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To investigate the immunomodulatory mechanism of low relative molecular mass seleno-aminopolysaccharide, a metabolomics method based on liquid chromatography-time-of-flight mass spectrometry (LC-TOF-MS) was used to analyze the endogenous metabolites changes in the liver of Acanthopagrus schlegelii . The potential biomarkers were screened using non-targeted mass spectrometry with the XCMS plus software, and the related metabolic pathways were analyzed using MetaboAnalyst3.0 website. The results showed that the liver metabolites in the low relative molecular mass seleno-aminopolysaccharide-fed group were significantly different from those in the blank group. Also, 32 biomarkers were identified. Additionally, low relative molecular mass seleno-aminopolysaccharide could enhance the immune function of Acathopagrus schlegelii via amino acid, nucleotide, and nitrogen metabolism, aminoacyl-transfer ribonucleic acid (tRNA) biosynthesis, and other metabolic pathways. This study therefore provides a scientific basis for elucidating the immunoenhancement mechanism of low relative molecular mass seleno-aminopolysaccharide.

Objective: To explore the effects of methylseleninic acid (MeSeA), selenomethionine (SeMet) and methylselenocysteine (MeSeCys) on proliferation, migration and adhesion of HeLa cells., Methods: HeLa cells were cultured and treated with MeSeA, SeMet and MeSeCys for 12 - 72 h respectively. MTT assay, healing assay and in vitro cell Matrigel adhesion assay were used to detect the proliferation, migration and adhesion of HeLa cells., Results: Compared to the control group, the proliferation of HeLa cells was remarkably inhibited by MeSeA (P <0. 01). The migration of HeLa cells in MeSeA group was inhibited by 34% (P < 0. 05) and 26% (P < 0. 05) in 4 h and 8 h, respectively. However, the migration of HeLa cells with inhibitions of 18% and 13% was in SeMet group in 4 h and 8 h. The inhibitions of HeLa cell migration in MeSeCys group was 28% (P < 0.05) and 5% in 4 h and 8 h, respectively. In addition, the adhesive function of HeLa cells in the MeSeA group, the SeMet group as well as the MeSeCys group were inhibited by 36% (P < 0. 01), 25% and 49% (P < 0. 01)., Conclusion: The proliferation and migration of HeLa cell were effectively inhibited by MeSeA, while the adhesive function of HeLa cell was remarkably inhibited by MeSeCys.

Taking 200 healthy broilers at 14 d of age as test materials, the free radicals in their blood and tissues were detected by electron spin resonance (ESR) and biochemical methods, aimed to investigate the effects of vitamin E (V(E)) and selenium (Se) on the metabolism of different free radicals and their dynamic changes in the broilers. The results showed that the content of NO free radicals in broilers tissues decreased with increasing supplementing level of V(E), while high supplementation of Se tended to induce the production of NO free radicals. High supplementation of V(E) and Se in feeds improved the GSH-Px and SOD activities in broilers serum and liver significantly. With the extension of experimental period, the SOD activity in tissues decreased, while GSH-PX activity increased gradually, implying that the deficiency of V(E) and/or Se might induce the overproduction of O2*- and H2O2 free radicals. H2O2 free radicals might be produced largely at early stage of V(E) and Se deficiency and declined then, while the over-production of O2*- free radicals could maintain for a long time. The deficiency of V(E) and/or Se could improve the MDA content significantly, and Se deficiency had higher effects than V(E) deficiency. There were synergic effects in the metabolism of NO, O2 and H2O2 free radicals.

Changes of lipid peroxidation reaction and NK cell activity in spleen of CCl4-induced liver injury mice with adding orgnoselenium from Se-enriched lactobacillus were studied to discuss the protective effect of orgnoselenium and its mechanism. Sixty healthy mice (female: male=1:1) were chosen and divided randomly into four groups: control group (group C), orgnoselenium group (group Se), CCl4-injection group (group CCl4) and CCl4-injection plus orgnoselenium group (group CCl4-Se). The liver injury was induced by abdominal injection of CCl4 (0.07ml/100g body weight) on every other day over four weeks. The spleens were collected at the 2nd and 4th week, and spleen NK cell activity, spleen homogenate GSH-Px, SOD, CAT activities and MDA concentration were determined. The results showed that during the entire experimental period, spleen homogenate GSH-Px, SOD and CAT activities in groups C, Se and CCl4-Se were higher or significantly higher than that in group CCl4, and three antioxidant enzyme activities in groups Se and CCl4-Se had no apparent differences from that in group C except that there were significant increases of SOD activity at the 4th week. Spleen homogenate MDA content of group CCl4 increased markedly compared with that of groups C, Se and CCl4-Se, MDA level of group CCl4-Se was close to that of group C, and that of group Se was lower. During the entire experimental period, NK cell activity of group Se was the highest and significantly higher than that of group C at the 4th week, a lowest value was observed in group CCl4, which was lower or markedly lower than that of groups C, Se and CCl4-Se, there were no significant differences between group CCl4-Se and group C. It is suggested that orgnoselenium from Se-enriched lactobacillus can enhance antioxidation ability in normal mice and play an effective role by means of improving and enhancing the spleen antioxidation enzymes and NK cell activities in the process of intervening liver injury.

