Inorganic Forms Of Selenium Research Articles

Producing of beef meat enriched with organically bound selenium

In this study, the effects of the organic and inorganic form of selenium, in the diet for finishing beef cattle, were investigated. Sell-Plex produced by American firm Alltech as a source of organic selenium with selenium concentration of 2000 mg/kg was used. The source of inorganic selenium was sodium selenite. The trial was conducted on Simmental fattening cattle in the final stage in the free housing system and it lasted 60 days. Selenium content in control and trial group (m. longissimus dorsi) was 78.65 and 125.03 ?g/kg (P<0.01), in kidneys 855.52 and 1026.04 ?g/kg(P <0.001); in liver 453.13 and 534.64 ?g/ kg(P<0.01) and in spleen 308.44 and 383.62 ?g/kg (P<0.001), respectively. There were no differences in main carcass characteristics, share of some tissues in the round and three rib chops, chemical composition and meat quality of m. longissimus dorsi (P>0.05).Considering the higher storage of organic selenium in meat and internal organs of the fattening cattle with respect to the inorganic form, it was concluded that the selenium supply in organic form has a better bioavailability. Inclusion of organic selenium into the diet in the final stage of fattening cattle and its deposition in meat and internal organs is a good and easy way to get meat with functional foods properties that in addition to nutritional value should positively affect human health.

Metabolism of selenite in human lung cancer cells: X-ray absorption and fluorescence studies.

Selenite is an inorganic form of selenium that has a cytotoxic effect against several human cancer cell lines: one or more selenite metabolites are considered to be responsible for its toxicity. X-ray absorption spectroscopy was used to monitor Se speciation in A549 human lung cancer cells incubated with selenite over 72 h. As anticipated, selenodiglutathione and elemental Se both comprised a large proportion of Se in the cells between 4 and 72 h after treatment, which is in accordance with the reductive metabolism of selenite in the presence of glutathione and glutathione reductase/NADPH system. Selenocystine was also present in the cells but was only detected as a significant component between 24 and 48 h concomitant with a decrease in the proportion of selenocysteine and the viability of the cells. The change in speciation from the selenol, selenocysteine, to the diselenide, selenocystine, is indicative of a change in the redox status of the cells to a more oxidizing environment, likely brought about by metabolites of selenite. X-ray fluorescence microscopy of single cells treated with selenite for 24 h revealed a punctate distribution of Se in the cytoplasm. The accumulation of Se was associated with a greater than 2-fold increase in Cu, which was colocalized with Se. Selenium K-edge extended X-ray absorption fine structure (EXAFS) spectroscopy revealed Se-Se and Se-S bonding, but not Se-Cu bonding, despite the spatial association of Se and Cu. Microprobe X-ray absorption near-edge structure spectroscopy (μ-XANES) showed that the highly localized Se species was mostly elemental Se.

Effect of organic and inorganic forms of selenium in diets on turkey semen quality

The effects of Se supplementation and its organic or inorganic form on semen quantitative parameters (ejaculate volume, sperm concentration, and total number of sperm) and biochemical parameters of seminal plasma (protein concentration, acid phosphatase activity, superoxide dismutase activity, and total antioxidant capacity) were investigated over a 25-wk reproductive season. Additionally, DNA fragmentation and motility characteristics of turkey spermatozoa were measured. The parameters of turkey semen in relation to yellow semen syndrome were also determined. Twenty-four males (Big 6) were divided into 3 experimental groups differing in form of Se supplementation (no Se supplementation, 0.3 mg/kg of inorganic Se from sodium selenite and 0.3 mg/kg of organic Se from Sel-Plex, Alltech Inc., Nicholasville, KY). Dietary Se supplementation enhanced the sperm concentration and total number of sperm and did not influence the antioxidative properties of turkey seminal plasma and most biochemical parameters. Only seminal plasma acid phosphatase activity was increased in turkeys fed inorganic Se. The main sperm DNA fragmentation parameters were not affected by dietary Se. The highest percentage of motile spermatozoa (85%) was recorded for the semen of turkeys fed organic Se. Values of the biochemical parameters (acid phosphatase, superoxide dismutase, total antioxidant capacity) of seminal plasma increased during the reproductive season. Yellow semen was characterized by increased biochemical parameters and decreased spermatozoa motility characteristics. However, the percentage of motile spermatozoa did not differ between white and yellow semen. Organic Se seemed to be the preferred form of diet supplementation in comparison with inorganic Se. Biochemical parameters of semen and spermatozoa motility parameters appear to be useful for evaluating the effect of age on semen quality. Monitoring the DNA fragmentation of spermatozoa at the end of the reproductive season could be a useful tool for monitoring turkey semen quality. Increased superoxide dismutase activity can be used as an indicator of yellow semen. A decline in the quality of yellow semen can be related to a decrease in the spermatozoa motility parameters of turkeys.

