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重铬酸钾处理人胚肺细胞A549的Hormesis效应及对某些修复基因表达的影响 被引量:2

Hormesis of potassium dichromate exposure on A549 cells and its effect on expression of some repair genes
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摘要 目的研究重铬酸钾(K2Cr2O7)对A549细胞的低剂量兴奋效应和修复基因的表达变化。方法 K2Cr2O7作用浓度为0.156、0.312、0.625、1.250、2.500和5.000μmol/L;对照纽K2Cr2O7浓度为0μmol/L;作用时间均为24 h。K2Cr2O7作用浓度为0.312μmol/L时,作用时间分别为12、24、36和48 h;对照组K2Cr2O7作用浓度为0μmol/L,作用时间为0 h。MTT法测人胚肺A549细胞的增殖活性,半定量RT-PCR检测修复基因转录水平。结果 K2Cr2O7浓度在0-0.312μmol/L之间可促进细胞增殖,K2Cr2O7浓度在0.625~5.000μmol/L之间对细胞的增殖抑制率有增大的趋势,各组与对照组和0.312μmol/L组比较,差异均有统计学意义(P〈0.05)。K2Cr2O7浓度在0-0.312μmol/L之间可促进修复基因hOGG1与hMTH1 mRNA的表达,Cr(Ⅵ)浓度在0.625-5.000μmol/L之间可抑制hOGGl及hMTHlmRNA的表达。K2Cr2O7作用浓度为0.312μmol/L时,随着时间的延长,最终将抑制细胞的增殖和修复基因的转录。结论低剂量K2Cr2O7作用于A549细胞可引起低剂量兴奋作用(Hormesis)效应,并导致hOGGl及hMTHl基因的表达变化。 Objective To study low-dose potassium dichromate on A549 cells and changes on the expression of repair genes hMTH1 and hOGG1 involved.Methods A549 cells were treated with potassium dichromate of 0.156,0.312,0.625,1.250,2.500 and 5.000 μmol/L for 24 h;the concentration of the control group was 0.000 μmol/L and 24 h.When the cells were exposed to 0.312 μmol/L,and the reaction times were 12,24,36 and 48 h,the control group was 0.000 μmol/L and 0 h.The proliferation viability was measured by the MTT assay.The expressions of repair genes hMTH1 and hOGG1 on hormesis were evaluated by examining the level of mRNA of hMTH1 and hOGG1 using semi-quantitative RT-PCR.Results Potassium dichromate could accelerate the proliferation viability of A549 cell when its concentrations was 0~0.312 μmol/L.When the potassium dichromate concentration was 0.625~5 μmol/L,the suppression rate of proliferation tends to enlarge.Compared with the control group and 0.312 μmol/L,the difference of all groups was statistically significant(P〈0.05).Potassium dichromate could promote the expressions of hOGG1 and hMTH1 when its concentrations were 0~0.312 μmol/L.When the Cr +6 concentration was 0.625~5 μmol/L,the expressions of hOGG1 and hMTH1 were suppressed.When the reaction concentration was 0.312 μmol/L,as the time prolonged the proliferation viability and genes repairmen would finally be inhibited.Conclusions The A549 cell might show obvious Hormesis effect after treated with low dosages of 0.156 and 0.312 μmol/L of potassium dichromate for 24 h and induce expression changes of hOGG1 and hMTH1 genes.
出处 《工业卫生与职业病》 CAS CSCD 北大核心 2010年第5期261-264,共4页 Industrial Health and Occupational Diseases
关键词 重铬酸钾 A549人胚肺细胞:Hormesis hOGGl hMTH1 Potassium dichromate Human lung cell A549 Hormesis hOGG1 hMTH1
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参考文献8

  • 1Calabrese EJ. Hormesis.. changing view of the doseresponse, a personal account of the history and current status [J].Mutat Res, 2002, 511(3): 181-189.
  • 2顾祖维.小资料[J].环境与职业医学,2004,21(6):498-498. 被引量:2
  • 3刘树铮.低剂量辐射兴奋效应发生机理若干问题的探讨[J].中华放射医学与防护杂志,2003,23(6):393-398. 被引量:31
  • 4Wenhua L, Ruming Z, Zhixiong X, etal. Effects of La^3+ on growth transformation and gene expression of Ecoli [J]. Biol Trace Elem Res, 2003, 94(2): 167- 177.
  • 5杨萍,刘起展,李爱萍,李婷,洪霞,周建伟.亚砷酸钠所致人胚肺成纤维细胞增殖兴奋效应与氧化应激的关系[J].中华劳动卫生职业病杂志,2006,24(2):103-105. 被引量:18
  • 6Bamham KJ, Masters CL, Bush AI. Neurodegenerative diseases and oxidative stress [J]. Nat Rev Drug Discov, 2004, 3(3): 205-214.
  • 7Miyake H, Hara I, Kamidono S, et al. Oxidative DNA damage inpatients with prostate cancer and its response to treatment [J]. J Urol, 2004, 171 (4):1533-1536.
  • 8Ichiba M, Maeta Y, Mukoyama T, etal. Expression of 8- hydroxy-2'-deoxyguanosinein chronic liver disease and hepatocellular carcinoma [J]. Liver Int, 2003, 23 (5) : 338-345.

二级参考文献17

  • 1刘树铮,苏旭,张迎春.小剂量X射线全身照射后淋巴细胞TCR/CD3表达和[Ca^(2+)]_i的变化[J].辐射研究与辐射工艺学报,1994,12(1):61-63. 被引量:11
  • 2赵勇,龚守良,刘树铮.乙酰胆碱对小剂量辐射小鼠脾细胞增殖反应的影响[J].辐射研究与辐射工艺学报,1996,14(4):231-238. 被引量:2
  • 3Calabrese EJ,Baldwin LA.Toxicology rethinks its central belief:Hormesis demands a reappraisal of the way risks are assessed.Nature,2003,421:691-692.
  • 4Calabrese E J,Baldwin LA.Hormesis:The hormetic dose response model is more common than threshold model in toxicology.Toxicol Sci,2003,71:246-250.
  • 5Calabrese EJ,Baldwin LA.Inorganics and hormesis.Crit Rev Toxicol,2003,33:215-304.
  • 6Delia D,Aiello A,Meroni L,et al.A Role of antioxidants and intracellular free radicals in retinamide induced cell death.Carcinogenesis,1997,18:943-948.
  • 7Lee TC,Oshimura M,Barrett JC,et al.Comparison of arsenic-induced cell transformation,cytotoxicty,mutation and cytogenetic effects in Syrian hamster embryo cells in culture.Carcinogenesis,1985,6:1421-1426.
  • 8Brown JL,Kitchin KT.Arsenite,but not cadmium,induces ornithine decarboxylade and heme oxygenase activity in rat liver:relevance to arsenic carcinogenesis.Cancer Lett,1996,98:227-231.
  • 9Allen RG,Tresini M.Oxidative stress and gene regulation.Free Radic Biol Med,2000,28:463-499.
  • 10Sauer H,Wartenberg M,Hescheler J.Reactive oxygen species as intercellular messengers during cell growth and differentiation.Cell Physiol Biochem,2001,11:173-186.

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