hydrogen peroxide, and very likely other cascading oxyradicals. The toxicity of selenium compounds is countered by plant and animal methylation reactions and antioxidant defenses. As carcinostasis is mostly known to occur at supranutritional levels of selenium in animals, carcinostasis appears to be directly correlated to selenium toxicity. The catalytic toxic selenium specie appears to be the metabolic selenide (RSe-) anion.

Animal Feed↗
PubMed1998

Study of the antioxidant effect of several selenium and sulphur compounds.

Four selenium derivatives (sodium selenate, sodium selenite, selenourea and selenomethionine) and the sulphur analogues (sodium sulfate, sodium sulfite, thiourea and methionine), together with urea, were examined by means of polarography to study their reactivity towards superoxide ion O2. In order that experimental results could be applied to physiological conditions and to control the electroreduction of oxygen, most reactions were carried out in model systems (in the presence and in the absence of triphenyl phosphine oxide and at increasing pH) which are briefly described and discussed. Sodium sulfite and thiourea react with molecular oxygen; selenourea originates an anodic wave, although under other pH conditions. Other compounds (selenate, selenite, seleno-methionine and methionine) display an interesting antioxidant capacity because they catalyse the disproportion of the superoxide ion, as documented by the increase in the limiting current. Methionine appears to be particularly efficient in this respect, since it retains its catalytic ability in a poorly protic environment. Experimental results support the view that exogenous compounds, administered for particular purposes, can display unanticipated, and sometimes positive, side effects.

Antioxidants↗
PubMed1998

Effect of organic forms of selenium on delta-aminolevulinate dehydratase from liver, kidney, and brain of adult rats.

The inhibitory effect of various forms of organic selenium compounds and of diphenyl ditelluride (PhTe)2 on delta-aminolevulinate dehydratase (delta-ALA-D) from liver, kidney, and brain of rats was investigated because it has been reported that organocalcogens catalyze the oxidation of thiols. Diphenyl diselenide (PhSe)2, rho-chloro-diphenyl diselenide (rho ClPhSe)2, propyl-2-2-diphenyl diselenide, and propyl-2-methoxy-2-phenyl selenide inhibited delta-ALA-D and the IC50 ranged from 2 to 32 microM depending on the selenium compound and whether it was preincubated with the enzyme. (rho ClPhSe)2 was the most potent inhibitor of delta-ALA-D, and preincubation increased the inhibitory potency of all the tested compounds. Inorganic selenium compounds (sodium selenite, Na2SeO3 and selenium dioxide, SeO2) inhibited delta-ALA-D, and the potency of SeO2 was greater than that of (rho ClPhSe)2. Diphenyl ditelluride (PhTe)2 also inhibited delta-ALA-D but with relatively lower potency than that of organic and inorganic selenium compounds. The inhibitory effect of propyl-2-2-diphenyl diselenide and propyl-2-methoxy-2-phenyl selenide seems to be mediated by (PhSe)2 since the compounds decomposed rapidly to (PhSe)2 in aqueous medium. The inhibitory action of selenium forms on delta-ALA-D from liver, kidney, and brain was antagonized by sulfhydryl protecting agents (dithiotreitol and reduced glutathione). The effects of organic selenium compounds on delta-ALA-D were related to the stability of the Se-Se (or Se-C) bond because the compound methyl-diphenyl diselenide (which possesses the most stable Se-C-Se bond) did not inhibit the enzyme. The inhibitory action of (PhSe)2 was not related to the formation of oxyradicals in the medium since superoxide dismutase and catalase did not affect the inhibition of delta-ALA-D by (PhSe)2. delta-ALA-D from cucumber leaves was not inhibited by selenium or tellurium compounds which suggests that these compounds act directly on the B or beta-site of the animal enzyme. These results suggest that delta-ALA-D from liver, kidney, and brain is a potential molecular target for the toxic effect of organic forms of selenium and tellurium.

Animals↗
PubMed1986

Syntheses of selenium labelled compounds--II. The exchange reaction with elemental selenium.

73Se labelled 2-selenouracil was prepared by the isotope exchange reaction method. It has been well known that in order to prepare labelled compounds in high specific activity by exchange reaction, the substrate compounds have to be used in small quantities. For 2-selenouracil, however, the reaction in low concentration is not always preferable for the labelling of high specific activity within a limited time. The optimum conditions for the preparation of [2-73Se]-2-selenouracil of maximum specific activity were determined.

Humans↗
PubMed1997

Chemopreventive and growth inhibitory effects of selenium.