Selenocysteine Is Selectively Taken Up by Red Blood Cells

Both organic and inorganic forms of selenium are utilized in the biosynthesis of selenoproteins. Selenite is taken up by red blood cells and then returned to the plasma after reduction, but little is known about the metabolic fate of selenocysteine. We found that selenocysteine was taken up into red blood cells without decomposition into selenide.

The effects of dietary oxidized fat and selenium source on performance, glutathione peroxidase, and glutathione reductase activity in broiler chickens

Normal or elevated selenium status of broilers, which is influenced by dietary selenium sources, improves the bird’s ability to overcome the adverse effects of reactive oxygen metabolites. The objective of this study was to evaluate the effects of feeding graded levels of peroxidized poultry fat on blood and hepatic glutathione peroxidase (GSH-Px), and hepatic glutathione reductase activity in broiler chickens fed either inorganic sodium selenite (SEL) or organic selenium enriched in the organic selenium yeast product Sel-Plex (SP). Nine starter diets, varying in levels of oxidized fat (0, 3, and 6 mEq/kg) and dietary selenium sources, were fed to 360 male chicks from hatch to 21 d of age. Sel-Plex or SEL was added to the basal diet to provide either 0 or 0.2 ppm of supplemental selenium in the diets. Blood and hepatic samples were obtained for each treatment group at 21 d of age. Neither peroxidized fat nor selenium source significantly altered the activity of hepatic glutathione reductase (P ≤ 0.05). Blood GSH-Px was influenced significantly by both fat and selenium source (P ≤ 0.05), but the fat × selenium source interaction was not significant (P ≥ 0.3). A selenium source effect on the hepatic GSH-Px activity (P ≤ 0.05) was evidenced by higher GSH-Px activity, even in the basal diet with no added peroxidized fat. An increase in GSH-Px activity was seen in the erythrocyte and hepatic samples in both the SEL and SP treatments when peroxidized fat was given at 3 mEq/kg, but in the erythrocytes and in the hepatic tissues from SEL-supplemented birds, there was an apparent inhibition of GSH-Px activity. This inhibition was not seen in the hepatic tissue samples from SP-fed birds. Because elevated GSH-Px activity is indicative of oxidative stress, it was concluded that dietary SP supplementation resulted in better selenium and redox status in broilers than did SEL. These results indicate that the dietary selenium supplied in an organic form (selenium yeast as SP) improved the selenium and redox status in broilers, leading to greater resistance to oxidative stress than when the inorganic form of selenium (SEL) was fed.

Comparison of glutathione peroxidase 1 and iodothyronine deiodinase 1 mRNA expression in murine liver after feeding selenite or selenized yeast

The experiment was conducted to compare the effect of different selenium sources on the expression of glutathione peroxidase 1 (GPx1) and iodothyronine deiodinase 1 (Dio1) mRNA in mice by quantitative real-time PCR. A total of 60 male Kunming mice at average body weight of 20 g were allotted to three groups in a randomized complete block design, namely two treatments and one control. Mice in Group 1 were fed a basal diet as control, while mice in Groups 2 and 3 were fed the basal diet supplemented with 0.1mg/kg selenium as sodium selenite or selenized yeast, respectively. Whole feeding experiment lasted for 30 d. At the end of the feeding trial, liver mRNA levels of GPx1 and Dio1 were determined by quantitative real-time PCR, as well as growth performance, body composition, blood and GPx activity were determined. The results showed that no significant differences in overall growth performance and body composition, including body weight, body length, heart weight, kidney weight and liver weight, were found between the experimental groups (P>0.05). Blood GPx activity increased in all of the selenium supplemented groups compared with control group (P<0.01). However, blood GPx activity in selenized yeast group was higher than that in sodium selenite group (P<0.05). Liver mRNA levels of GPx1 and Dio1 also increased in the two selenium supplemented groups compared with the control group (P<0.05), while there was no significant difference between the sodium selenite and selenized yeast groups (P>0.05). In conclusion, selenium increased the mRNA expression of GPx1 and Dio1 genes in murine liver, and there was no significant difference between the organic or inorganic form of selenium used.

