Inhibitory Effect Of Selenium Research Articles

Influence of selenium and silicon salts and nanoparticles on the growth of <i>Fusarium avenaceum</i> (Fr.) Sacc. and <i>Bipolaris sorokiniana</i> (Sacc.) Shoem. mycelium and grain seeds germination

The effect of selenium and silicon in nanoform in comparison with sodium selenite and sodium silicofluoride on the growth of pathogenic fungi Fusarium avenaceum and Bipolaris sorokiniana was evaluated. The influence of nanoparticles on wheat and corn seed germination and seedling growth was also studied. The inhibitory effect of selenium and silicon nanoparticles on the growth of Fusarium avenaceum and Bipolaris sorokiniana was revealed. Nanosilicon at a concentration of 5–50 mg/l inhibited the growth of pathogenic fungi Fusarium avenaceum and Bipolaris sorokiniana to a greater extent than selenium nanoparticles and was more effective than sodium silicofluoride. Fusarium avenaceum was shown to be more resistant to nanoselenium and sodium selenite compared to Bipolaris sorokiniana. Nanoparticles had practically no effect on seed germination and the growth of wheat and corn seedlings, while sodium selenite and sodium silicofluoride at the same concentrations caused a decrease in seed germination energy and dry weight of the shoots and roots of seedlings.

Inhibitory Effects of Selenium on Arsenic-Induced Anxiety-/Depression-Like Behavior and Memory Impairment.

Elevated arsenic (As) contamination in drinking water was detected in many areas of Pakistan. The intoxication of As causes various neurological diseases in humans, which can be inhibited by the administration of potent antioxidants. Trace elements are also found in drinking water such as selenium (Se), which possess antioxidant potential. The main purpose of the current study is to find out the protective effect of Se against As toxicity which can cause anxiety- and depression-like behaviors as well as memory impairment. Thirty-six male rats were divided into six groups: (1) distilled water (dw)+dw, (2) dw+Se (0.175 mg/ml/kg), (3) dw+Se (0.35mg/ml/kg), (4) dw+As (2.5mg/ml/kg), (5) As (2.5mg/ml/kg) + Se (0.175 mg/ml/kg), and (6) As (2.5mg/ml/kg) + Se (0.35 mg/ml/kg). Rats were treated with respective treatment for 4 weeks. Sub-chronic treatment of As reduced time spent in open arm (elevated plus maze), and lightbox (light-dark activity test) and increased immobility time in forced swim test indicate anxiety- and/or depression-like behavior, respectively. Conversely, rats treated with As+Se (at both doses) increased time spent in open arm (elevated plus maze), and lightbox (light-dark activity test) and decreased immobility time in forced swim test indicate the anxiolytic and anti-depressive effect of Se, respectively. Co-administration of Se (0.175 and 0.35) inhibited As instigated reduction of spatial memory performed in Morris water maze. The reversal in the reduced level of malondialdehyde and activity of acetylcholinesterase in the hippocampus by Se was observed in As-treated animals, while the activity of antioxidant enzymes in the hippocampus was increased in As+Se than dw+As-treated animals. Histopathological studies have shown the reversal of hippocampus deterioration by Se in As-treated rats. The results may imply to prevent the intoxication of As instigated impairment in behavioral and biochemical indices by Se supplementation and/or increased safer intake.

Inhibitory Effect of Selenium on Esophagus Cancer Cells and the Related Mechanism.

Selenium has been associated with many malignant tumors including esophagus cancer (EC). In current study, we examined the effects of three types of selenium, sodium selenite (SSE), methylseleninic acid (MSA) and methylselenocysteine (MSC) on EC cell line Eca109. Here, selenium attenuated cell viability and increased cell apoptosis, especially in MSC, when compared with control group (p<0.05). Meanwhile, MSC and MSA, but no SSE, arrested cell cycle in G0/G1 phase (p<0.05). Mechanistically, FAL1 and PTEN were found to participate in regulating cell cycle and cell apoptosis process by decreasing cyclinD1, CDK2, and promoting caspase-3, caspase-8. In addition, we found that cyclinD1, CDK2 were significantly downregulated by MSA and MSC, while caspase-3, caspase-8 were dramatically upregulated by SSE (p<0.05). Based on these results, we concluded that MSC and MSA inhibit the viability of Eca109 mainly through reducing cell proliferation, while SSE by promoting apoptosis.