Objective: To investigate the mechanisms underlying the effect of selenium dioxide (SeO(2)) on the proliferation, apoptosis, and apoptosis-related gene expressions of Bcl-2 and p53 in 3 leukemia cell lines NB4, K562 and HL-60., Methods: The three leukemia cell lines were treated with 3, 10 and 30 mmol/L SeO(2) and apoptosis detected by flow cytometry and analysis of p53 and Bcl-2 expressions., Results: SeO(2) at 10 and 30 mmol/L could inhibit the proliferation of three leukemia cell lines. SeO(2) treatment at 30 mmol/L for 48 h induced an apoptosis rate of 54.0 %, 46.5 %, 49.6 % in NB4, K562, and HL-60 cells respectively, and down-regulated Bcl-2 expression in NB4 and K562 but not in HL-60 cells., Conclusion: SeO(2) can induce apoptosis in NB4, K562 and HL-60 leukemia cells, involving the down-regulation of Bcl-2 and up-regulation of p53.

Background & Objective: It was reported that selenium could induce apoptosis of cancer cells; moreover, apoptosis of cancer cells and telomerase activity were closely related to the development of cancer. This study was designed to investigate the effect of selenium dioxide on human pulmonary adenocarcinoma GLC-82 cell to reveal its probable mechanism and the relationship between apoptosis and telomerase activity., Methods: Methyl thiazolyl tetrazolium(MTT) method was used to determine the growth inhibition rates of lung cancer GLC-82 cells by various concentrations of selenium dioxide at different time. TRAP-PCR-ELISA assay was used to examine the changes of GLC-82 cells treated with selenium dioxide. The cell apoptotic rate was measured by flow cytometry (FCM). DNA ladder was showed by DNA agarose gel electrophoresis. The morphological changes of the cancer cells were examined under light and electron microscope., Results: After being treated with 3, 10, 30 micromol/L selenium dioxide, the proliferation and telomerase activity of GLC-82 cells were markedly inhibited. The growth inhibition rates in GLC-82 cells for 24 hours were 0.7%, 12.8%, and 31.8%; for 72 hours were 15.1%, 51.2%, and 61.1%, respectively. Telomerase activity of GLC-82 cells for 24 hours were 1.173+/-0.029,1.127+/-0.067, and 1.050+/-0.098(P< 0.05); for 48 hours were 1.150+/-0.026, 1.047+/-0.060, and 0.950+/-0.036(P< 0.05), respectively (control group: 1.227+/-0.032 and 1.167+/-0.023, respectively). An apoptosis peak appeared before diploid peak in FCM. Agarose gel electrophoresis showed overt ladder-shape band of cell apoptosis. GLC-82 cells treated by selenium dioxide showed morphological characteristics of apoptotic cells., Conclusion: Selenium dioxide could significantly inhibit the growth of lung cancer GLC-82 cells through inducing apoptosis and inhibiting the telomerase activity. Selenium dioxide has strong growth inhibitory effect in a dose-and time-dependent manner.

Background & Objective: This study was designed to investigate the impact of selenium dioxide (SeO2) on regulatory regions P250 of c-fos gene and to seek possible regulation mechanism., Methods: HeLa cells were transfected with plasmids containing upstream regulating regions of c-fos chloramphenicol acetyl-transferase (CAT). The cells were cultured in various concentration of selenium dioxide. CAT expression in transfected cells was observed., Results: After transfected HeLa cells were exposed to selenium dioxide, CAT expression showed obvious increase, especially in 10 micromol/L and 30 micromol/L selenium dioxide group (P< 0.05)., Conclusion: Trough affecting regulatory regions P250 of c-fos gene, Selenium dioxide plays biological effect of regulating tumor cells. Selenium dioxide possibly has anti-tumor effects.

It is reported that selenium (Se) incorporation into garlic increases the bioactivities of garlic. Hence, the chemical changes of selenocompounds during processing and storage will influence the bioactive effectiveness of Se-enriched garlic. The principal selenocompounds in Se-enriched garlic are water-soluble, and several comparative experiments are thus conducted to examine the stabilities of the selenocompounds in water extracts of Se-enriched garlic and Se-enriched onion. The results show that preparing the garlic powder by freeze-drying technique can maintain the chemical properties of the selenium compounds in Se-enriched garlic. Se-methyl-selenocysteine is unstable in water extract of Se-enriched garlic when the extract is prepared and stored at room temperature. Specific alliinase inhibitor hydroxylamine (NHOH.HCl) effectively prevents the loss of Se-methyl-selenocysteine, which suggests that the decomposition of Se-methyl-selenocysteine may be catalyzed by alliinase. Se-methyl-selenocysteine is one of the main bioactive selenocompounds in Se-enriched garlic. The procedures of processing and storage should be carefully chosen to prevent the loss of selenocompounds and the decrease of the bioactivity of Se-enriched garlic. Se-enriched onion also contains alliinase and Se-methyl-selenocysteine, but its Se-methyl-selenocysteine is proved to be stable in the same water extract as that of Se-enriched garlic. The stability differences of Se-methyl-selenocysteine in Se-enriched garlic and onion, the mechanism of selenocompound decomposition and the bio-activities of decomposed compounds in Se-enriched garlic need to be further studied.

