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In vivo investigation of the distribution and the local speciation of selenium in Allium cepa L. by means of microscopic X-ray absorption near-edge structure spectroscopy and confocal microscopic X-ray fluorescence analysis.

In this work, microscopic X-ray absorption near-edge structure spectroscopy (mu-XANES) and confocal microscopic X-ray fluorescence analysis (mu-XRF) were used for the in vivo determination of the distribution of total selenium and for the local speciation of selenium in roots and leaves of onion. Selected Allium cepa L. plants were grown hydroponically in a standard medium containing inorganic selenium compounds (selenite or selenate). The measurements were performed in vivo, that is, on living plants without the need for any form of sampling or sample pretreatment and without the necessity for cutting plant tissues into pieces. Distinct energy differences of the XANES spectra of various selenium reference compounds having different oxidation states allow adjusting the excitation energies used for mu-XRF mapping in such a manner that the distribution of selenium in various oxidation states is obtained with a spatial resolution of a few tens of micrometers within the virtual cross section of the onion tissues. We find that the ratio of inorganic to amino acid selenium compounds differs in various subparts of the plant. Detailed in vivo investigation of the distribution of various selenium species in virtual cross sections of root tips and green leaf shows that the selenium transport takes place via different mechanisms, depending on the nature of the selenium compounds originally taken up.

Amino Acids↗

Bioavailability of enteral yeast-selenium in preterm infants.

There is no data or literature on the effects of supplementing infants with yeast selenium, although its intestinal absorption and bioavailability are higher in adults compared with other selenium compounds. The aim of the present investigation was to study the impact of selenium enriched yeast on the serum selenium concentration of preterm infants living in a low selenium area (Hungary). Twenty-eight preterm infants with mean+/-SD birth weight of 962+/-129 g and gestational age 27+/-1 wk were randomized into two groups at birth with respect to selenium supplementation. In the supplemented group (n=14) infants received 4.8 mg yeast selenium containing 5 microg selenium daily via nasogastric drip during the first 14 postnatal days. The nonsupplemented infants were used as a reference group. In the supplemented group, the serum selenium concentration increased from 32.1+/-8.5 microg/L to 41.5+/-6.5 microg/L and in the nonsupplemented group it decreased from 25.9+/-6.8 microg/L to 18.2+/-6.4 microg/L from birth in two weeks time. Compared with previous studies, our results suggest that the bioavailability of selenium in the form of yeast selenium is higher than that of other selenium compounds used for preterm infants. We did not observe any complications or side-effects owing to enteral yeast selenium supplementation. We conclude that selenium enriched yeast is a safe and an effective form of short-term enteral selenium supplementation for infants.

Biological Availability↗

Adverse health effects of selenium in humans.

Epidemiologic studies and case reports have shown that chronic exposure to selenium compounds is associated with several adverse health effects in humans. An early toxic effect of selenium is on endocrine function, particularly on the synthesis of thyroid hormones following dietary exposure of around 300 micrograms Se/d, and on the metabolism of growth hormone and insulin-like growth factor-1. Other adverse effects of selenium exposure can be the impairment of natural killer cells activity and at higher levels, hepatotoxicity and gastrointestinal disturbances. Dermatologic effects, such as nail and hair loss and dermatitis, occur after exposure to high levels of environmental selenium. Assessing the toxicity and morbidity after long-term exposure to environmental selenium is difficult: neurotoxicity, particularly the degeneration of motor neurons leading to increased risk of amyotrophic lateral sclerosis, might occur after chronic exposure to both organic and inorganic selenium compounds. The results of laboratory investigations and cohort studies suggest that selenium species exhibit a bivalent effect in cancer, either increasing or decreasing risk. Current environmental selenium exposure limits appear to be inadequate for averting adverse health effects.

Biomarkers↗

Is the selenium drinking water standard justified?

