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PubMed2003

Effects of an inorganic and two new organic compounds of selenium on morphologic blood elements and antioxidant status in mice.

Two organic compounds, 4-(o-tolilo-)-selenosemicarbazide of p-chlorobenzoic acid and 3-(p-chlorobenzoylamino-)-2-(o-tolylimino-)-4-phenyl-4-selenazoline were compared to the effects of the supplementation with inorganic Na2SeO3. Studies were carried out in four groups consisting of 10 female mice each of SWISS strain. Three of them were supplemented with different selenium formula at the dose of 10(-3) mg Se per g over the period of 10 day. The blood samples were collected to heparinized test tubes; the red blood and white blood count, hematocrit and haemoglobin concentration were studied. The influence of selenium compounds on phagocytosis and NBT test was determined.

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↗
PubMed2004

Methioninase and selenomethionine but not Se-methylselenocysteine generate methylselenol and superoxide in an in vitro chemiluminescent assay: implications for the nutritional carcinostatic activity of selenoamino acids.

Methylselenol from selenium metabolism is postulated to be and most experimental evidence now indicates that it is the selenium metabolite responsible for the dietary chemoprevention of cancers. Using the recombinant enzyme methioninase, methylselenol-generating chemiluminesence by superoxide (O2*-) is shown to be catalytically produced from L-selenomethionine and D,L-selenoethionine, but not from methionine or L-Se-methylselenocysteine (SeMC). Methylselenol enzymaticaly generated by methioninase activity from the substrate selenomethionine arises from an initial putative selenium radical as measured by chemiluminesence in the absence of glutathione (GSH). In the presence of GSH, superoxide was generated as measured by chemiluminesence and superoxide dismutase inhibition of chemiluminescence. Ascorbic acid also quenched the chemiluminesence from the activity of methioninase with selenomethionine. Methylselenol and other redox cycling selenium compounds are almost assuredly accountable for inducing cell-cycle arrest and apoptosis in cancer cells in vitro and in vivo. Methylselenol generated from selenomethionine by methioninase is catalytic alone in oxidizing thiols, i.e. GSH, generating superoxide and inducing oxidative stress in direct proportion to its concentration. Se-methylselenocysteine in vivo is very likely carcinostatic in like manner to selenomethionine by generating methylselenol from other enzymatic activity, i.e. beta-lyase or amino acid oxidases.

Apoptosis↗
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↗
PubMed2000

Lack of chemopreventive efficacy of DL-selenomethionine in colon carcinogenesis.

Epidemiologic observations and laboratory research have suggested that dietary selenium reduces the risk of colon cancer. Selenium-enriched brewer's yeast as a dietary supplement reduces the incidence of and mortality from cancer of the colon in humans. It is not clear whether the observed inhibitory effect is due to selenomethionine, or to other forms of selenium, or to a mixture of the selenium compounds present in selenium-enriched brewer's yeast. Therefore, bioassay described in this study examined the chemopreventive efficacy of 10 and 15 ppm selenomethionine, equivalent to 3.6 and 5.4 ppm as selenium, against azoxymethane (AOM)-induced colon carcinogenesis. At five weeks of age, groups of male F344 rats were fed diets containing 0 (control diet), 10 or 15 ppm selenomethionine. At seven and eight weeks of age, all rats except those in vehicle-treated groups received s.c. injections of AOM at a dose rate of 15 mg/kg body wt. The rats were maintained on their respective diets for 52 weeks and were then sacrificed. Colon tumors were processed and evaluated histopathologically. Colon tumor incidence and multiplicity were analyzed statistically. No obvious toxic effects were observed following dietary administration of 10 or 15 ppm selenomethionine as indicated by body weight gain. Administration of 10 or 15 ppm selenomethionine had no significant effect on colon tumor incidence and multiplicity. This study suggests that i) selenomethionine lacks chemopreventive efficacy against AOM-induced colon carcinogenesis and ii) other forms of selenium or a mixture of selenium compounds present in selenium-enriched brewer's yeast need to be evaluated for their chemopreventive efficacy.

Adenocarcinoma↗
PubMed2006

Effect of selenium-containing compounds on hepatic chemoprotective enzymes in mice.