The optimum Se application time for reducing Cd uptake by rice (Oryza sativa L.) and its mechanism

The inhibitory effect of selenium (Se) on cadmium accumulation in brown rice (BR-Cd) is controversial, which may be related to the Se application time. The optimum Se application time for reducing the BR-Cd is investigated. A pot experiment was conducted to examine the changes in the dynamics of iron plaque on root surface and Cd accumulation in rice as Se was applied at different growth stages to two Cd-contaminated soils, and explore its mechanisms. Field trials were conducted to verify the results. Iron plaque formed mainly at the middle stage (tillering to booting stage) of rice and then decreased at the mature stage. Se application at the seeding, tillering, and booting stages reduced the BR-Cd by 10.6–18.4%, 14.9–23.7%, and 10.8–20.9% in the neutral soil, 18.3–32.4%, 40.3–63.0%, and 22.7–40.6% in the acid soil, respectively. Two field trials demonstrated that tillering application of Se caused significant reductions (27.1–35.1%) of BR-Cd. Tillering stage is optimal for Se application to reduce BR-Cd, mainly because tillering application of Se causes the maximum amount iron plaque at the booting stage, maximumly inhibit Cd uptake by the root; meanwhile, the transport of Cd from the root to brown rice is inhibited.

Inhibitory effects of selenium on cadmium-induced cytotoxicity in PC12 cells via regulating oxidative stress and apoptosis

Purpose of this study is to investigate mechanism/s of cyto-protection by selenium (Na2SeO3; Se4+) against cadmium (CdCl2; Cd2+)-induced cytotoxicity using PC12 cells. In addition, Se (5, 10, 20 and 40 μM) and Cd (2.5, 5 and 10 μM)-induced cytotoxicity is determined. Cytotoxicity assays and western blot analyses confirmed that Se (≥10 μM) promotes autophagic cell death via inhibition of mTOR activation and p62 accumulation due to increase of cellular oxidative stress. On the other hand, co-presence of non-toxic Se (5 μM) and toxic Cd (5 μM) showed to increase cell viability, glutathione and glutathione peroxidase 1 (GPx1) levels, and to decrease DNA fragmentation and lactate dehydrogenase (LDH) activity compared to Cd-treated (5 μM) cells alone. Furthermore, western blot analyses of cytochrome c and ERK1 indicated that Cd-induced apoptotic cell death in PC12 cells. However, the co-exposure of Se with Cd significantly decreases the release of cytochrome c into cytosol from mitochondria, and up-regulates ERK1 protein to inhibit Cd-induced apoptosis. In conclusion, Se (≥10 μM) possess cytotoxicity in PC12 cells; however, co-presence of Se (5 μM) with Cd (5 μM) protects against Cd-induced apoptosis in PC12 cells due to inhibition of Cd-induced oxidative stress and subsequently suppression of mitochondrial apoptosis pathway.

Protective Role of Selenium Compounds on the Proliferation, Apoptosis, and Angiogenesis of a Canine Breast Cancer Cell Line

We herein examined the effects of different doses, forms, and compatibilities of selenium on a canine mammary gland tumor cell line, CTM1211, and explored the related mechanisms. Three selenium compounds, sodium selenite (SSE), methylseleninic acid (MSA), and methylselenocysteine (MSC), were selected for these experiments, and cyclophosphamide (CTX) served as a positive control. In the cell viability assay, the cell viability of each group at 48/72h decreased significantly compared with the control group (p < 0.05), and the cell viability of the CTX + MSA group was lower than that of CTX and MSA groups (p < 0.05). Moreover, the inhibitory effect of selenium on cell proliferation was time-dependent but not concentration-dependent. In the cell apoptosis assay, the apoptosis values of each group increased significantly compared with the control group, and the apoptosis values of the CTX + MSA group increased the most significantly (p < 0.01). The protein and mRNA expression levels of vascular endothelial growth factor-alpha (VEGF-alpha), angiopoietin-2 (Ang-2), and hypoxia inducible factor-1 alpha (HIF-1 alpha) were downregulated in each group, while that of phosphatase and tensin homolog (PTEN) were upregulated (p < 0.05). In conclusion, these three selenium compounds, especially MSA, could significantly inhibit the viability and growth of the CTM1211 cell line, which is partly due to the induction of apoptosis and regulation of tumor angiogenesis.