Growth and fruit body formation of Pleurotus ostreatus on media supplemented with inorganic selenium

Selenium is a trace mineral chemically related to sulfur and tellurium. In the body selenium combines with protein molecules to form selenoproteins and it is distributed in low concentrations and unequally in air, soil and water all over the world. Edible mushrooms are known to be selenium accumulators. Since mushrooms contain relatively high protein levels, and they can accumulate large amounts of selenium, it is reasonable to expect that selenium could be incorporated into proteins. The growth of mycelia and fruit body formation of different medicinal mushroom strains of Pleurotus ostreatus (Hk-35 and P70) over the wide range of concentrations of inorganic form of selenium were examined. Mushrooms were cultivated on agar base media and on substrates based on sawdust. Vegetative growths of mycelium were measured as colony diameter in pure cultures supplemented with inorganic form of Se supplements, prepared as Na2SeO4 and Na2SeO3 in concentrations of: 1, 10, 25, 50, 75, 100 and 150 mg/l. Inorganic form of Se supplements, showed stimulation effects (in concentration of 1-50 mg/l) and toxic effects in higher concentration. On the standard industrial sawdust based substrate, supplemented with 100 mg/kg Na2SeO4 and Na2SeO3, accumulation of Se in fruit bodies was determined by the method of flameless atomic absorption spectrophotometer. The readings were performed on Varian SpectrAA-10 spectrophotometer equipped with VGA-76. Se as Na2SeO4 and Na2SeO3 was effectively taken up from substrates and accumulated in fruit bodies. Mushrooms accumulated selenium between 120 and 250 mg/kg dry weight. In mushrooms cultivated without Se supplement, Se contents were only about 1 mg/kg and in substrate about 0.1 mg/kg.

Selenite Treatment Inhibits LAPC-4 Tumor Growth and Prostate-Specific Antigen Secretion in a Xenograft Model of Human Prostate Cancer

Selenium compounds have known chemopreventive effects on prostate cancer. However selenite, an inorganic form of selenium, has not been extensively studied as a treatment option for prostate cancer. Our previous studies have demonstrated the inhibition of androgen receptor expression and androgen stimulated prostate-specific antigen (PSA) expression by selenite in human prostate cancer cell lines. In this study, we investigated the in vivo effects of selenite as a therapy to treat mice with established LAPC-4 tumors. Male mice harboring androgen-dependent LAPC-4 xenograft tumors were treated with selenite (2 mg/kg intraperitoneally three times per week) or vehicle for 42 days. In addition, androgen-independent LAPC-4 xenograft tumors were generated in female mice over 4 to 6 months. Once established, androgen-independent LAPC-4 tumor fragments were passaged into female mice and were treated with selenite or vehicle for 42 days. Changes in tumor volume and serum PSA levels were assessed. Selenite significantly decreased androgen-dependent LAPC-4 tumor growth in male mice over 42 days (p < 0.001). Relative tumor volume was decreased by 41% in selenite-treated animals compared with vehicle-treated animals. The inhibition of LAPC-4 tumor growth corresponded to a marked decrease in serum PSA levels (p < 0.01). In the androgen-independent LAPC-4 tumors in female mice, selenite treatment decreased tumor volume by 58% after 42 days of treatment (p < 0.001). These results suggest that selenite may have potential as a novel therapeutic agent to treat both androgen-dependent and androgen-independent prostate cancer.

