Redifferentiation of Human Gastric Cancer Cells Induced by Ascorbic Acid and Sodium Selenite

Objective To explore the effects and mechanisms of ascorbic acid (AA) and sodium selenite (SS) on growth inhibition and redifferentiation in human gastric cancer cells. Methods In the present study, trypan blue dye exclusion method was used to determine the cell growth curve and mitotic index, cell electrophoresis and colonogenic potential were used as the indexes of redifferentiation. In order to find out the mechanisms of redifferentiation, the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT) were assayed, the content of malondialdehyde (MDA), reduced glutathione (GSH) and H2O2 were evaluated. Results After treatment with AA 3 mol/L + SS 2μmol/L, the growth rate and mitotic index of human gastric cancer cells (MGc-803) decreased remarkably. The indexes related with cell malignancy were alleviated. For example, cell surface charge was obviously decreased, the electrophoresis rate was dropped from 2.21 to 1.15μm·s-1·V-1·cm-1. The indexes related with cell redifferentiation were promoted. For example, the colonogenic potential was decreased to 93.5%. These results indicated that redifferentiation of human gastric cancer cells was successfully induced by AA + SS. The activities of SOD and GPX were significantly higher, while the activity of CAT was slower in treated group than that in the control. The content of MDA was slightly decreased, GSH was sharply decreased, and H2O2 content was dramatically increased. Conclusion These results indicated that combination of ascorbic acid and sodium selenite may induce the redifferentiation of human gastric cancer cells and inhibit cell growth by virtue of enhancing the activities of antioxidative enzymes and inducing the formation of H2O2, and altering the cell redox status. Combination of ascorbic acid and sodium selenite may be a potent anticancer agent for human gastric cancer.

Sodium selenite ameliorates dextran sulfate sodiuminduced chronic colitis in mice by decreasing Th1, Th17, and γδT and increasing CD4(+)CD25(+) regulatory T-cell responses

AIM To assess the effect of sodium selenite on the severity of dextran sulfate sodium(DSS)-induced colitis in C57BL/6 mice.METHODS Mice were randomly divided into four groups(n = 10/group): normal group, selenium(Se) group, chronic colitis group, and Se + chronic colitis group. The mice were sacrificed on day 26. Survival rates, clinical symptoms, colon length, and histological changes were determined. The percentages and absolute numbers of immune system cells in the lamina propria lymphocytes(LPL) of the colon, the expression of m RNA in colon tissue, and the concentrations of Th1, Th17, and Treg cytokines in LPL from the large intestine, were measured.RESULTS Se significantly ameliorated the symptoms of colitis and histological injury(P < 0.05 each), increasing the proportions of neutrophils and CD4+ CD25+ T cells(P < 0.05 each) and decreasing the proportions of γδT cells, CD4+, CD4+CD44+, and CD4+ CD69+ T cells in LPL(P < 0.05 each). Moreover, Se reduced the expression of IL-6, IFN-γ, IL-17 A, IL-21, T-bet, and RORγt(P < 0.05 each), but enhanced the expression of IL-10 and Foxp3(P < 0.05 each). CONCLUSION These results suggest that Se protects against DSSinduced chronic colitis perhaps by increasing the number of CD4(+)CD25(+) Tregs that suppress the secretion of proinflammatory cytokines and populations of Th1, Th17, and γδT cells.

Sodium selenite promotes neurological function recovery after spinal cord injury by inhibiting ferroptosis

Ferroptosis is a recently discovered form of iron-dependent cell death,which occurs during the pathological process of various central nervous system diseases or injuries,including secondary spinal cord injury.Selenium has been shown to promote neurological function recovery after cerebral hemorrhage by inhibiting ferroptosis.However,whether selenium can promote neurological function recovery after spinal cord injury as well as the underlying mechanism remain poorly understood.In this study,we injected sodium selenite(3μL,2.5μM)into the injury site of a rat model of T10 vertebral contusion injury 10 minutes after spinal cord injury modeling.We found that sodium selenite treatment greatly decreased iron concentration and levels of the lipid peroxidation products malondialdehyde and 4-hydroxynonenal.Furthermore,sodium selenite increased the protein and mRNA expression of specificity protein 1 and glutathione peroxidase 4,promoted the survival of neurons and oligodendrocytes,inhibited the proliferation of astrocytes,and promoted the recovery of locomotive function of rats with spinal cord injury.These findings suggest that sodium selenite can improve the locomotive function of rats with spinal cord injury possibly through the inhibition of ferroptosis via the specificity protein 1/glutathione peroxidase 4 pathway.

