期刊文献+

硫氧还蛋白系统与高氧肺损伤 被引量:1

下载PDF
导出
摘要 动物实验和临床研究表明,长期高浓度供氧可引起新生儿尤其早产儿产生氧化应激性损伤,多数学者认为这种氧化应激损伤在高氧肺损伤发生发展中起关键作用。高氧时,氧化应激对肺泡Ⅱ型上皮细胞(alveolar epithelial cell typeⅡ,AECⅡ)的影响包括对肺泡上皮细胞的损伤和对肺泡上皮细胞的保护。AECⅡ存活与凋亡有赖于细胞内的氧化还原状态,通过改变细胞内的氧化还原状态可干预氧化应激。硫氧还蛋白系统(thioredoxin system)在生物体内通过抗氧化和氧化还原调节,在基因表达、信号转导、细胞生长、细胞凋亡等方面起重要作用。
作者 蔡成 常立文
出处 《生理科学进展》 CAS CSCD 北大核心 2008年第2期172-174,共3页 Progress in Physiological Sciences
基金 国家自然科学基金资助课题(30672261 30471824)
  • 相关文献

参考文献2

二级参考文献117

  • 1[1]Alpini G,Phillips JO,Vroman B,LaRusso NF.Recent advances in the isolation of liver cells.Hepatology 1994;20:494-514
  • 2[2]Loeffler M,Kroemer G.The mitochondrion in cell death control:certainties and incognita.Exp Cell Res 2000;256:19-26
  • 3[3]Crompton M.Mitochondrial intermembrane iunctional complexes and their role in cell death.J Physiol 2000;529 (Pt 1):11-21
  • 4[4]Chelli B,Falleni A,Salvetti F,Gremigni V,Lucacchini A,Martini C.Peripheral-type benzodiazepine receptor ligands:mitochondrial permeability transition induction in rat cardiac tissue.Biochem Pharmacol 2001;61:695-705
  • 5[5]Zamzami N,Susin SA,Marchetti P,Hirsch T,Gomez-Monterrey I,Castedo M,Kroemer G.Mitochondrial control of nuclear apoptosis.J Exp Med 1996;183:1533-1544
  • 6[6]Ding WX,Shen HM,Ong CN.Critical role of reactive oxygen species and mitochondrial permeability transition in microcystin-induced rapid apoptosis in rat hepatocytes.Hepatology 2000;32:547-555
  • 7[7]Gohil VM,Gvozdenovic-Jeremic J,Schlame M,Greenberg ML.Binding of 10-N-nonyl acridine orange to cardiolipindeficient yeast cells:implications for assay of cardiolipin.Anal Biochem 2005;343:350-352
  • 8[8]Woo SH,Park IC,Park MJ,Lee HC,Lee SJ,Chun YJ,Lee SH,Hong SI,Rhee CH.Arsenic trioxide induces apoptosis through a reactive oxygen species-dependent pathway and loss of mitochondrial membrane potential in HeLa cells.Int J Oncol 2002:21:57-63
  • 9[9]Anuradha CD,Kanno S,Hirano S.Oxidative damage to mitochondria is a preliminary step to caspase-3 activation in fluoride-induced apoptosis in HL-60 cells.Free Radio Biol Med 2001; 31:367-373
  • 10Raijmakers MT,Dechend R,Poston L.Oxidative stress and preeclampsia:rationale for antioxidant clinical trials.Hypertension 2004; 44:374-380.

共引文献60

同被引文献13

  • 1卢红艳,常立文,汪鸿,李文斌,王华.高氧对早产大鼠Ⅱ型肺泡上皮细胞转分化的影响[J].细胞与分子免疫学杂志,2006,22(6):706-709. 被引量:8
  • 2卢红艳,常立文,汪鸿,李文斌,王华.高浓度氧对早产鼠Ⅱ型肺泡上皮细胞增殖和细胞周期的影响[J].中国小儿急救医学,2007,14(1):32-34. 被引量:1
  • 3常立文.新生儿支气管肺发育不良诊治进展[J].临床儿科杂志,2007,25(3):161-165. 被引量:46
  • 4Kinsella JP, Greenough A,Abman SH. Bronchopulmonary dysplasia [ J ]. Lancet,2006,367 (9520) : 1421 - 1431.
  • 5Fernandez - Vizarra E, Tiranti V, Zeviani M. Assembly of the oxidative phosphorylation system in humans:What we have learned by studying its defects [ J ]. Biochim Biophys Acta,2009,1793 ( 1 ) :200 - 211.
  • 6Park JS, Li YF, Bai Y. Yeast NDI1 improves oxidative phosphorylation capacity and increases protection against oxidative stress and cell death in cells carrying a Leber's hereditary optic neuropathy mutation[ J]. Biochim Biophys Acta,2007,1772 (5) :533 - 542.
  • 7Walters DM, Cho HY, Kleeberger SR. Oxidative stress and antioxidants in the pathogenesis of pulmonary fibrosis:A potential role for Nrf2 [ J ]. A ntioxid Redox Signal, 2008,10 ( 2 ) : 321 - 332.
  • 8Roper JM, Mazzatti D J, Watkins RH ,et al. In vivo exposure to hyperoxia induces DNA damage in a population of alveolar type Ⅱ epithelial ceils [ J ]. Am J Physiol Lung Cell Mol Physiol, 2004,286 ( 5 ) : 1045 - 1054.
  • 9Brzezinski P, Reimann J, Adelroth P. Molecular architecture of the proton diode of cytochrome c oxidase [ J ]. Biochem Soc Trans, 2008,36 (6) :1169 - 1174.
  • 10Callejon R,de Rojas M,Ariza C, et al. Cytochrome oxidase subunit 1 and mitochondrial 16S rDNA sequences of Trichuris skrjabini (Tricocephalida:Trichuridae) [J]. Parasitol Res,2009,104(3) :715 -716.

引证文献1

二级引证文献1

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