期刊文献+

无机砷调节小鼠胚胎干细胞中含硒蛋白质的表达 被引量:2

下载PDF
导出
摘要 在人类体内至少有25种硒蛋白(含有硒代半胱氨酸),啮齿动物体内也已经分离出24种相似的蛋白质,它们在氧化应激,氧化还原调控以及解毒方面发挥重要的作用。无机砷(iAs)暴露调节硒蛋白的表达可能揭示砷毒性的分子机制。为研究iAs暴露对硒蛋白表达的影响,研究者在培养基中添加iAs来调节小鼠胚胎干细胞中已知的含硒蛋白质的表达,小鼠胚胎干细胞分别用亚砷酸盐(iAsⅢ)(0.25~0.5μmol/L)、砷酸盐(iAsⅤ)(1.0~2.0μmol/L),对照亚硒酸钠(SeⅣ)(0.5μmol/L)处理。实时定量PCR检测含硒蛋白质mRNA的表达水平,蛋白免疫印迹分析和酶活性检测来证实硒蛋白的表达上调。结果表明:CGR8干细胞亚砷酸盐(iAsⅢ)(0.25~0.5μmol/L)、砷酸盐(iAsⅤ)(1.0~2.0μmol/L)处理组活性氧自由基(ROS)的产生和核转录因子(Nrf2)的聚集均有显著增加。iAsⅢ(0.5μmol/L)、iAsⅤ(2.μmol/L)处理24 h可引起抗氧化含硒蛋白质(Gpx1、Gpx4、Tr1)的表达显著增加,而硒蛋白H和内质网相关硒蛋白(15-Sep、SelK、SelM、SelS)mRNA的表达显著降低。SeⅣ(0.5μmol/L)处理组未见到明显的硒蛋白表达下调。这些结果表明iAs暴露不仅调节抗氧化硒蛋白而且可以调节内质网弹性相关硒蛋白。但仍需进一步的研究证实这些硒蛋白调节基因是补硒预防无机砷毒性的作用基因。.
出处 《国外医学(医学地理分册)》 CAS 2013年第1期38-41,共4页 Foreign Medical Sciences:Section of Medgeography
  • 相关文献

参考文献19

  • 1Huang Z. Inorganic arsenic modulates the expression of selenoproteins in mouse embryonic stem cel[J]. Toxicol Letter,2009, doi: 10. 1013.
  • 2Andrew AS,Jewell DA,Mason RA,et al. Drinking-water arsenic exposure modulates genc expression in human lymphocytcs from a U.S. Population[J]. Environ Health Perspect, 2008, 116,524-531.
  • 3Ahuja Yr, Vijayalakshmi V, Polasa K. Stem cell test: a practical tool in toxicogenomics[J]. Toxicology, 2007,231,1-10.
  • 4Argos M,Kibriya MG,Parvez F,et al. Gene expression profiles in peripheral lymphocytes by arsenic exposure and skinlesion status in a Bangladeshi population[J]. Cancer Epidemiol Biomarkers Prev, 2006,15,1367-1375.
  • 5Banning A,Deubel S,Kluth D,et al. The GI-GPx gene is a target for Nrf2 Mol[J]. Cell Biol, 2005,25,4914-4923.
  • 6Brigelius-flohe R. Selenium compounds and selenoproteins in cancer[J]. Chem. Biodivers, 2008,5,389-395.
  • 7Chen Y, Hall M, Graziano JH, et al. A prospective study of blood selenium levels and the risk of arsenic-relatedpremalig- nant skin lesions[J]. Cancer Epidemiol Biomarkers Prev,2007, 16,207-213.
  • 8Curran JE,Jowett JB, Elliott KS, et al. Geneticvariation in selenoprotein S influences inflammatory response[J]. Nat Genet, 2005,37,1234-1241.
  • 9Dinkova-kostova AT, Holtzclaw WD, Wakabayashi N. Keapl, the sensorfor electrophiles and oxidants that regulates the phase 2 response,is a zincmetalloprotein[J]. Biochemistry, 2005,44: 6889-6899.
  • 10Du YZ, Wang KK,Fang H,et al. Coordination of intrinsic,extrinsic,and cndoplasmic reticulum-mediated apoptosis by imatinib mesylate combined with arsenictrioxidv in chronic myeloid leukcmia[J]. Blood,2006,107 : 1582-1590.