Four cases are presented which suggest that the present U.S.E.P.A. drinking water standard for selenium of 10 micrograms/L in inappropriate. The rationale upon which this standard is based is that selenium is carcinogenic, induces dental caries formation, and is highly toxic to animals. However, a critical assessment of this literature can not support these claims. Case no. 1 demonstrates that there is insufficient evidence to classify selenium as a carcinogen. Data derived from the three respective groups of researchers claiming a carcinogenic effect induced by selenium are obscure due to 1) the inability to accurately identify malignancies, 2) the apparent opposite effects of different selenium compounds, and 3) the lack of proper controls. Case no. 2 reviews recent evidence that selenium reduces the incidence of cancer in laboratory animals and in man, an effect which can probably be attributed to the antioxidant properties of selenium compounds. Case no. 3 provides evidence which does not permit the classification of selenium as a cariogenic element. Epidemiological studies supporting such a claim are inadequate since they lack properly matched control groups. Animal data do not support this link as well. Case no. 4 is a review of studies which clearly demonstrate the essentiality of selenium, an aspect of selenium metabolism that was not considered when the 10 micrograms/L standard was promulgated. In light of the four cases presented and an assessment of selenium toxicity in man, it is concluded that the 10 micrograms/L standard can not be justified. Instead, it is suggested that 50 micrograms/L selenium should provide sufficient protection from the toxic effects of this element. This is consistent with the current state of knowledge with respect to the potential adverse health effects associated with selenium.

9,10-Dimethyl-1,2-benzanthracene↗

Effect of pH on one-electron oxidation chemistry of organoselenium compounds in aqueous solutions.

Pulse radiolysis coupled with absorption detection has been employed to study one-electron oxidation of selenomethionine (SeM), selenocystine (SeCys), methyl selenocysteine (MeSeCys), and selenourea (SeU) in aqueous solutions. Hydroxyl radicals (*OH) in the pH range from 1 to 7 and specific one-electron oxidants Cl2*- (pH 1) and Br2*- (pH 7) have been used to carry out the oxidation reactions. The bimolecular rate constants for these reactions were reported to be in the range of 2 x 10(9) to 10 x 10(9) M(-1) s(-1). Reactions of oxidizing radicals with all these compounds produced selenium-centered radical cations. The structure and stability of the radical cation were found to depend mainly on the substituent and pH. SeM, at pH 7, produced a monomer radical cation (lambdamax approximately 380 nm), while at pH 1, a dimer radical cation was formed by the interaction between oxidized and parent SeM (lambdamax approximately 480 nm). Similarly, SeCys, at pH 7, on one-electron oxidation, produced a monomer radical cation (lambdamax approximately 460 nm), while at pH 1, the reaction produced a transient species with (lambdamax approximately 560 nm), which is also a monomer radical cation. MeSeCys on one-electron oxidation in the pH range from 1 to 7 produced monomer radical cations (lambdamax approximately 350 nm), while at pH < 0, the reaction produced dimer radical cations (lambdamax approximately 460 nm). SeU at all the pH ranges produced dimer radical cations (lambdamax approximately 410 nm). The association constants of the dimer radical cations of SeM, MeSeCys, and SeU were determined by following absorption changes at lambdamax as a function of concentration. From these studies it is concluded that formation of monomer and dimer radical cations mainly depends on the substitution, pH, and the heteroatoms like N and O. The availability of a lone pair on an N or O atom at the beta or gamma position results in monomer radical cations having intramolecular stabilization. When such a lone pair is not available, the monomer radical cation is converted into a dimer radical cation which acquires intermolecular stabilization by the other selenium atom. The pH dependency confirms the role of protonation on stabilization. The oxidation chemistry of these selenium compounds is compared with that of their sulfur analogues.

Cystine↗

Evaluation of organoselenium compounds for potential chemopreventive properties in colon carcinogenesis.