Comparison of the impact of epigallocatechin gallate and ellagic acid in an experimental cataract model induced by sodium selenite

AIM：To compare the potential protective effects of epigallocatechin gallate（EGCG） and ellagic acid（EA） in an experimental cataract model.●METHODS：Twenty-eight Spraque-Dawley rat pups were assigned into four groups.All the rats,except for those in the control group,were injected subcutaneously sodium selenite to induce experimental cataract on the postpartum ninth day,and between 10 th and 14 th days.Rats in the sham,EGCG,and EA groups were intraperitoneally administered 50 mg/（kg·d） saline solution,50 mg/（kg·d） EGCG and 200 mg/（kg·d） EA,respectively.The reduced glutathione（GSH） and malondialdehyde（MDA） levels,total antioxidant status（TAS） and total oxidant status（TOS） in lens supernatants were measured.RESULTS：The mean cataract gradings in EGCG and EA groups were found to be significantly lower than that in sham group（P〈0.001）.The mean GSH levels and TASs in EGCG and EA groups were significantly higher than that in sham group while mean MDA levels and TOSs in EGCG and EA groups were significantly lower than that in the sham group（P〈0.001）.CONCLUSION：EGCG and EA have protective effects on cataract development via the inhibition of oxidative stress.

Change of choline compounds in sodium selenite-induced apoptosis of rats used as quantitative analysis by in vitro 9.4T MR spectroscopy

AIM: To study liver cell apoptosis caused by the toxicity of selenium and observe the alteration of choline compounds using in vitro 9.4T high resolution magnetic resonance spectroscopy. METHODS: Twenty male Wistar rats were randomly divided into two groups. The rats in the treatment group were intraperitoneally injected with sodium selenite and the control group with distilled water. All rats were sacrifi ced and the livers were dissected. 1H-MRS data were collected using in vitro 9.4T high resolution magnetic resonance spectrometer. Spectra were processed using XWINNMR and MestRe-c 4.3. HE and TUNEL staining was employed to detect and confi rm the change of liver cells. RESULTS: Good 1H-MR spectra of perchloric acid extract from liver tissue of rats were obtained. The conventional metabolites were detected and assigned. Concentrations of different ingredient choline compounds in treatment group vs control group were as follows: total choline compounds,5.08 ± 0.97 mmol/L vs 3.81 ± 1.16 mmol/L (P = 0.05); and free choline,1.07 ± 0.23 mmol/L vs 0.65 ± 0.20 mmol/L (P = 0.00). However,there was no statistical signif icance between the two groups. The hepatic sinus and cellular structure of hepatic cells in treatmentgroup were abnormal. Apoptosis of hepatic cells was confi rmed by TUNEL assay. CONCLUSION: High dose selenium compounds can cause the rat liver lesion and induce cell apoptosis in vivo. High resolution 1H-MRS in vitro can detect diversified metabolism. The changing trend for different ingredient of choline compounds is not completely the same at early period of apoptosis.

Protective Role of C-Phycocyanin Against Secondary Changes During Sodium Selenite Mediated Cataractogenesis

Age related cataract is the leading cause of blindness associated with accumulation of oxidative stress in the eye lens.The present investigation reveals the rational of the beneficial effects of the natural compound C-phycocyanin(CPC)is beneficial when administered to rat pups to protect against the secondary effects of sodium selenite induced cataractogenesis.A single subcutaneous dose of sodium selenite(19 lmol/kg body weight)on the 10th day of postpartum is adequate to induce cataract in rat pups.Serum biochemical parameters,such as the level of electrolytes,mean activities of anti-oxidant enzymes i.e.superoxide dismutase,catalase and reduced glutathione were observed to be significantly altered during selenite induced cataractogenic process.Histopathological examination revealed signs of degradation of normal cell architecture in the liver,kidney and eye lens.Interestingly,the deleterious effects of sodium selenite toxicity were restored with the simultaneous treatment with C-PC.The results suggest that an administration of 200 mg/kg body weight of C-PC has the ability to prevent/alter the secondary changes reflected in the serum biochemical and histological modifications in rats exposed to sodium selenite.These results complement the beneficial role of C-PC of cyanobacterial origin as a efficacious anti-cataractogenic agent against sodium selenite toxicity.