Selenite and organoselenium compounds have been examined at supranutritional levels for their ability to influence the activity and mRNA levels of chemoprotective enzymes in the livers of selenium-sufficient mice and the changes compared to those elicited by oltipraz. Compounds investigated included novel selenocysteine prodrugs that have previously been evaluated for their ability to reduce the tumorigenicity of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in mice. Following seven daily doses (i.g.), all compounds except 2-methylselenazolidine-4(R)-carboxylic acid (MSCA) increased thioredoxin reductase activity (43-92%) but only for 2-oxoselenazolidine-4(R)-carboxylic acid (OSCA) was there an accompanying increase in mRNA. No compound enhanced glutathione peroxidase activity, although sodium selenite significantly elevated the mRNA of this enzyme. Oltipraz was an efficacious inducer of both thioredoxin reductase and glutathione peroxidase mRNAs. Sodium selenite, selenazolidine-4(R)-carboxylic acid (SCA), and OSCA elevated NAD(P)H-quinone oxidoreductase mRNA but only for OSCA was the elevation in mRNA accompanied by an increase in enzyme activity. L-Selenocystine significantly increased this activity without increasing mRNA levels. Sodium selenite, L-selenocystine, L-selenomethionine, and Se-methyl-L-selenocysteine all enhanced glutathione S-transferase activity. The increased activity with sodium selenite was accompanied by increases in mRNAs of Gst alpha, Gst mu and Gst pi classes, while for L-selenocystine and Se-methyl-L-selenocysteine, only an elevation in the mRNA for the Gst alpha class was observed. Gst alpha and Gst mu class mRNAs were elevated by OSCA without a significant elevation in enzyme activity. SCA and MSCA both elevated a Gst pi mRNA and MSCA elevated Gst mu in addition. By comparison, oltipraz only significantly elevated the mRNA of Gst mu, adding to the conclusion that across the entire study, no selenium compound appears to be acting purely through the antioxidant response typified by oltipraz. Despite their chemical similarity, the three cysteine prodrugs, SCA, MSCA, and OSCA, each produced its own unique pattern of effects on protective enzymes and none was identical to the pattern elicited by sodium selenite, L-selenocystine, L-selenomethionine, and Se-methyl-L-selenocysteine. The study also shows that after 7 days of administration, there was only occasional concordance between elevations in mRNA and enzyme activity for any selenium compound and for any protective enzyme, there was no response in common for all selenium compounds.

Animals↗
PubMed1999

Selenium redox biochemistry of zinc-sulfur coordination sites in proteins and enzymes.

Selenium has been increasingly recognized as an essential element in biology and medicine. Its biochemistry resembles that of sulfur, yet differs from it by virtue of both redox potentials and stabilities of its oxidation states. Selenium can substitute for the more ubiquitous sulfur of cysteine and as such plays an important role in more than a dozen selenoproteins. We have chosen to examine zinc-sulfur centers as possible targets of selenium redox biochemistry. Selenium compounds release zinc from zinc/thiolate-coordination environments, thereby affecting the cellular thiol redox state and the distribution of zinc and likely of other metal ions. Aromatic selenium compounds are excellent spectroscopic probes of the otherwise relatively unstable functional selenium groups. Zinc-coordinated thiolates, e.g., metallothionein (MT), and uncoordinated thiolates, e.g., glutathione, react with benzeneseleninic acid (oxidation state +2), benzeneselenenyl chloride (oxidation state 0) and selenocystamine (oxidation state -1). Benzeneseleninic acid and benzeneselenenyl chloride react very rapidly with MT and titrate substoichiometrically and with a 1:1 stoichiometry, respectively. Selenium compounds also catalyze the release of zinc from MT in peroxidation and thiol/disulfide-interchange reactions. The selenoenzyme glutathione peroxidase catalytically oxidizes MT and releases zinc in the presence of t-butyl hydroperoxide, suggesting that this type of redox chemistry may be employed in biology for the control of metal metabolism. Moreover, selenium compounds are likely targets for zinc/thiolate coordination centers in vivo, because the reactions are only partially suppressed by excess glutathione. This specificity and the potential to undergo catalytic reactions at low concentrations suggests that zinc release is a significant aspect of the therapeutic antioxidant actions of selenium compounds in antiinflammatory and anticarcinogenic agents.

Animals↗
PubMed2006

Pro-angiogenesis action of arsenic and its reversal by selenium-derived compounds.

Inorganic arsenic (arsenite and arsenate) in drinking water has been associated with skin cancers and increased incidence of cardiovascular diseases. Additionally, studies have demonstrated the pro-angiogenic effect of arsenite and its potential promotion of tumor angiogenesis and tumor progression. Furthermore, recent reports demonstrated reversal of skin co-carcinogenesis by an organoselenium compound. The present study was undertaken to determine the effect and mechanism on angiogenesis of arsenite at low level and its potential reversal by various selenium-derived compounds. The pro-angiogenesis effects and mechanisms of sodium arsenite were determined using the chick chorioallantoic membrane (CAM) model over 3 days and compared with standard pro-angiogenesis factors, such as basic fibroblast growth factor (b-FGF). Additionally, the potential effect of various selenium-derived compounds--such as dimethyl selenone, diphenyl selenone, sodium selenite or Se-methyl selenocysteine--in reversing the pro-angiogenesis effect of arsenite or b-FGF was also determined in the CAM model. The pro-angiogenesis effect of arsenite or b-FGF was significantly (P < 0.01) blocked by dimethyl selenone, diphenyl selenone, sodium selenite or Se-methyl selenocysteine. The pro-angiogenesis effect of either sodium arsenite at 33 nM or b-FGF was blocked (P < 0.01) by the extracellular signal-regulated kinases 1 and 2 (ERK1/2) activation inhibitor, PD 98059. Additionally, the pro-angiogenic effect of arsenic or b-FGF was blocked as well (P < 0.01) by the alphavbeta3 antagonist, XT199. These data suggest that the pro-angiogenesis effect of arsenic is initiated at the plasma membrane integrin alphavbeta3, involves activation of the ERK1/2 pathway and is effectively reversed by various selenium-derived compounds.