二级参考文献31

  • 1高建忠,黄克和.动物硒蛋白研究进展[J].畜牧与兽医,2004,36(7):39-42. 被引量:33
  • 2HU YJ,DIAMOND AM.Role of glutathione peroxidase 1 in breast cancer:loss of heterozygosity and allelic differences in the response to selenium[J].Cancer Research,2003,63:3347-3351.
  • 3HU YJ,DOLAN ME,RICHARD B,et al.Allelic loss at the GPx-1 locus in cancer of the head and neck[J].Bid Trace Element Res,2004,101:97-106.
  • 4HU YJ,KOROTKOV KV,MEHTA R,et al.Distribution and functional consequences of nucleotide polymorphisms in the 3'-untranslated region of the human Sep15 gene[J].Cancer Res,2001,621(5):2307-2310.
  • 5NASR MA,HU YJ,DIAMOND AM.Allelic loss at the SEP15 locus in breast cancer[J].Cancer Therapy,2003,1:293-298.
  • 6JABLONSKA E,GROMADZINSKA J,SOBALA W,et al.Lung cancer risk associated with selenium status is modified in smoking individuals by Sep15 polymorphism[J].Eur J Nutr,2008,47:47-54.
  • 7PETERS U,CHATTERJEE U,HAYES RB,et al.Variation in the Selenoenzyme genes and risk of advanced distal colorectal adenoma[J].Cancer Epidemiol Biomarkers Prev,2008,17(5):1144-1153.
  • 8MENTUCCIA D,PROIETTI-PANNUNZI L,TANNER K.et al.Association between a novel variant of the human type 2 deiodinase gene thr92ala and insulin resistance[J].Diabetes,2002,51:880-883.
  • 9GRARUP N,ANDERSEN MK,CAMILLA H.et al.Studies of the common dio2 thr92ala polymorphism and metabolic phenotypes in 7342 danish white subjects[J].J Clin Endocrinol Metab,2007,92(1):363-366.
  • 10CANANI LH,CAPPC,DORA JM.et al.The type 2 deiodinase a/g (thr92ala) polymorphism is associated with decreased enzyme velocity and increased insulin resistance in patients with type 2 diabetes mellitus[J].J Clin Endocrinol Metab,2005,90(6):3472-3478.

共引文献10

同被引文献24

  • 1Yoshida T. Yamauchi H. Sun GF. Chronic health effects in people exposed to arsenic via the drinking water: dose-response relationships in review [J]. Toxicol Appl Pharmacol , 2004 .198 (3) :243-252.
  • 2Sun G. Arsenic contamination and arsenicosis in China [J]. Toxicol Appl Pharmacol , 2004 .198(3) : 268-271.
  • 3Uddin R. Huda NH. Arsenic poisoning in Bangladesh[J]. Oman Med.2011.26(3): 207-209.
  • 4Sham KW. Comparative Study of Liver Cancer Patients in Arsenic Exposed and Non-exposed Areas of Pakistan [J]. Biol Trace Elem Res. 2011.144(1-3) :86-96.
  • 5Asutosh Ghosh. Evaluation of Chronic Arsenic Poisoning Due to Consumption of Contaminated Ground Water in West Bengal. India[J]. Int J Prev Med.2013.4(8) :976-979.
  • 6Guha M, Effect of chronic intake of arsenic-contaminated water on liver [J]. Toxicol Appl Pharrnacol , 2005.206 (2): 169- 175.
  • 7任先云.内蒙古自治区自然科学学术年会优秀论文集[C].内蒙古科技出版社,2003.
  • 8Cohen SM, Arnold LL, Eldan M, et al. Methylated arsenicals: the implications of metabolism and carcinogenicity studies in rodents to human risk assessment[J]. Crit Rev Toxicol, 2006, 36(2) :99-133.
  • 9Coppin JF, Qu W, Waalkes MP. Interplay between cellular methyl metabolism and adaptive efflux during oncogenic trans- formation from chronic arsenic exposure in human cells[J]. Bi- ol Chem,2008,283(28) : 19342-19350.
  • 10Zhao CQ, Young MR, Diwan BA,et al. Association of arsenic- induced malignant transformation with DNA hypomethylation and aberrant gene expression[J]. Proc Natl Acad Sci USA, 1997,94(20) :10907-10912.

引证文献2

二级引证文献9

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部