Selenite induces topoisomerase I and II‐DNA complexes in K562 leukemia cells

The essential trace element selenium is one of the most promising cancer chemopreventive agents. Data from preclinical studies have revealed that selenite, an inorganic form of selenium, may also be useful in cancer chemotherapy. DNA topoisomerases (topos) are the target of several useful anticancer drugs. These drugs induce DNA complexes with either topo I or topo II; then cellular processing coverts these topo-DNA complexes into permanent DNA strand breaks that ultimately lead to cell death. Previous reports have revealed that selenite can induce apoptosis in cancer cells selectively and that selenite-induced apoptosis is preceded by the formation of DNA strand breaks. In vitro experiments have shown that selenite induces topo II-DNA complexes, which seem to be involved in selenite-induced apoptosis. Using the cell-based assay TARDIS, here we show that selenite induces topo II-DNA complexes (topo IIalpha and topo IIbeta) in K562 leukemia cells; these complexes appeared in a time-dependent manner and correlated with the induction of apoptosis. Cells lacking topo IIbeta were resistant to selenite-induced cell growth inhibition, suggesting that this isoenzyme is a target for selenite. We report for the first time that selenite induces topo I-DNA complexes in K562 cells; the levels of these complexes were high at short exposure times and seem to appear before the induction of apoptosis. Overall, our results show that selenite induces topo-DNA complexes in cells with both topo I and II, and support previous data that suggest that this agent has potential for the treatment of cancer.

Cysteine supplementation reduces the bioavailability of selenomethionine in mice

Summary Background & aims Selenomethionine, a common form of dietary selenium that is sometimes used to supplement patients with selenium deficiency, must be degraded to an inorganic form of selenium for incorporation into selenium-specific proteins (selenoprotein), and cysteine, which is occasionally added in the total parenteral nutrition preparation, might influence the degradation of selenomethionine. The purpose of this research is to study the influence of cysteine on the metabolism of selenomethionine. Methods An animal study was conducted. Mice were fed a selenomethionine diet with or without cysteine. The control mice were fed a selenite diet. The total selenium concentration and glutathione peroxidase (GPx) activity were measured. Results The mouse experiment showed that the selenium contents in liver, plasma, red blood cells, muscle, and brain were higher in the selenomethionine groups than in the selenite control group. However, the activities of GPx, which were measured in liver, red blood cells, and blood plasma, were lower in the group fed selenomethionine with the addition of cysteine than in the other groups, especially in red blood cells, where the activities were significantly lower than those in mice fed a diet containing only selenomethionine or selenite. Conclusions The results show that the addition of cysteine to a selenomethionine diet may inhibit the selenium metabolism from selenomethionine to selenoproteins, such as extracellular GPx.

Toxicity of selenate and selenite to the potworm Enchytraeus albidus (Annelida: Enchytraeidae): a laboratory test

Little information is available about the toxicity of inorganic selenium forms in soil animals. Therefore, the effects of selenate and selenite on the mortality and reproduction of Enchytraeus albidus were examined in standard laboratory tests with chronic exposure. Total and available amount of selenate and selenite were tested in a calcareous loamy chernozem soil. The LC(50) of selenate was 5.69 (2.7-8.12) mg kg(-1) dry wt. for total Se and 4.74 (2.14-6.98) mg kg(-1) dry wt. for available Se. Selenite LC(50) was as high as 22.5 (19.6-25.7) mg kg(-1) dry wt. for total Se and 8.10 (6.8-9.6) mg kg(-1) dry wt. for available Se. The EC(50) of selenate was 0.41 (0.35-0.48) mg kg(-1) dry wt. for total Se and 0.28 (0.24-0.34) mg kg(-1) dry wt. for available Se. Selenite EC(50) was as high as 7.3 (6.2-8.5) mg kg(-1) dry wt. for total Se and 2.46 (2.05-2.91) mg kg(-1) dry wt. for available Se. The response in reproduction was more sensitive to Se toxicity than the response in mortality. Selenate proved to be more toxic than selenite. Available data show that E. albidus may function as a biological indicator for some inorganic selenium forms in the soil.