There is very convincing evidence that a high dietary level of selenium substantially reduces the incidence of a wide variety of animal cancers. The human epidemiological evidence is less clear cut, but overall suggests that selenium may be protective: the evidence is strongest in men in relation to gastro-intestinal cancers. There is evidence that dietary selenium compounds reduce the formation of DNA adducts by carcinogens. Selenium compounds also inhibit growth in vitro and induce apoptosis. In general, there is a good correlation between the effectiveness of selenium compounds in chemoprevention and growth inhibition, implying that the mechanisms of growth inhibition and chemoprevention may be similar and that a major factor in the chemopreventive effects of selenium compounds in vivo is their ability to retard outgrowth of pre-malignant cells. Various hypotheses have been advanced as to how selenium compounds might prevent tumour cell growth. One is that they cause apoptosis by inducing oxidative stress. However, we have shown that the most potent selenium compound, selenodiglutathione (SDG), a natural metabolite of selenite, does not induce oxidative stress, at least not in the same way as other oxidants such as H2O2 and diamide. Firstly, a partially selenium-resistant variant cell line does not show increased resistance to H2O2. Moreover, SDG does not induce widespread tyrosine phosphorylation, including MAP and SAP kinases, like other oxidants such as H2O2 and diamide and its effects are not reversed by pretreatment with the tyrosine kinase inhibitor, herbimycin. Our experiments with the selenium-resistant variant suggest that a novel selenium-binding protein may be involved in growth inhibition by selenium.

Anticarcinogenic Agents↗
PubMed1986

Intestinal absorption of 75Se-labeled sodium selenite and selenomethionine in chicks: effects of time, segment, selenium concentration and method of measurement.

The purpose of the present experiments was to obtain information on the intestinal transport of different selenium compounds in chicks. Absorption of selenium was studied in 3-wk-old white Leghorn cockerels both by introducing the radiolabeled selenium compounds into ligated intestinal loops of the anesthetized birds and after oral or parenteral administration of the isotope to previously fasted animals. Increasing the stable selenite concentration slightly reduced the percentage of [75Se]selenite transferred from the intestinal lumen to the body, while the transport of [75Se]selenomethionine was not similarly affected by the carrier concentration. Selenomethionine was more rapidly removed from the ligated intestinal segment and more efficiently retained after oral or parenteral administration. It was shown that the liver selenium cannot be used as an indicator of the efficiency of selenium absorption in short-term studies, since after dosing the liver accumulates sodium selenite more efficiently than selenomethionine, in spite of the greater percentage absorption of the latter compound. The percentage absorption of both selenium compounds was greatest from the duodenal segment of the small intestine. The transport of these selenium compounds does not appear to depend on the dietary level of selenium since the percentage absorption was not altered by feeding the birds diets supplemented with 0.4 or 4.0 ppm selenium prior to the measurement of absorption. The data imply that there are differences, in the chick, in the processes by which various selenium compounds are transported across the intestinal epithelium and retained in the body. The differences in absorption are not of nutritional importance, since, regardless of the chemical form, selenium is efficiently absorbed.

Administration, Oral↗
PubMed1995

Cellular and metabolic effects of triphenylselenonium chloride in a mammary cell culture model.

Triphenylselenonium chloride, a novel synthetic organic selenium compound in which selenium is bonded to three unsubstituted benzene rings, possesses significant chemopreventive activity against chemically-induced mammary carcinogenesis. The effects of triphenylselenonium chloride on a mammary tumor cell line (MOD) were compared to selenite, a reference compound in selenium chemoprevention research. It was observed that triphenylselenonium chloride treatment exerted a cytostatic effect in the absence of membrane damage or DNA strand breaks. The observed cytostasis was associated with a selenium concentration-dependent inhibition of cell proliferation, measured by [3H]thymidine incorporation into DNA, and delayed cell cycle progression. In contrast, selenite treatment rapidly induced DNA damage and cell death. These marked differences were observed across the same levels of cellular selenium. In addition, triphenylselenonium chloride treatment increased glucose consumption and lactate production, indicating an effect of the compound on cellular energy metabolism. Collectively these observations demonstrate that the toxic activities associated with selenite treatment do not occur when cells are treated with triphenylselenonium chloride. This compound represents a new type of selenium compound that exerts significant cellular effects through mechanisms distinct from those induced by selenite.

Animals↗
PubMed1995

Fish consumption and exposure to persistent organochlorine compounds, mercury, selenium and methylamines among Swedish fishermen.

OBJECTIVES: This study assessed dietary habits and exposure to selenium, persistent organochlorine compounds, methylmercury, and methylamines among Swedish fishermen. METHODS: Two hundred and fifty randomly selected subjects from a cohort of 2896 fishermen from the Swedish east coast (Baltic Sea) and 8477 fishermen from the west coast (Skagerrak and Kattegatt) were interviewed along with 250 referents. Subgroups of fishermen and referents from different coastal areas were also selected for blood and urine sampling. RESULTS: The interview data showed that fishermen ate almost twice as much fish as the 250 referents from the general population. The blood levels of mercury were twice as high, and the plasma selenium levels were 10-15% higher in the fishermen than in the referents. There was, however, no difference between the fishermen's cohorts with respect to these variables. Fishermen from the east coast ate more fatty fish than fishermen from the west coast, and they also had higher blood levels of persistent organochlorine compounds such as polychlorinated biphenyls and polychlorinated dibenzo p-dioxins and furans (present in fatty fish species in the Baltic Sea) than both the westcoast fishermen and the referents. CONCLUSIONS: A cohort of Swedish eastcoast fishermen might be a suitable study base for epidemiologic studies on the mortality and cancer morbidity associated with dietary exposure to persistent organochlorine compounds.

Animals↗