As a part of a program aimed to develop less toxic and more effective chemopreventive organoselenium compounds than inorganic selenium, we have evaluated benzyl selenocyanate (BSC) and its o-, m-, p-nitro and -methoxy isomers, o-, m-, and p-isomers of phenylenebis(methylene)selenocyanate (XSC), dibenzyl diselenide (DDS), and 2,2'-diselenobis[((N,N-dimethylamino)methyl)- benzene]bis(hydrochloride salt) (DSBDB) for their potential colon tumor inhibitory properties using azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF), a preneoplastic lesion, in male F344 rats prior to preclinical efficacy study. In the first experiment, the effect of these agents administered during initiation and postinitiation periods of carcinogenesis was investigated. Male F344 rats were fed diets containing 8 ppm Na2SeO3 or 10 ppm of each BSC and its analogues, DDS and DSBDB or 20 ppm of each XSC analogue, two weeks prior to AOM (15 mg/kg body wt., once weekly for two weeks, s.c.) administration and during and until 8 weeks after AOM treatment. Formalin-fixed and methylene blue stained colons were scored for AOM-induced ACF using the light microscope. Taking body weight gains and multiplicity of 4 or more AC/focus, the inhibitory effects of Na2SeO3, o-, m- and p-methoxy-BSC, p-XSC and DDS were much greater than those of the other selenium compounds. In the second study, the effects of these agents when administered during the initiation or postinitiation periods were investigated. The results indicated that o-, m-, and p-methoxy-BSC, DDS and p-XSC significantly inhibited crypt multiplicity during the initiation period whereas o-, and p-methoxy-BSC, p-XSC and DDS suppressed crypt multiplicity during the postinitiation period. It is concluded that o-, and p-methoxy-BSC, p-XSC and DDS possess potential chemopreventive properties in colon cancer. Further studies are warranted to evaluated these agents for chemopreventive properties in preclinical efficacy studies.

Animals↗

Inhibition of colony formation of Hela cells by naturally occurring and synthetic agents.

The present study compared the effects of naturally occurring extracts or compound in combination with synthetic selenium compounds on the colony formation and nucleic acid synthesis of cultured human cervical epitheloid carcinoma cells (Hela). Crude extract of bean (Phaseolus vulgaris) or purified lectin from red kidney bean (Phaseolus vulgaris) in combination with selenomethionine were more effective in inhibiting the colony formation of Hela cells than when these cells were treated with these agents alone. Extracts of saffron (Crocus sativus) and selenite have previously been shown to inhibit the colony formation and nucleic acid synthesis by Hela cells in vitro. In the present study we examined the effects of saffron extract in combination with selenite on the colony formation and DNA and RNA synthesis in Hela cells. We found that the treatment of tumor Hela cells with saffron extract in combination with selenite increased the level of inhibition of the colony formation and nucleic acid synthesis in comparison with cells that were treated with only one of these agents. The inhibitory effect of saffron extract in combination with selenite was modified by intracellular sulfhydryl compounds.

Cell Division↗

Efficacy of trimethylselenonium versus selenite in cancer chemoprevention and its modulation by arsenite.

Selenite, which has been demonstrated to be an effective prophylactic agent in experimental carcinogenesis, is metabolized to trimethylselenonium as an excretory product. Previous reports in the literature have shown that arsenite decreases the toxicity of selenite but increases that of trimethylselenonium. The present study was designed to compare the anti-carcinogenic efficacy of selenite and trimethylselenonium and their interactions with arsenite in chemoprevention, using the dimethylbenz[a]anthracene-induced mammary tumor model in rats. The results of this experiment indicated that supplementation of selenite (3 p.p.m. Se) alone produced approximately 50% reduction in tumor yield, and arsenite (5 p.p.m. As) reduced the response to selenite. In contrast, arsenite greatly enhanced the protective effect of trimethylselenonium (40 p.p.m. Se); this combination was nearly as effective as selenite, although either trimethylselenonium or arsenite alone was inactive. Thus, arsenite has the capacity to influence the anti-carcinogenic action of selenium, and can either potentiate or attenuate the protective effect depending on the methylation state of the selenium compound. The metabolism of selenium and its perturbation by arsenite are discussed in relation to the above findings.

Animals↗

High-performance liquid chromatography-ultrasonic nebulizer high-power nitrogen microwave-induced plasma mass spectrometry, real-time on-line coupling for selenium speciation analysis.