Sodium selenite may be not the optimal speciation as an effective therapy for arsenic-induced anxiety-/depression-like behavior

Major depressive disorder is a serious and prevalent neuropsychiatric disorder,affecting more than 350 million people worldwide.Here,sodium selenite(SS)was selected as the selenite supplement to improve the behavior in a mouse model of depression induced by As.SS may be not the optimal speciation for selenite supplementation and the source of the SS used in the study was not disclosed.There are many mouse models of depression and anxiety;however,in the current study,a classical mouse model of depression was not used.Thus,several questions still need to be further discussed.Taken together,the results indicate that SS may be not the optimal speciation as an effective therapy for As-induced anxiety-/depression-like behavior.

Effect of Sodium Selenite-Chitosan Compound Preservative on Storability of Kumquats

[Objectives]To explore the effect of sodium selenite-chitosan compound preservative on storability of kumquats.[Methods]Under the condition of room temperature,fresh kumquats were coated with different concentrations of sodium selenite-chitosan compound preservative,respectively.[Results]Sodium selenite-chitosan compound preservative reduced the weight loss rate,delayed the decline of vitamin C,soluble solids,titratable acid and GSH contents,slowed down the accumulation of MDA,inhibited the increase of PPO activity,and increased to a certain extent the activity of SOD in fresh kumquats.[Conclusions]Sodium selenite-chitosan compound preservative maintained the quality and prolonged the shelf life of kumquats.The preservation effect of compound preservative composed of 4 mg/L sodium selenite and 8 g/L chitosan was the best.

Systematic pharmacology analysis of Sodium 8-(((carboxymethyl)amino)methyl)-4',7-bishydroxy-isoflavone-3'-sulfonate

The purpose of this study is to use the newly synthesized molecule Sodium 8-(((carboxymethyl)amino)methyl)-4',7-bishydroxy-isoflavone-3'-sulfonate(M)as a research object,the pharmacological mechanism of the molecule was analyzed by using a series of Systematic pharmacology methods.The results show that the M molecule has a higher drug-like DL value of 0.59 and better molecular property parameters,namely Hdon=4,Hacc=10 and AlogP=0.94;A total of 11 M molecules related targets,namely F2,ESR1,AR,F10,CA2,DPP4,CCNA2,PRSS1,CDK2,GSK3B and PTPN1;A total of 140 diseases are associated with M molecule targets,and these diseases are mainly related to cancer and cardiovascular diseases;A total of 52 pathways involve the pharmacological mechanisms of M molecules,which are mainly related to cancer and other related diseases;GO-enriched analysis showed that these targets are closely related to the regulation of peptidase activity and biological processes such as blood coagulation and hemostasis.This article clearly demonstrated the pharmacological mechanism of M molecule,which provides references for exploring the pharmacological mechanism of new compounds.

亚硒酸钠通过活性氧(ROS)/谷胱甘肽(GSH)/谷胱甘肽过氧化物酶4(GPX4)轴诱导非小细胞肺癌A549细胞铁死亡

硒作为人体必需的微量元素,具有抗癌作用,但其抗癌机制尚不明确,因此,通过探讨亚硒酸钠是否可以通过铁死亡途径抑制肺癌A549细胞增殖及其肺癌A549细胞发生铁死亡的具体机制。通过细胞增殖实验(CCK-8实验)及细胞计数实验评价亚硒酸钠对A549细胞增殖的影响,通过流式细胞术分析亚硒酸钠对肺癌A549细胞内线粒体膜电位(MMP)及活性氧(ROS)水平的影响,通过亚铁离子检测试剂盒检测亚硒酸钠作用后肺癌A549细胞内亚铁离子含量变化,MDA检测试剂盒分析亚硒酸钠作用后肺癌A549细胞内脂质氧化产物丙二醛(MDA)含量,分光光度法分析亚硒酸钠对肺癌A549细胞内谷胱甘肽过氧化物酶4(GPX4)及谷胱甘肽(GSH)的表达影响。研究发现:亚硒酸钠能够显著抑制肺癌A549细胞增殖,且亚硒酸钠抑制肺癌A549细胞的半数抑制率(IC_(50))为10μmol/L;亚硒酸钠能诱导肺癌A549细胞内ROS过度积累并使细胞内谷胱甘肽耗竭;亚硒酸钠作用后,细胞内线粒体膜电位水平显著降低,MDA含量升高而GPX4蛋白表达下调。研究表明,亚硒酸钠能通过诱导肺癌A549细胞内ROS过度积累,引起细胞内GSH大量耗竭,导致GPX4表达下降,诱导细胞发生铁死亡。