The protective effect of selenium inorganic forms against cadmium and silver toxicity in mycelia of Pleurotus ostreatus

The effect of two inorganic selenium forms has been investigated in the mycelia of Pleurotus ostreatus exposed to cadmium and silver salts in the shaken cultures. The degree of toxicity was assessed by the determination of malondialdehyde (MDA; a common biomarker of lipid peroxidation). The mycelia were exposed to one element form (up to 5 mg l −1) and also to the following combinations: cadmium(II) + selenium(IV); cadmium(II) + selenium(VI); silver(I) + selenium(IV); silver(I) + selenium(VI). The concentrations of cadmium, silver, selenium, and MDA were assessed in the mixed cytosol and cell membrane fractions (CCM). A positive correlation between MDA and cadmium was found in the CCM (β = 0.7775, P = 0.0001), whereas the effect of silver was less significant (β = 0.4642, P = 0.039). These results indicate that silver(I) and cadmium(II) have different capacities to induce lipid peroxidation in P. ostreatus. The protective role of selenium against metal-induced oxidative damage was found to be dependent on the oxidation state of the element form in the growth medium. The strongest beneficial effect was observed in mycelia exposed to cadmium(II) + selenium(IV) (inverse correlation between MDA and selenium in the CCM: β = −0.7129, P = 0.009) and it has been ascribed to a lower incorporation of the toxic metal and/or to possible intracellular interaction between selenium and cadmium. Under exposure to silver(I), the protective effect of selenium(IV) was less noticeable (correlation between MDA and selenium in the CCM; β = −0.6068, P = 0.036); in the presence of selenium(VI), no beneficial effect was observed.

Selenomethionine‐Catalyzed Nickel Ion Reduction at a Mercury Electrode: Applications in the Analysis of Nutritional Supplements

AbstractSelenomethionine (SeMet) is a catalyst for Ni2+ reduction at a mercury electrode in a borax buffer at pH around 9 and gives rise to a differential pulse voltammetric peak, A, at −0.74 V vs. the Ag|AgCl, (3 M KCl) reference electrode. Peak current is directly proportional to SeMet concentration over the concentration range 0.4–10 μM. Alkali and alkali‐earth ions depress to some extent the sensitivity but the current‐concentration relationships remains linear even under these conditions. Differential pulse cathodic stripping voltammetry (DPCSV) in 0.01 M borax results in two partially overlapped peaks. The more negative (A, at about −0.74 V) is similar to that recorded with no deposition and is due to the catalysis by nonadsorbed SeMet, whereas the more positive one (B, at about −0.60 V) results from the catalysis by adsorbed SeMet. Only the DPCSV peak A appears if 0.1 M KNO3 is also present along with 0.01 M borax. Stearic acid, which is present in nutritional supplement tablets, improves the separation of the DPCSV peaks. Consequently, the peak B recorded with 0.01 M borax buffer allows determining SeMet in nutritional supplement tablets by the standard addition method and enables discriminating between the organic and inorganic selenium forms.

Comparative Toxicosis of Sodium Selenite and Selenomethionine in Lambs

Excess consumption of selenium (Se) accumulator plants can result in selenium intoxication. The objective of the study reported here was to compare the acute toxicosis caused by organic selenium (selenomethionine) found in plants with that caused by the supplemental, inorganic form of selenium (sodium selenite). Lambs were orally administered a single dose of selenium as either sodium selenite or selenomethionine and were monitored for 7 days, after which they were euthanized and necropsied. Twelve randomly assigned treatment groups consisted of animals given 0, 1, 2, 3, or 4 mg of Se/kg of body weight as sodium selenite, or 0, 1, 2, 3, 4, 6, or 8 mg of Se/kg as selenomethionine. Sodium selenite at dosages of 2, 3, and 4 mg/kg, as well as selenomethionine at dosages of 4, 6, and 8 mg/kg resulted in tachypnea and/or respiratory distress following minimal exercise. Severity and time to recovery varied, and were dose dependent. Major histopathologic findings in animals of the high-dose groups included multifocal myocardial necrosis and pulmonary alveolar vasculitis with pulmonary edema and hemorrhage. Analysis of liver, kidney cortex, heart, blood, and serum revealed linear, dose-dependent increases in selenium concentration. However, tissue selenium concentration in selenomethionine-treated lambs were significantly greater than that in lambs treated with equivalent doses of sodium selenite. To estimate the oxidative effects of these selenium compounds in vivo, liver vitamin E concentration also was measured. Sodium selenite, but not selenomethionine administration resulted in decreased liver vitamin E concentration. Results of this study indicate that the chemical form of the ingested Se must be known to adequately interpret tissue, blood, and serum Se concentrations.

