期刊文献+

不同低氧暴露对人红细胞硫氧还蛋白过氧化物酶PeroxiredoxinⅡ的影响 被引量:1

Effect of Different Hypoxic Environment Exposure on PeroxiredoxinⅡ
下载PDF
导出
摘要 目的:观察模拟高住组和间歇性低氧组经过四周低氧暴露后,人红细胞硫氧还蛋白过氧化物酶Peroxiredoxin2的变化。方法:男性大学生20名随机分成对照组、模拟高住组和间歇性低氧组,三组从事相同的身体活动、学习和生活作息,模拟高住组每天8hr低氧环境睡眠,间歇性低氧组每天安静状态吸低氧(浓度14%-10%)50-60min,连续4周。三组均在实验开始前、结束后按Bruce方案进行力竭运动,并在安静和运动后取血测试Prx2、MDA。在低氧训练实验开始前一天、实验的最后一天取血测定红细胞数目、血红蛋白及红细胞压积。结果:(1)一次性力竭运动后,Prx2的变化不大,而经过四周低氧暴露后,在完成力竭运动前,模拟高住组Prx2有升高趋势,在间歇性低氧组则达到显著性;力竭运动后,Prx2的升高在低氧组都达到了显著性;(2)力竭运动后,三组MDA明显增多,低氧暴露前后低氧组无明显变化;(3)低氧组都未观察到红细胞计数和压积、血红蛋白浓度的明显变化。结论:长时间低氧暴露可诱导Prx2的生成增多。 Objective The paper investigated the effects of different hypoxia exposure on Peroxiredoxin Ⅱ. Methods Twenty healthy male students were randomly assigned to three group with following protocols: control group( C), intermittent hypoxia exposure(IH) and mimic lived high and trained low group (MH). The IH group intermittently inhaled different hypoxic gas mixtures (02 were 14 %, 12%, 10%, respectively), 50 -60 rain daily for 4 weeks. M H group was exposed to hypoxic environment for 8 hours each night. Three groups completed Bruce protocol exercise on the treadmill before and after hypoxic exposure. Results 1 ) Before hypoxic exposure, there were no significantly changes of Prx2 after exhaustive exercise. After 4 weeks of hypoxic exposure, Prx2 in MH and IH group were significantly increased. 2) MDA in three groups were significantly change after exhaustive exercise. There were no change between before and after hypoxic exposure. 3 )Changes of RBC ,HCT and Hb were not investigated between three groups after hypoxic exposure. Conclusion 4 weeks hypoxic exposure is effective on impro- ving Prx2.
作者 胡永欣
出处 《广州体育学院学报》 CSSCI 北大核心 2012年第3期84-87,共4页 Journal of Guangzhou Sport University
关键词 Prx2 RBC MDA 间歇性低氧 高住低练 Prx2 RBC MDA intermittent hypoxia exposure lived high and trained low
  • 相关文献