7.0 T MRI评估青藏高原环境下亚硒酸钠改善大鼠肺动脉高压后左心室功能的初步研究

目的利用心脏磁共振(cardiac magnetic resonance,CMR)组织追踪技术评估高原低氧环境下亚硒酸钠(sodium selenite,SE)对肺动脉高压(pulmonary arterial hypertension,PAH)后左心室功能的改善作用并初步探索SE提升PAH后左心室功能的潜在机制。材料与方法46只雄性SD大鼠于购置第二日从成都(海拔500 m)陆运至青海省玉树藏族自治州高原动物实验室(海拔4250 m),随机分为对照组(n=10)、模型组[野百合碱(monocrotaline,MCT)组,n=20]和治疗组(SE组,n=16)。高原低氧环境下饲养28周后,MCT组和SE组大鼠均接受一次性腹腔注射60 mg/kg的MCT以建立PAH模型,而对照组则接受等量的生理盐水注射。一周后,SE组大鼠通过灌胃方式给予0.7 mg/kg的SE持续治疗一个月,对照组和MCT组进行常规饲养。干预完成后将大鼠运回成都。随机从三组中各选取8只大鼠进行CMR成像,以评估左心室功能、应变和T2弛豫时间。CMR扫描结束后取材大鼠心脏组织和血液分别进行病理、血生化检测。结果相较于对照组,MCT组的左心室射血分数(left ventricular ejection fraction,LVEF)(61.36%±4.50%)和左心室整体周向应变(left ventricular global circumferential strain,LVGCS)(−19.81%±0.84%)显著降低(P值均<0.05)。然而,与MCT组相比,SE组的LVEF(75.29%±5.67%)、左心室整体径向应变(left ventricular global radial strain,LVGRS)(42.90%±5.94%)和LVGCS(−21.43%±1.33%)明显提高(P值均<0.05),表明SE治疗提高了PAH后左心室功能。对照组和MCT组血清中谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)的含量差异具有统计学意义[对照组vs.MCT组:(16544.38±3734.02)U/mL vs.(9974.00±900.80)U/mL,P<0.05],MCT组血清中丙二醛(malondialdehyde,MDA)相较于对照组有所增加[MCT组vs.对照组:9.00(7.60,13.20)μmol/L vs.3.86(3.60,6.20)μmol/L,P<0.01],提示MCT组大鼠抗氧化能力下降。经SE干预后,SE组的大鼠表现出血清中超氧化物歧化酶(superoxide dismutase,SOD)(292.60±44.38)U/mL和GSH-Px(17843.26±3585.44)U/mL水平的升高以及MDA[5.37(5.10,6.20)μmol/L]水平的降低(P值均<0.05)。凋亡染色表明,与对照组相比,MCT组左心室的相对荧光强度显著增高(P<0.001),而治疗后SE组的相对荧光强度较MCT组明显降低(P<0.001)。结论CMR组织追踪技术能够定量评估肺动脉高压后左心室功能的异常;SE在高原低氧环境下能改善PAH后左心室功能,其机制可能与其提高大鼠抗氧化能力、减轻心肌细胞凋亡有关。

蚯蚓处理添加不同硒源牛粪的比较研究

根据蚯蚓的生长繁殖和蚓体富硒情况,选出两种不同的硒源按不同的浓度混入牛粪中,利用蚯蚓处理牛粪,实现养殖业粪污的资源化利用。试验利用亚硒酸钠(Sodium selenite,SS)与富硒酵母(Selenium enriched yeast,SY)易富硒、价格低廉优势,选取亚硒酸钠和富硒酵母作为硒源添加剂,促进蚯蚓对硒富集,生产优质富硒肥料。探索有机硒与无机硒对蚯蚓生长繁殖的影响,以期实现蚯蚓养殖处理粪污的同时生产富硒肥料,提高特种养殖经济效益。试验通过在牛粪基料中添加2种硒源(亚硒酸钠SS、富硒酵母SY)、3个水平(5、10、15 mg·kg^(-1)),以硒元素计,选择出两种硒源的最适富硒量。结果表明,随着牛粪中硒添加量升高,蚯蚓的生长繁殖逐渐被抑制,硒浓度越高,蚯蚓的生长繁殖被抑制程度越高,当SY的硒添加量为15 mg·kg^(-1)时,蚯蚓有明显的中毒现象;硒浓度越高,蚯蚓体硒含量越高,二者成正比;牛粪中添加同一水平的SS与SY,SY组蚯蚓的硒含量明显高于SS组。