Angiogenesis Inducing Agents↗
PubMed1991

Chemical form of selenium, critical metabolites, and cancer prevention.

Methylated selenides are prominent metabolites at the dietary levels used for obtaining anticarcinogenic effects with selenium. The present study reports the chemopreventive activities of 2 novel selenium compounds, Se-methylselenocysteine and dimethyl selenoxide, in the rat dimethylbenz(a)anthracene-induced mammary tumor model. Other treatment groups were supplemented with either selenite or selenocystine for comparative purposes. Each selenium compound was tested at different levels and was given to the animal starting 1 week before dimethylbenz(a)anthracene administration and continued until sacrifice. Results of the carcinogenesis experiments showed that the relative efficacy with the four compounds was Se-methylselenocysteine greater than selenite greater than selenocystine greater than dimethyl selenoxide. In correlating the chemical form and metabolism of these selenium compounds with their anticarcinogenic activity, it is concluded that: (a) selenium compounds that are able to generate a steady stream of methylated metabolites, particularly the monomethylated species, are likely to have good chemopreventive potential; (b) anticarcinogenic activity is lower for selenoamino acids, such as selenocysteine following conversion from selenocystine, which have an escape mechanism via random, nonstoichiometric incorporation into proteins; and (c) forms of selenium, as exemplified by dimethyl selenoxide, which are metabolized rapidly and quantitatively to dimethyl selenide and trimethylselenonium and excreted, are likely to be poor choices. We also undertook a separate bioavailability study using Se-methylselenocysteine, dimethyl selenoxide, and trimethylselenonium as the starting compounds for delivering selenium with one, two, or three methyl groups, and measured the ability of these compounds to restore glutathione peroxidase activity in selenium-depleted animals. All three compounds were able to fully replete this enzyme, although with a wide range of efficiency (Se-methylselenocysteine greater than dimethyl selenoxide greater than trimethylselenonium), suggesting that complete demethylation to inorganic selenium is a normal process of selenium metabolism. However, the degree to which this occurs under chemoprevention conditions would argue against the involvement of selenoproteins in the anticarcinogenic action of these selenium compounds.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1986

Fatal poisoning with selenium dioxide.

Two hours after suicidal ingestion of an unknown amount of selenium dioxide, a 17-year-old male was admitted to hospital with asystolia and apnea. Attempts at resuscitation failed and the patient was pronounced dead. Findings at autopsy included congestion of lungs and kidneys, diffuse swelling of the heart, and brain edema. The most impressive finding was an orange-brown discoloration of the skin and all viscera, probably due to hemolysis and/or pigmentation related to ingestion of selenium dioxide. Selenium blood and tissue levels were increased by a factor of 100-1000 as compared to normal. The highest concentrations were found in pancreas, spleen, liver, and adipose tissue. For elucidation of the chemical nature of selenium in tissues, a new analytical method which was based on carbon disulfide extraction was developed. Carbon disulfide is a good solvent for non-polar selenium compounds like elemental selenium and selenium disulfide, but not for polar compounds like selenite and selenoproteins. A major fraction of selenium in tissues was extractable by carbon disulfide, which seems to indicate the presence of elemental selenium and/or selenium disulfide. The color of these substances is red and orange, respectively. This might explain at least part of the discoloration of skin and tissues. In vitro experiments suggested that trace amounts of hydrogen selenide, which is an intermediate of selenite metabolism, probably induced hemolysis. For evaluation of the therapeutic value of hemoperfusion in selenium poisoning in vitro hemoperfusion experiments were performed, which revealed only a moderate effect on selenium blood levels.

Adolescent↗
PubMed2004

Speciation of selenium in selenium-enriched shiitake mushroom, Lentinula edodes.

The major selenium compound in an aqueous extract of the most popular mushroom in Eastern Asian countries, shiitake ( Lentinula edodes), fortified with selenium (Se) was identified by means of hyphenated techniques, i.e. HPLC-inductively coupled argon plasma mass spectrometry and HPLC-electrospray ionization mass spectrometry (HPLC-ICP MS and HPLC-ESI MS). Sixty-eight per cent of the total Se in the selenized shiitake was extracted with water, and 49.8% of the Se in the water extract was eluted in the high molecular mass fraction (>40,000 kDa) before incubation at 37 degrees C. After incubation, 40.6% of the Se in the water extract was eluted in a lower molecular mass fraction and the Se eluted in the high molecular mass fraction had decreased to 14.0%, suggesting that the major selenium compound in the water extract was initially in a form bound to macromolecule(s) and was then enzymatically liberated from the macromolecule(s). The retention time of the liberated selenium compound in HPLC-ICP MS matched that of selenomethionine (SeMet), and the masses of molecular and fragment ions detected by HPLC-ESI MS also suggested that the selenium compound was SeMet. The selenized shiitake accumulated Se as SeMet, and SeMet might be bound to the water extractable high molecular mass protein(s).

Chromatography, High Pressure Liquid↗