Objective: To compare the effects of selenium-enriched garlic (Se-garlic), garlic, Na2SeO3, and garlic + Na2SeO3 on growth of human gastric carcinoma cells., Methods: In vivo and in vitro assays were carried out in the cultured human gastric carcinoma cell line MGC803 transplanted in the nude mice by cell count, flow cytometry, Western blot and neoplasm volume measurement., Results: The inhibition effect of garlic was similar to that of Se-garlic, but Na2SeO3 was weaker than Se-garlic. Combination of garlic and Na2SeO3 was stronger than Se-garlic. In flow cytometry assay, the proportion of G1 phase was increased after 24 hour treatment of Se-garlic, garlic and Na2SeO3 in the non-synchronized cells. However, the proportion of S phase was increased in the synchronized cells. The proportion of G2 + M phase was increased both in non-synchronized and synchronized cells on treatment with the combination of garlic and Na2SeO3. The amount of Cdk2-CyclinE complex and Cdk4-CyclinD1 complex was decreased in all treated synchronized cells in immunoprecipitation and immunoblot assays. The growth of MGC803 tumor in male Balb/c nude mice was inhibited by administration of 1.67% of Se-garlic (Se 2 micrograms/g) in diet with an inhibition rate of 29.92% in tumor weight. Treatment of either 0.83% of Se-garlic or 1.67% of garlic or 4.38 micrograms/g of Na2SeO3 (Se 2 micrograms/g) could not appreciably inhibit the growth of tumor. Wrapping of a number of monocytes around the tumor was induced in 62.50% of tumors in 0.83% of the Se-garlic group., Conclusion: In vitro, Se-garlic is able to inhibit the growth of MGC803 cell through action of garlic. In vivo, Segarlic is able to inhibit growth of MGC803 tumor in nude mice by being better than garlic and selenite.

Ninety white rats were treated with liquid lead acetate. When the concentration of lead in urine was more than (0.81 +/- 0.26) mg/L and blood lead was more than (4.8 +/- 0.33) mg/L, the rats were divided into three groups randomly. The oxygenic damage indicators in serum showed SOD activity decreased and MDA content increased. In one group of lead rats fed with an organic selenium compound (code FCQY) the SOD activities were high and the lipid peroxidation was inhibited compared with controls without selenium supplementation. The lead contents of bone, kidney and liver were measured. The results suggested that the organic selenium compound could interfere with the absorption and accumulation of lead.

The effects of selenium polysaccharide and sodium selenite administered by single or repetitive intraperitoneal injection (i.p.) on blood selenium concentration, the activities of liver cytochrome P450, b5 as well as NAD(P)H cytochrome C reductase, glutathione S-transferase and glutathione were studied in rats. The biological effects of selenium polysaccharide and sodium selenite were also compared. The results indicated that the blood selenium concentration was increased rapidly and reached the peak in 2 hours followed by gradual decline after selenium polysaccharide and sodium selenite were i.p. injected at a dose of Se 0.6 mg/kg. The absorption and eliminating rates of Se from sodium selenite were faster than that from selenium polysaccharide. Administration of selenium polysaccharide and sodium selenite at a dose of 0.2 mg/kg by i.p. increased the blood selenium concentration to 2.6 and 2.1 times of those of control group, respectively, and the blood selenium concentration of selenium polysaccharide group was significantly higher than that of sodium selenite group (P < 0.05). The activities of liver cytochrome P450, b5 and GST were inhibited by selenium polysaccharide and sodium selenium in vivo and in vitro experiments. Those proteins were decreased to 57%, 70% and 62% of the control, respectively, by selenium polysaccharide which has particularly stronger effects on cytochrome P-450 monooxygenase system (P < 0.05). The two selenium compounds did not appear to affect the activity of NAD(P)H cytochrome C reductase. Both of the selenium polysaccharide and sodium selenite could enhance the activity of glutathion peroxidase significantly (P < 0.05).

Effect of selenium on the protein kinase c-alpha (PKC-alpha) gene expression was observed in the preneoplastic lesions in liver of S.D. rat Solt-Farber model. Overexpression of PKC-alpha was found in preneoplastic liver but not in partially hepatectomized liver. Administration of 4PPm Na2SeO3 in water 2 weeks before i.p injection of DEN (200 ng/kg bw) for 8 weeks reduced the PKC-alpha gene overexpression in preneoplastic liver and the formation of hyperplastic foci, alpha-GT-altered foci and preneoplastic lesions.