亚硒酸钠通过增加ROS抑制PI3K/AKT通路改善肺癌PC-9/GR细胞对吉非替尼的耐药性

目的:探讨亚硒酸钠对肺癌耐药细胞PC-9/GR增殖、凋亡的影响,研究其是否能改善吉非替尼耐药及可能机制。方法:不同浓度(0、5、10、20、40μmol/L)亚硒酸钠处理细胞24、36、48 h后,CCK-8法检测亚硒酸钠对细胞增殖的影响并选择合适浓度用于后续实验。不同浓度(0、2.5、5、10、20、40μmol/L)吉非替尼单药及联合亚硒酸钠(6μmol/L)处理细胞48 h,分别计算半数抑制浓度(IC50),得出亚硒酸钠对PC-9/GR逆转倍数;流式细胞术检测各组细胞凋亡;DCFH-DA法检测细胞内ROS水平;Western blot实验检测各组细胞中p-PI3K、p-AKT、Bax、Bcl-2表达水平。结果:随亚硒酸钠浓度升高及作用时间延长,细胞增殖抑制率逐渐升高(P<0.05);单药吉非替尼组的IC50值为16.051μmol/L,联合亚硒酸钠后IC50值为5.406μmol/L,表明亚硒酸钠能够逆转吉非替尼的耐药,其逆转耐药倍数为2.969倍。与吉非替尼和亚硒酸钠单药组相比,联合治疗组的细胞凋亡率显著升高,ROS水平及Bax蛋白表达上调,p-PI3K、p-AKT、Bcl-2表达下调,经N-乙酰半胱氨酸(NAC)消除ROS后抵消了亚硒酸钠对PI3K/AKT通路的抑制作用(P<0.05)。结论:亚硒酸钠联合吉非替尼能提高肺腺癌耐药细胞的敏感性,抑制细胞的增殖,同时诱导细胞凋亡,这一过程可能通过ROS依赖性下调PI3K/AKT通路的表达实现。

Mechanistic research:Selenium regulates virulence factors,reducing adhesion ability and inflammatory damage of Helicobacter pylori

BACKGROUND The pathogenicity of Helicobacter pylori is dependent on factors including the environment and the host.Although selenium is closely related to pathogenicity as an environmental factor,the specific correlation between them remains unclear.AIM To investigate how selenium acts on virulence factors and reduces their toxicity.METHODS H.pylori strains were induced by sodium selenite.The expression of cytotoxin-associated protein A(CagA)and vacuolating cytotoxin gene A(VacA)was determined by quantitative PCR and Western blotting.Transcriptomics was used to analyze CagA,CagM,CagE,Cag1,Cag3,and CagT.C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite induction,and H.pylori colonization,inflammatory reactions,and the cell adhesion ability of H.pylori were assessed.RESULTS CagA and VacA expression was upregulated at first and then downregulated in the H.pylori strains after sodium selenite treatment.Their expression was significantly and steadily downregulated after the 5th cycle(10 d).Transcriptome analysis revealed that sodium selenite altered the levels affect H.pylori virulence factors such as CagA,CagM,CagE,Cag1,Cag3,and CagT.Of these factors,CagM and CagE expression was continuously downregulated and further downregulated after 2 h of induction with sodium selenite.Moreover,CagT expression was upregulated before the 3rd cycle(6 d)and significantly downregulated after the 5th cycle.Cag1 and Cag3 expression was upregulated and downregulated,respectively,but no significant change was observed by the 5th cycle.C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite induction.The extent of H.pylori colonization in the stomach increased;however,sodium selenite also induced a mild inflammatory reaction in the gastric mucosa of H.pylori-infected mice,and the cell adhesion ability of H.pylori was significantly weakened.CONCLUSION These results demonstrate that H.pylori displayed virulence attenuation after the 10th d of sodium selenite treatment.Sodium selenite is a low toxicity compound with strong stability that can reduce the cell adhesion ability of H.pylori,thus mitigating the inflammatory damage to the gastric mucosa.