Abstract 245: Consumption of a high-fat diet abrogates inhibitory effects of selenium on spontaneous metastasis of Lewis lung carcinoma in mice

Abstract The present study investigated the effects of dietary supplementation with selenium (Se) on spontaneous metastasis of Lewis lung carcinoma (LLC) in mice fed a high-fat diet using a 2x2 design. Three-week-old male C57BL/6 mice were fed the AIN93G diet or that diet modified with 45% calories from fat supplemented with or without 2.5 mg Se/4029 kcal as methylseleninic acid for 6 weeks, at which time they were injected subcutaneously with 2.5x105 LLC cells. The resulting primary tumor was removed surgically 10 days later, and the experiment was terminated after an additional 10 days. Consumption of the high-fat diet significantly increased the body fat mass, regardless of Se supplementation, compared to the AIN93G diet (p&amp;lt;0.01). The high-fat diet increased lung metastases by 17% compared to the AIN93G diet (p&amp;lt;0.01). Selenium supplementation reduced the metastases by 11% compared to non-supplemented controls (p&amp;lt;0.05); however, the reduction was greater in AIN93G-fed mice (18%) than in mice fed the high-fat diet (5%). Supplemental Se reduced plasma concentrations of proteolytic proteases (uPA, p&amp;lt;0.01; MMP-9, p&amp;lt;0.05) and angiogenic factors (VEGF, p&amp;lt;0.01; TIMP-1, p&amp;lt;0.01) compared to non-supplemented controls. The high-fat diet significantly increased plasma concentrations of adipokines PAI-1, MCP-1, TNF-α and leptin regardless of the level of dietary Se; however, supplemental Se reduced plasma PAI-1 (p≤0.05) and MCP-1 (p≤0.05) in AIN93G-fed mice. These results demonstrate that consumption of a high-fat diet abrogated the anti-metastatic effects of Se, and that such an abrogation may involve adipose-derived inflammatory cytokines. Citation Format: Lin Yan. Consumption of a high-fat diet abrogates inhibitory effects of selenium on spontaneous metastasis of Lewis lung carcinoma in mice. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 245. doi:10.1158/1538-7445.AM2014-245

Inhibitory Effect of Selenium Against Penicillium expansum and Its Possible Mechanisms of Action

Some organic and inorganic salts could inhibit the growth of many pathogens. Selenium (Se), as an essential micronutrient, was effective in improving the plant resistance and antioxidant capacity at a low concentration. Penicillium expansum is one of the most important postharvest fungal pathogens, which can cause blue mold rot in various fruits and vegetables. In this study, the inhibitory effect of Se against P. expansum was evaluated. The result showed that Se strongly inhibited spore germination, germ tube elongation, and mycelial spread of P. expansum in the culture medium. The inhibitory effect was positively related to the concentration of Se used. Fluorescence microscopy observation of P. expansum conidia stained with propidium iodide (PI) indicated that the membrane integrity decreased to 37 % after the conidia were treated with Se (20 mg/l) for 9 h. With the use of an oxidant-sensitive probe 2,7-dichlorofluorescin (DCHF-DA), we found that Se at 15 mg/l could induce the generation of intracellular reactive oxygen species (ROS). Furthermore, methane dicarboxylic aldehyde (MDA) content, hydrogen peroxide (H2O2), and superoxide anion (O2 (-)) production rate in P. expansum spores exposed to Se increased markedly. Compared with the control, the activities of superoxide dismutase (SOD) and the content of glutathione (GSH) were reduced, confirming that damage of Se to cellular oxygen-eliminating system is the main reason. These results suggest that Se might serve as a potential alternative to synthetic fungicides for the control of the postharvest disease of fruit and vegetables caused by P. expansum.