The coupling of a high-power nitrogen (N2) microwave-induced plasma (MIP) mass spectrometry--(MS) (1.3 kW) with high-performance liquid chromatography, connected with concentric nebulizer (CN), ultrasonic nebulizer (USN) and a hydride generation (HG) systems, for the optimization and determination of selenium compounds, has been carried out. The MIP-MS system fulfils the ideal requirement being an on-line real-time chromatographic detector for Se speciation analysis. Interchanging of MIP-MS system fabricated nebulizer (concentric) with an ultrasonic nebulizer increases about 3.4-12 (peak height) and 6.5-10 (peak area) times ion signals for the selenium compounds. The detection limits for selenate, selenite, trimethylselenonium ion (TmSe), selenomethionine (Semet) and selenoethionine (Seet) (in Milli-Q-water) obtained with the optimized HPLC-USN-N2MIP-MS system are 0.11, 0.14, 0.09, 0.14 and 0.10 microg L(-1), respectively, about 12-48 times lower than the HPLC-CN-MIP-MS and 1.5-4.4 (peak height) times lower compared to the HPLC-CN-inductively coupled plasma (ICP)-MS coupling. Considering peak area, the repeatability (R.S.D. for three successive analyses) and intermediate precision (R.S.D. for three successive analyses performed on three different days), achieved for five Se compounds are 0.8-5.6, and 1.1-5.9%, comparable with the HPLC-CN-ICP-MS, HPLC-HG-MIP-MS and HPLC-CN-MIP-MS systems. The combined HPLC-USN-N2MIP-MS has been adequately applied for the determination of Se compounds in certified National Institute for Environmental studies human urine CRM No. 18. The results reasonably agree with the HPLC-CN-ICP-MS values. This encouraging combination may be an alternative ion source of mass spectrometry for coming generation in regard to the selenium speciation analysis.

Chromatography, High Pressure Liquid↗

Facilitation of long-term object recognition memory by pretraining administration of diphenyl diselenide in mice.

Selenium compounds display antioxidant and neuroprotective properties. Diphenyl diselenide (PhSe)(2) is an organic selenium compound that affects a number of neuronal processes. The aim of the present study was to evaluate the effects of the systemic administration of (PhSe)(2) on novel object recognition memory in mice. Adult male CF1 mice were given an i.p. injection of (PhSe)(2) (0.2, 1.0, 5.0, or 25.0 micromol/kg) 30 min before training in an object recognition task. (PhSe)(2) did not affect short-term memory or the total time exploring both objects, but induced a facilitation of retention measured 24 h after training. The present findings show that systemic administration of (PhSe)(2) induces a facilitation of formation of long-term object recognition memory.

Animals↗

Selenite inhibition of Coxsackie virus B5 replication: implications on the etiology of Keshan disease.

Keshan disease is a cardiomyopathy of unknown origin reported in some areas of China. Because of epidemiologic features, this disease was ascribed to an infectious agent, likely a Coxsackie virus, but it has also been thought to depend on selenium deficiency, mainly because selenite is effective in its prophylaxis. We examined the hypothesis that pharmacological activity of selenite on Coxsackie virus growth was associated with prevention of Keshan disease. We studied the antiviral effects of three selenium compounds on Coxsackie virus B5 replication: five microM selenite reduced viral replication, whilst 10 microM selenate and selenomethionine did not exhibit any antiviral activity. The inhibitory activity of selenite on viral replication was due to its toxicity following its interaction with thiols, as that activity could be blocked by dithiothreitol, a sulfhydryl-protecting agent known to reverse several toxic effect of selenite. Zinc, another inhibitor of selenite toxicity, also counteracted the antiviral effect of selenite. The selenium compounds showed only limited activity against herpes simplex 1 virus and IHD strain of vaccinia virus. A direct inhibitory effect of selenite on Coxsackie virus replication might explain the efficacy demonstrated by this compound in the prophylaxis of Keshan disease.

Animals↗

The influence of selinium on methyl mercury toxicity in rat hepatoma cells, human embryonic fibroblasts and human lymphocytes in culture.