基于网络药理学联合分子对接技术探讨色苷酸钠预防低氧性急性肺动脉高压的作用机制

目的基于网络药理学联合分子对接技术探讨肥大细胞(Mast cells,MCs)脱颗粒抑制剂—色苷酸钠(Sodium Cromolyn,SCG)预防低氧性急性肺动脉高压(Acute Pulmonary Hypertension,APH)的作用机制。方法(1)从Swiss Target Predicition、TargetNet、UniProt、OMIM、GeneCards、NCBI gene数据库中获取色苷酸(Cromolyn)治疗APH的靶基因,使用Venny 2.1.0在线工具绘制Venn图并获取交集基因。通过String数据库构建蛋白质相互作用(protein-protein interaction,PPI)网络。使用Cytoscape软件对PPI网络进行拓扑分析,使用DAVID数据库做基因本体(Gene Ontology,GO)功能分析、京都基因与基因组百科全书(Kyoto Encyclopedia of Genes and Genomes,KEGG)富集分析,并筛选出相关信号通路,使用Autodock Vina软件进行分子对接分析。(2)给予SD大鼠SCG预处理(100 mg/kg,ig,Bid,3 d),利用低压舱(模拟海拔7000 m,12 h)构建急性低氧动物模型。将SD大鼠随机分为低氧对照组(HC组,12只)和低氧SCG处理组(HSCG组,12只)。将低压舱海拔由7000 m降至3500 m,应用颈外静脉插管术监测肺动脉压(Pulmonary arterial pressure,PAP),通过蛋白质印迹(Western Blot,WB)实验检测FcεRⅠ、SYK、mTOR蛋白和p-mTOR(Ser2448)蛋白在SD大鼠肺组织中的表达水平。结果(1)基于网络药理学分析方法筛选出FcεRⅠ蛋白和mTOR信号通路及核心蛋白FcεRⅠ、SYK、mTOR。FcεRⅠ、SYK、mTOR分别与Cromolyn对接,均具有良好的结合活性,构象较稳定。(2)SD大鼠mPAP结果:与HC组比较,HSCG组的mPAP下降(P<0.05)。(3)肺组织WB结果:与HC组比较,HSCG组SD大鼠肺组织中的FcεRⅠ、SYK、mTOR蛋白和p-mTOR(Ser2448)蛋白表达均下降(P<0.05),p-mTOR(Ser2448)/mTOR亦下降(P<0.05)。结论经SCG预处理,可减弱急性低氧应激SD大鼠肺组织MCs中的FcεRⅠ、SYK、mTOR蛋白和p-mTOR(Ser2448)蛋白表达、降低p-mTOR(Ser2448)/mTOR,致FcεRⅠ、mTOR信号通路的激活水平降低,进而抑制肺组织中MCs的活化脱颗粒过程,减少收缩血管活性物质的释放,达到预防低氧性APH的作用。

Selenium: The Cancer Shield

Introduction: Breast cancer is one of the most common types of cancer in the world and the treatments are being improved day by day. Although chemotherapy agents have begun to be used, side effects, resistance development and toxicity seen with these drugs are still steps that limit treatment. Objective: Our aim in this study is to show whether sodium selenate (NaS), which has different effects on many different cells, has antiproliferative and apoptotic effects on MCF-7 breast cancer cells, considering the dose-time relationship, and to reveal its effect on oxidant stress parameters. Methods: 10, 20, 30, 40 and 50 μM sodium selenate was applied to the cells for 24, 48 and 72 hours. MTT test was applied to show the proliferative effect. Apoptosis was also measured with Annexin V/7AAD in MCF7 cells. Malondaldehyde (MDA) and Glutathione (GSH) levels were studied to reveal the oxidant/antioxidant balance. Results: It has been shown that as the NaS dose increases in MCF-7 cells, cell viability decreases (p 0.05), but at all subsequent increasing NaS doses, viability was found statistically significant decreased (p: 0.001, p 0.05, respectively). Conclusion: Considering that NaS has an antitumor effect on breast cancer, increases oxidative stress and increases apoptosis by supressing the antioxidant protection system, and does not have a toxic effect on normal body cells at certain doses. When all these features evaluated, we think, selenium should be considered as a natural option in the treatment of breast cancer.