Organic and inorganic forms of selenium inhibited differently fish (Rhamdia quelen) and rat (Rattus norvergicus albinus) δ-aminolevulinate dehydratase

Selenium contamination in the aquatic environment can produce severe toxic effects to fish. The mammalian sulfhydryl-containing enzyme, δ-aminolevulinate dehydratase (δ-ALA-D), is inhibited after exposure to organic and inorganic forms of selenium. In the present study, the inhibitory effect of (PhSe)2, (BuSe)2, and Na2SeO3 on the activity of fish hepatic and gill δ-ALA-D was investigated and compared with the rat liver enzyme. Results indicated that δ-ALA-D activity varied considerably depending on the tissue, selenium form, and species considered. For fish (liver and gill), the IC50 values for δ-ALA-D inhibition by (PhSe)2, (BuSe)2, and Na2SeO3 were 274 and 76, 985 and 693, and 386 and 902μM, respectively. For rat liver these values were 7, 10, and 5μM, respectively. In contrast, fish and rat subcellular fractions similarly increased the oxidative effect of (PhSe)2 toward sulfhydryl groups from DTT. These catalytic properties of subcellular fractions from fish and rat liver were abolished by heat treatment. Taking into account that aquatic organisms can be in contact with higher concentrations of selenium for longer periods of time and accumulate more selenium than terrestrial animals, it is reasonable to suppose that fish δ-ALA-D can be a potential target for organic and inorganic selenium forms present in aquatic contaminated environments. From an ecotoxicological point of view, our results suggest a link between selenium-induced anemia signs in fish and the sensitivity of fish δ-ALA-D to selenium in natural habitats.

Selenium speciation in subantarctic and subtropical waters east of New Zealand: trends and temporal variations

Surveys examining selenium speciation in two South Pacific water masses were conducted during austral autumn, winter, spring and summer to investigate the in situ effect of phytoplankton growth on the speciation and recycling of oceanic selenium. The water masses studied, subantarctic surface water (SASW) and subtropical surface water (STW), possess distinct biological signatures. SASW is a high nitrate low chlorophyll (HNLC) water mass, while in STW algal growth exhibits a classical cycle of spring and autumn blooms. The ‘nutrient type’ vertical profiles obtained for selenite and selenate in the study area, and the observed selenium content of phytoplankton (4.4±1.7 μg Se g dw −1), indicate that selenium is biologically utilized by phytoplankton in SASW and STW. Surface selenium concentration in the two water masses (Se(tot)=0.62–0.95 nM; 0–50 m) was similar to previously reported sub-tropical surface ocean concentrations. For the majority of the year, inorganic forms of selenium (selenite and selenate) were dominant over organic forms (typically, Se(org) ∼0.10 nM). In seasons with different primary production rates selenium speciation trends in the HNLC SASW remained relatively constant. In contrast, at the end of the algal growth season in STW, following spring phytoplankton blooms, decreased levels of bio-available inorganic selenium coincided with a decrease in concentration of the nutrient phosphate. Thus, the reduction in inorganic selenium concentration was presumably due to the uptake of inorganic selenium by phytoplankton. A corresponding increase in organic selenium concentration observed in STW is likely due to the regeneration of biogenic particles (derived from algal cells) that contain selenium. This study, representing the first report of significant short-term variations in oceanic selenium speciation related to phytoplankton processes, indicates that seasonality can be important in the interpretation of trends in oceanic selenium speciation.

Freshwater bacteria can methylate selenium through the thiopurine methyltransferase pathway.