The effect of methyl mercury and two selenium compounds have been studied in cell cultures. Methyl mercury in concentrations above 1 microM had a pronounced inhibiting effect on the growth of rat Morris hepatoma cells. Glucose and lactate uptake in relation to cell protein was appreciably stimulated by the organic mercury compound. Selenite in low concentration (0.5 microM) and seleno-di-N-acetyl glycine in thousandfold higher concentrations offered considerable protection against these effects of methyl mercury. The same selenite concentration (0.5 microM), which did not affect cell growth, caused an appreciable protection against methyl mercury (6 microM), even if it was added 3 days after methyl mercury. The methyl mercury inhibited the growth of human embryonic fibroblasts and the DNA-synthesis in the human lymphocytes. However, no protective effect of selenite were observed in these cell types. These results suggest that selenium compounds exert their protective effect through cell specific processes rather than by a direct chemical reaction between selenite and methyl mercury.

Animals↗

Mercury, silver, and gold inhibition of selenium-accelerated cysteine oxidation.

In vivo, cysteine in proteins or glutathione is the major amino acid involved in sulfhydryl oxidation-reduction reactions. An in vitro model of cysteine oxidation accelerated by selenium compounds was used to study the interaction of selenocystine and sodium selenite with metal ions. The interaction of metal ions with selenium compounds inhibited cysteine oxidation. The ionic forms of three toxic soft-acid metals, mercury, silver, and gold, were the most effective inhibitors. The antiarthritic gold drugs, aurothiomalate and aurothioglucose, were of particular interest as they inhibit the activity of selenium-glutathione peroxidase. The effect of gold ligands on gold(I) inhibition of selenocystine-accelerated cysteine oxidation was tested. Sodium cyanide partially reversed inhibition and potassium iodide had no effect. Inhibition of selenium-accelerated oxidation-reduction reactions by soft-acid metal ions may be of biological relevance during toxicities or during antiarthritic gold therapy.

Cysteine↗

Susceptibility of methicillin-resistant Staphylococcus aureus to the selenium-containing compound 2-phenyl-1,2-benzoisoselenazol-3(2H)-one (PZ51).

The growth of Staphylococcus aureus 209P was inhibited by 0.20 micrograms of 2-phenyl-1,2-benzoisoselenazol-3(2H)-one (PZ51) per ml, while strains of the family Enterobacteriaceae were more resistant to the drug. The MIC for 90% of methicillin-resistant S. aureus strains was 1.56 micrograms/ml, and the drug was bactericidal. The selenium in PZ51 was essential, since its sulfur analog (PZ25) lost the antibacterial activity.

Azoles↗

Antigenotoxic properties of selenium: studies in the wing spot test in Drosophila.

The genotoxic activity of three selenium compounds (sodium selenite, sodium selenate, and selenious acid) and the antigenotoxic effects of sodium selenite in combination with the chromium compound potassium dichromate were studied using the wing spot test of Drosophila melanogaster. This assay is based on the principle that the loss of heterozygosity of suitable recessive markers, multiple wing hairs (mwh) and flare-3 (flr[3]), can lead to the formation of mutant clones of larval cells, which are then expressed as spots on the wings of the adult flies. Pretreatment and chronic cotreatment was comparatively used for the antigenotoxicity study. From the results obtained, it was evident that all selenium compounds are unable to increase the frequency of any of the three categories of spots recorded (small, large, and twin spots). Nevertheless, the antigenotoxic effects of sodium selenite were clearly demonstrated, in both cotreatment and pretreatment, by a complete suppression of those clones induced by potassium dichromate. Therefore, the D. melanogaster wing spot test was revealed to be a good assay, not only for evaluating genotoxic activity but also for detecting antigenotoxic effects in vivo.

Animals↗

Fluoride-selenium interaction in the hard and soft tissues of the rat.

The interaction of dietary fluoride and selenium in the hard and soft tissues of rats was studied by providing drinking solutions containing 50 ppm F, as NaF, alone or plus 1 or 3 ppm Se as one of the following selenium compounds: NaSeO3, Na2SeO4, DL-selenomethionine, or DL-selenocystine. The following parameters were measured: symptoms of selenium toxicity, soft tissue uptake of fluoride and selenium, histology of liver and kidney tissues, fluoride uptake into growing femur bones, and fluoride uptake onto calcified molar enamel. No evidence was found that fluoride interacted with any of the four selenium compounds.

Animals↗