不同浓度外源硒对魔芋球茎硒含量和营养指标的影响

为探明花魔芋、白魔芋以及两者杂交后代优选品系ZL-19的富硒和耐硒能力,以及外源硒对魔芋球茎营养物质的影响,采用盆栽的方式开展不同浓度亚硒酸钠(0、5、10、20、40 mg·kg^(-1))灌根试验。结果表明,不同品种(系)球茎最高含硒量为:ZL-19与白魔芋相当,为0.192 mg·kg^(-1),低于花魔芋(0.265 mg·kg^(-1))。在耐硒能力方面:ZL-19>白魔芋>花魔芋,而在富硒能力方面花魔芋>ZL-19>白魔芋。花魔芋在外源硒浓度为10 mg·kg^(-1)时,球茎各项营养指标综合表现较优,球茎鲜质量增加了13.13%,球茎总糖、还原糖、总蛋白、可溶性蛋白含量和GSH-Px活性分别达到了71.265、27.019、50.811、17.605 mg·g^(-1)和1.845 U·g^(-1);白魔芋在外源硒浓度为20 mg·kg^(-1)时,球茎各项营养指标综合表现较优,球茎鲜质量增加了12.94%,球茎总糖、还原糖、总蛋白和可溶性蛋白含量和GSH-Px活性分别达到了97.012、29.632、52.773、16.892 mg·g^(-1)和1.642 U·g^(-1);ZL-19同样在外源硒浓度为20 mg·kg^(-1)时,球茎各项营养指标综合表现较优,球茎鲜质量增加了28.80%,球茎总糖、还原糖、总蛋白和可溶性蛋白含量和GSH-Px活性分别达到了84.717、31.819、49.402、17.709 mg·g^(-1)和1.719 U·g^(-1)。

罗伊氏乳杆菌富集有机硒转化条件的研究

为筛选富有机硒罗伊氏乳杆菌添加剂的最优生产条件,试验以罗伊氏乳杆菌为研究对象,对其富集有机硒的理想条件进行探索。将不同质量浓度的无菌亚硒酸钠(0、20、40、60、80、100、120μg/mL)加入到改良的乳酸菌培养基(MRS培养基)中,进行耐硒试验,并观察菌落数(CFU)及菌落颜色,判定不同质量浓度的亚硒酸钠对罗伊氏乳杆菌生长的影响;采用3,3’-二氨基联苯胺(3,3’-DAB)分光光度法测定罗伊氏乳杆菌富集有机硒的含量。结果表明,每克菌体转化的硒量不同亚硒酸钠浓度组之间差异极显著(P <0.01),当亚硒酸钠浓度在100μg/mL时,罗伊氏乳杆菌有机硒的转化量为4.40 mg/g,转化率为13.3%,达到有机硒富集的最大临界值,且此浓度对罗伊氏乳杆菌增殖影响较小。

硒化物在文蛤响应镉胁迫过程中作用的转录组学分析

研究两种硒化物在文蛤富集、排出镉过程中的作用,对文蛤进行转录组测序,并进行生物信息学分析,以探讨硒化物对Cd^(2+)代谢相关机制。硒化卡拉胶组和亚硒酸钠组共产出587 855条高质量reads。基因本体分析功能注释到15 380条unigenes, KEGG通路注释到18 866条unigenes。差异基因主要富集到肌球蛋白复合物(myosin complex)、离子通道抑制(ion channel suppression)等基因本体分析功能中。差异基因KEGG通路富集显示,在嘌呤代谢(purinemetabolism)、ECM受体相互作用(extracellularmatrix receptor interaction)、硒化合物代谢(metabolism of selenium compounds)等通路显著富集。从结果分析Cd^(2+)可以使文蛤体内蛋白转录修饰出现异常;有机硒可以通过调控金属离子通道活性来排出细胞内的Cd^(2+);无机硒主要作用于文蛤细胞表面,增强其表面活性抵御Cd^(2+)进入细胞;差异基因KEGG注释结果表明有机硒与无机硒在文蛤重金属代谢中作用机制以及途径不相同。