Involvement of the bacterial thiopurine methyltransferase (bTPMT) in natural selenium methylation by freshwater was investigated. A freshwater environment that had no known selenium contamination but exhibited reproducible emission of dimethyl selenide (DMSe) or dimethyl diselenide (DMDSe) when it was supplemented with an organic form of selenium [(methyl)selenocysteine] or an inorganic form of selenium (sodium selenite) was used. The distribution of the bTPMT gene (tpm) in the microflora was studied. Freshwater bacteria growing on 10 micro M sodium selenite and 10 micro M sodium selenate were isolated, and 4.5 and 10% of the strains, respectively, were shown by colony blot hybridization to hybridize with a Pseudomonas syringae tpm DNA probe. Ribotyping showed that these strains are closely related. The complete rrs sequence of one of the strains, designated Hsa.28, was obtained and analyzed. Its closest phyletic neighbor was found to be the Pseudomonas anguilliseptica rrs sequence. The Hsa.28 strain grown with sodium selenite or (methyl)selenocysteine produced significant amounts of DMSe and DMDSe. The Hsa.28 tpm gene was isolated by genomic DNA library screening and sequencing. BLASTP comparisons of the deduced Hsa.28 bTPMT sequence with P. syringae, Pseudomonas aeruginosa, Vibrio cholerae, rat, and human thiopurine methyltransferase sequences revealed that the levels of similarity were 52 to 71%. PCR-generated Escherichia coli subclones containing the Hsa.28 tpm open reading frame were constructed. E. coli cells harboring the constructs and grown with sodium selenite or (methyl)selenocysteine produced significant levels of DMSe and DMDSe, confirming that the gene plays a role in selenium methylation. The effect of strain Hsa.28 population levels on freshwater DMSe and DMDSe emission was investigated. An increase in the size of the Hsa.28 population was found to enhance significantly the emission of methyl selenides by freshwater samples supplemented with sodium selenite or (methyl)selenocysteine. These data suggest that bTPMT can play a role in natural freshwater selenium methylation processes.

Effects of selenium supplementation on four agricultural crops.

Agricultural crops can be used either to remediate selenium-contaminated soils or to increase the daily selenium intake of consumers after soil supplementation using inorganic or organic selenium sources. In this study, four agricultural crops were examined for potential selenium enhancement. Soils containing tomato, strawberry, radish, and lettuce plants were supplemented with either an inorganic or an organic form of selenium. Two different soils, i.e., low Se and high Se containing, were also used. Statistically significant differences in appearance, fruit production, and fresh weights of the fruit produced were studied. Next, the amount of selenium retained in the edible fruits, nonedible plant, and soil for each was analyzed by acid digestion followed by hydride generation atomic absorption analysis. Finally, inhibition effects on the seeds of the agricultural plants were studied. The results show that supplementation with an inorganic form of selenium led to higher retention in the plants, with a maximum of 97.5% retained in the edible portion of lettuce plants.

Selenium compounds inhibit the biological activity of blood platelets

The action of inorganic forms of selenium (Se) on blood platelet aggregation, secretion and the arachidonate pathway in vitro was studied. It was shown that sodium selenite, after 30 min preincubation, inhibited platelet aggregation induced by 0.1 U/ml of thrombin and by 10 microM ADP (about 30% inhibition of aggregation after pretreatment of platelets with 10(-4) M of Se). Contrary to sodium selenite, sodium selenate did not affect the platelet aggregation induced by either agonist. Pretreatment of blood platelets with sodium selenite resulted in a statistically significant decrease in adenine nucleotide secretion ( P < 0.01) and release of malonyldialdehyde (MDA), produced in equal amounts to TXA(2) , in thrombin-stimulated platelets ( P <0.001). However, selenite did not change the level of MDA/TXA(2) in sodium arachidonate-stimulated platelets. We conclude that the inhibitory effects of sodium selenite on platelet activation could be the result of decreased synthesis and release of secondary agonists (TXA(2), ADP) in stimulated platelets. It is also possible that sodium selenite blocks the release of arachidonic acid from platelet membranes via phospholipases.

Selenium compounds inhibit the biological activity of blood platelets

The action of inorganic forms of selenium (Se) on blood platelet aggregation, secretion and the arachidonate pathway in vitro was studied. It was shown that sodium selenite, after 30 min preincubation, inhibited platelet aggregation induced by 0.1 U/ml of thrombin and by 10μxM ADP (about 30% inhibition of aggregation after pretreatment of platelets with 10−4 M of Se). Contrary to sodium selenite, sodium selenate did not affect the platelet aggregation induced by either agonist. Pretreatment of blood platelets with sodium selenite resulted in a statistically significant decrease in adenine nucleotide secretion (P< 0.01) and release of malonyldialdehyde (MDA), produced in equal amounts to TXA2, in thrombin-stimulated platelets (P<0.001). However, selenite did not change the level of MDA/TXA2 in sodium arachidonate-stimulated platelets. We conclude that the inhibitory effects of sodium selenite on platelet activation could be the result of decreased synthesis and release of secondary agonists (TXA2, ADP) in stimulated platelets. It is also possible that sodium selenite blocks the release of arachidonic acid from platelet membranes via phospholipases.