参考文献7

二级参考文献88

  • 1Bae YA, Cai GB, Kim SH, et al. Modular evolution of glutathione peroxidase genes in association with different biochemical properties of their encoded proteins in invertebrate animals. BMC Evol Biol, 2009, 9(4) :72-84.
  • 2Park SG, Cha MK, Jeong W, et al. Distinct physiological functions of thiol peroxidase isoenzymes in Saccharomyces cerevisiae. J Biol Chem, 2000, 275(8):5723-5732.
  • 3Rhee SG, Chae I-IZ, Kim K. Peroxiredoxins: A historical overview and speculative preview of novel mechanisms and emerging concepts in cell signaling. Free Radic Biol Med, 2005, 38 (12) : 1543-1552.
  • 4Johnson RM, Goyette G J, Ravindranath Y, et al. Hemoglobin autoxidation and regulation of endogenous H2 02 levels in erythrocytes. Free Radic Biol Med, 2005, 39(11):1407-1417.
  • 5Chae HZ, Chung SJ, Rhee SG. Thioredoxin-dependent peroxide reductase from yeast. J Biol Chem, 1994, 269 ( 44 ) : 27670- 27678.
  • 6Stuhlmeier KM, Kao J J, Wallbrandt P, et al. Antioxidant protein 2 prevents methemoglobin formation in erythrocyte hemolysates. Eur J Biochem, 2003, 270(2):334-341.
  • 7Low FM, Hampton MB, Peskin AV, et al. Peroxiredoxin 2 functions as a noncatalytic scavenger of low-level hydrogen peroxide in the erythrocyte. Blood, 2007, 109(6) :2611-2617.
  • 8Manta B, Hugo M, Ortiz C, et al. The peroxidaae and peroxynitrite reductase activity of human erythrocyte peroxiredoxin 2.Arch Bioehem Biophys, 2009, 484(2) :146-154.
  • 9Schroder E, Ponting CP. Evidence that peroxiredoxins are novel members of the thioredoxin fold superfamily. Protein Sci, 1998,7 ( 11 ) :2465-2468.
  • 10Schroder E, Littlechild JA, Lebedev AA, et al. Crystal structure of decameric 2-Cys peroxiredoxin from human erythrocytes at 1.7 A resolution. Structure, 2000, 8(6) :605-615.

共引文献58

同被引文献11

  • 1谢美容,王章进,林翠英,史河秀,吕俊杰,张卫玉,王世鄂.硫氧还蛋白过氧化物酶Ⅵ在小鼠卵巢、输卵管和子宫中的分布[J].解剖学研究,2008,30(6):405-408. 被引量:2
  • 2杨柳,米粲,霍艳英.Peroxiredoxin在H_2O_2介导的信号通路中的作用[J].国际病理科学与临床杂志,2006,26(5):417-419. 被引量:7
  • 3傅春玲,霍艳英,胡迎春,李刚,米粲,吴德昌.Pten基因敲除对过氧化物酶家族表达和活性氧水平的影响[J].军事医学科学院院刊,2007,31(3):201-203. 被引量:3
  • 4Zeidler P, Hubbs A, Battelli L, et al. Role of inducible nitric oxidesynthase-derived nitric oxide in silica-induced pulmonary inflammationand fibrosis [J]. S Toxicol Environ Health A, 2004, 67 ( 13 ):1001-1026.
  • 5Kim S U, Hwang C N, Sun H N, et al. Peroxiredoxin I is an indi-cator of microglia activation and protects against hydrogen peroxide me-diated micro glial death [ J ] . Biol Pharm Bull,2008, 31 ( 5 );820-825.
  • 6Lee Y M, Park S H, Shin D I, et al. Oxidative modification of per-oxiredoxin is associated with drug-induced apoptotic signaling in experi-mental models of Parkinson disease [ J ]. Biol Chem,2008,283(15); 9986-9998.
  • 7Wang X,Phelan S A, Forsman-Semb K. Mice with targeted mutationof peroxiredoxin 6 develop normally but are susceptible to oxidativestress [J]. J Biol Chem, 2003, 278 (27) : 25179-25190.
  • 8Park K J, Kim Y J, Kim J, et al. Protective effects of peroxiredoxinon hydrogen peroxide induced oxidative stress and apoptosis in cardi-onyocytes [J]. Korean Circ J, 2012, 42 (1〉: 23-32.
  • 9Srinivasa K, Kim N R, Kim J, et al. Characterization of a putativethioredoxin peroxidase Prx I of Candida albicans [ J ]. Mol Cells,2012,33 (3): 301-307.
  • 10Lee D H, Lim B S, Lee Y K, et al. Effects of hydrogen peroxide(H202 ) on alkaline phosphatase activitity and matrix mineralizationof odontoblat and osteoblast cell lines [J]. Cell Biol Toxicol,2006,22 (1): 3946.

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