Nutrition classics. Journal of the National Cancer Institute, April 1970, Vol. 44, No. 4: Relationship of selenium to cancer. I. Inhibitory effect of selenium on carcinogenesis. By Raymond J. Shamberger.

Nutrition classics. Journal of the National Cancer Institute, April 1970, Vol. 44, No. 4: Relationship of selenium to cancer. I. Inhibitory effect of selenium on carcinogenesis. By Raymond J. Shamberger.

Influência do zinco sobre o efeito do selênio na atividade da enzima δ-ALA-D de fígado, rim e cérebro de camundongos adultos in vitro

Selenium is an essential dietary trace element and its deficiency can cause some pathologies such as cardiac diseases. However, investigations have evidencied the toxicologic effect of organic and inorganic selenium compounds in the organs and enzymes.The present work examined the toxic effect of selenium on δ-ALA-D an enzyme involved in the biosynthesis of tetrapyrrol heme. A possible protective role of zinc on inhibitory effect of selenium was also evaluated. The organic selenium compound, (CH3)2C (Seφ) (0CH3) caused a dose dependent inhibition of renal, hepatic and cerebral δ-ALA-D (p&lt; 0.01). Also was evidencied that the selenium and zinc interaction not was able to restore the δ-ALA-D activity inhibited by selenium but increasing the inhibitory effect from the compound on the renal and cerebral enzyme.

Inhibitory Effect of Selenium on Biliary Secretion of Methyl Mercury in Rats

The inhibitory effect of sodium selenite on biliary secretion of methyl mercury was examined in rats. The biliary secretion of methyl mercury in rat treated with 1 μmol/kg of methyl mercury was significantly decreased by administration of selenite at doses of 0.05 μmol/kg or higher. In rats given 10 μmol/kg of methyl mercury, marked depression of biliary secretion of mercury was observed when selenite was injected at a dose of 0.2 μmol/kg. On the other hand, secretion of substantial amounts of selenium was observed when biliary secretion of mercury was depressed. When the concentration of selenium in the bile was higher than 5 nmol/ml, biliary secretion of mercury was markedly depressed independently of the dose of methyl mercury administered (1 μmol/kg or 10 μmol/kg). These results suggest that the degree of inhibitory effect of selenite may be determined by the selenium concentration in the liver or the bile after treatment with selenite rather than the molar ratio of the dose of methyl mercury and selenite. We concluded that the decrease in biliary secretion of methyl mercury induced by selenite may result from inhibition of pathway for secretion of methyl mercury from liver to bile rather than the direct formation of a compex between methyl mercury and selenium. Methyl mercury has been considered to be secreted from liver to bile as a complex with glutathione (GSH). However, administration of selenite did not affect biliary secretion of GSH or hepatic glutathione S-transferase activity. Moreover, gel filtration of liver cytosol demonstrated that the distribution pattern of hepatic methyl mercury between macromolecules and GSH was not significantly changed by administration of selenite. These results suggest that selenite does not affect complex formation of methyl mercury with GSH at least in the liver. Selenite might specifically inhibit the activity of the canalicular transporter(s) which transport complexes of methyl mercury and GSH from the liver to bile.

Inhibitory effect of selenium and change of glutathione peroxidase activity on rat glioma.

The inhibitory effect of selenium (Se) and change of glutathione peroxidase activity during the development of brain tumors was investigated in Wistar rats. Four rat groups classified to match by age and weight were fed a diet containing 0, 0.5, 2.0, and 4.0 micrograms Se/g. After 6 wk, the rats were injected with 3 x 10(6) C6 cells into the right frontal lobe parenchyma. Survival was significantly longer in the 0.5 and 2.0 micrograms Se/g groups than in the Se-free and 4.0 micrograms Se/g groups. The activity of glutathione peroxidase after development of tumors was significantly higher in the high Se group at 18 and 30 d.

Inhibitory effect of selenium on enzymes involved in heme biosynthetic pathway in chick embryos.

Effect of different concentrations of selenium (Se) on heme biosynthesis was studied at different developmental stages of chick embryo. The first rate limiting enzyme ALA-synthase (ALA-S; E.C.2.3-1.37) activity was enhanced by selenium, while hepatic and blood ALA-dehydratase activity (ALA-d; E.C.3.2.1.24) was decreased. Hepatic and blood free-sulfhydryl (-SH) group contents were significantly decreased by Se. Further, hepatic aminolevulinic acid (ALA) and total blood porphyrin levels were enhanced and hepatic heme levels were depleted by selenium exposure. Heme biosynthesis was maximally inhibited in the E4 (4th day injected embryos) when compared to later periods.

The anti-leukaemic effects and the mechanism of sodium selenite

The anti-proliferative effects of selenium were studied both in vivo and in vitro. At a selenium concentration of 0.6 μg/ml, cells from patients with ALL-L1, L2 and AML-M1, M3 and M5 were more sensitive than cells from patients with CML. Cells from patients with AML-M2, CLL and leukaemic lymphoma were least sensitive. Normal bone marrow or peripheral blood cells were not sensitive to selenium at this concentration. In the mouse leukaemia models (L797, L615, L7712), the sensitivity of leukaemic cells were: L797 (93% cytotoxicity) > L615 (49.7% cytotoxicity) > L7712 (4.4% cytotoxicity). Sodium selenite injected i.p. increased the longevity of L797-inoculated mice. Administration of 40 μg selenium daily for 7 days resulted in a significant increase in the longevity of mice inoculated with 10 5 L797 cells. However, no remarkable increase of the longevity was observed in either L615- or L7712-inoculated mice after treatment with sodium selenite for 7 days. Treatment of the HL-60 leukaemic cell line with selenium caused a dose- and time-related decrease in DNA, RNA and protein syntheses as measured by [ 3H]-thymidine, [ 3H]-uridine and [ 3H]-leucine uptake respectively. The inhibitory effect of selenium on DNA synthesis was reversed when selenium was removed from the medium, demonstrating that selenium-induced inhibition of DNA synthesis was due to interference with DNA biosynthesis rather than DNA template damage. These results suggest that the anti-leukaemic effect of sodium selenite is associated with inhibition of DNA replication, transcription and translation.

Inhibition of hamster tongue carcinogenesis by selenium and retinoic acid.

The inhibitory effect of selenium, 13-cis-retinoic acid, and their combination was studied in an animal model in which squamous cell carcinoma of the tongue was induced by 0.5% 9,10 dimethyl-1,2 benzanthracene (DMBA). A controlled, blinded experiment was carried out using 60 Syrian hamsters divided into four groups of 15 each. When compared to controls, the mean day of carcinoma onset was delayed 3 weeks for animals given selenium, 6 weeks for animals given retinoic acid, and 5.5 weeks for animals given selenium plus retinoic acid. The differences between each experimental group and the control group are statistically significant. We conclude that both selenium and retinoic acid inhibit the development of DMBA-induced squamous cell carcinoma of the tongue in hamsters. The dose of retinoic acid used produces a stronger inhibitory effect, but is associated with significant toxicity. At the doses used, combined inhibitory effect is no greater than that for retinoic acid alone.

The inhibitory effect of selenium on mice inoculated with B16 melanoma cells.

AbstractThe influence of selenium dioxide on the in vitro and in vivo growth of transplantable B16 melanoma was studied. In the in vivo study, melanoma tissues showed a decrease in development of tumor growth and a tendency toward higher levels of free radical signal (ESR). Cultured B16 melanoma cells revealed a marked disturbance of cell growth especially in the solution with a high dose of selenium.These results may indicate that selenium has an antitumorigenic effect on B16 melanoma cells.

Mode of Action of Selenium Inhibition of 7,12-Dimethylbenz[&lt;italic&gt;a&lt;/italic&gt;]anthracene-Induced Mouse Mammary Tumorigenesis&lt;xref ref-type="fn" rid="FN1"&gt;2&lt;/xref&gt;

Possible mechanisms for the inhibitory effect of selenium on mouse mammary gland tumorigenesis were evaluated in two different mouse models, in 7,12-dimethylbenz[a]anthracene [(DMBA) CAS:57-97-6]treated and hormonally stimulated mammary glands with two dietary levels of Se (0.2 and 2.0 ppm). In (C57BL X DBA/2f)F1 (BD2F1) and BALB/c strains of female mice, Se at 2.0 ppm decreased mammary tumor incidences by 36 and 68%, respectively. Selenium-dependent glutathione peroxidase (GSH-Px) activity in the mammary glands of BD2F1 female mice decreased at 6 months of age and then increased to the highest levels at 9 months of age. Mammary glands from DMBA-treated mice had lower GSH-Px activity than those from control mice. The increase of dietary Se to 2.0 ppm did not overcome this DMBA effect. These results indicate that GSH-Px activity does not correlate with the tumorigenic inhibitory effects of Se. In the hormonally stimulated mammary gland, increasing dietary Se to 2.0 ppm increased GSH-Px activity threefold and decreased mammary-gland-membrane-localized lipid peroxidation by 16%. In vitro peroxidation of hormonally stimulated mammary glands was inversely proportional to the level of GSH present in the incubation mixture. The marginal decrease in lipid peroxidation found in the mammary glands exposed to 2.0 ppm Se could not explain the inhibitory effect of Se on tumorigenesis.

Selenium retention and inhibition of cell growth in mouse mammary epithelial cell lines in vitro

The steady state levels of growth inhibitory doses of inorganic selenium were examined in five different mammary epithelial cell lines: MOD, COMMA-D, COMMA-F, COMMA-T, and YN-4. The retention of selenium was monitored using a radioactive isotope,(75)Se. Growth inhibition correlated with high levels of selenium in the cell. Generally, the retention of intracellular selenium was not dependent upon cell density, cell number, net growth rate, or tumorigenicity of the mammary cell lines. One cell line, COMMA-D, exhibited an unique response wherein the amount of selenium retained was low and the growth inhibitory effects of selenium were negligible when the cells were exposed to selenium at low density. However, at high cell densities, the COMMA-D cells responded like the other four cell lines. The growth inhibitory effect of selenium was reversible; upon removal of selenium from the medium, cells start synthesizing DNA within 24h. The retention of selenium was influenced by constituents in the growth medium. In particular, cysteine, but not methionine, purines, or pyrimidines altered selenium retention and counteracted the growth inhibitory effects of selenium. These results indicated that the mammary cell lines, particulary COMMA-D and MOD are good model systems to examine the uptake, retention, localization, and function of inorganic selenium under conditions where it acts as a growth inhibitory agent.

Inhibitory effects of selenium on the growth of du-145 human prostate carcinoma cells in vitro

The growth of DU-145 human prostate carcinoma cells is reduced to 50% of control by 1 × 10 −6M to 2 × 10 −6M selenium and to 2% of control at 10 −4M selenium. These cells show greater sensitivity to inhibition of growth or DNA synthesis by selenium than human W1-38 and HeLa cells and mouse mammary tumor cells. It has been shown that selenium inhibits carcinogenesis and reduces the incidence of chemical carcinogen and virus-induced tumors of a variety of organs in animals. Selenium may also inhibit the growth of certain tumor cells of non-human origin. To our knowledge, this is the first study on the effects of selenium on the growth of human tumor cells. From extrapolation, it is deduced that selenium serum levels in humans living in high selenium areas may be as high as 10 −6M and could be effective inhibiting the growth of tumor cells in vivo. These findings have implications in the prevention and intervention of prostate cancer in man.

Inhibitory effects of selenium on mutagenicity

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTInhibitory effects of selenium on mutagenicityScott E. Martin and Michael SchillaciCite this: J. Agric. Food Chem. 1984, 32, 3, 426–433Publication Date (Print):May 1, 1984Publication History Published online1 May 2002Published inissue 1 May 1984https://doi.org/10.1021/jf00123a002RIGHTS & PERMISSIONSArticle Views54Altmetric-Citations20LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InReddit PDF (864 KB) Get e-Alerts Get e-Alerts