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低剂量长期砷暴露对HaCat细胞增殖及凋亡水平的影响 被引量:2

Influence of low level and long-term arsenite exposure to cell proliferation and apoptosis of HaCat cells
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摘要 目的探讨低剂量长期砷暴露对HaCat细胞增殖及凋亡水平的影响。方法 HaCat细胞暴露于浓度为0、0.05、0.10μmol/L的NaAsO215周后,用直接细胞计数法计数对照组及染砷组细胞数,检测细胞增殖水平;用流式细胞仪测定10 000个细胞的细胞凋亡发生水平。结果各染砷组细胞增殖速率与对照组相比均显著增高(P<0.05),且0.10μmol/L组细胞增殖率(245.00±8.66)%显著高于0.05μmol/L组(165.00±15.00)%(P<0.05),细胞增殖水平与染砷剂量间呈显著剂量-效应关系;0.05μmol/L组(0.28±0.08)%及0.10μmol/L组(0.34±0.09)%细胞凋亡率均明显低于对照组(0.74±0.18)%(P<0.05)。结论长期低剂量砷暴露可使HaCat细胞的增殖能力明显增强,并诱导细胞凋亡率显著降低。 Objective To discuss the influence of low level and long - term arsenite exposure to cell proliferation and apoptosis of HaCat cells. Methods HaCat cells were exposed to arsenic (0,0.05,0. 10μmol/L) for 15 weeks, then cell numbers of each group were counted by direct cell count assay to detect the cell proliferation level. Ten thousand ceils were measured to detect the cell apoptosis level. Results The cell proliferation rate of arsenic exposed groups was significantly higher than that of control group ( P 〈 0.05 ) ; Cell proliferation rate of 0.1μmol/L group ( 245.00 ± 8.66 ) % was significantly higher than that of 0.05 μmol/L group ( 165.00 ± 15.00) % [ P 〈 0.05 ) ; Cell proliferation level increased significantly with a dose - effect relation; apoptosis rate of 0.05 μmol/L group ( 0.28 ± 0.08 ) % and 0.1 μmol/L group ( 0.34 ± 0.09 ) % were significantly lower than that of control group ( 0.74 ± 0.18 ) % ( P 〈 0.05 ). Conclusion Low level and long term arsenite exposure induce increased cell proliferation and decreased apoptosis level in HaCat cells.
作者 刘世宜 李昕
出处 《中国地方病防治》 2013年第1期1-3,共3页 Chinese Journal of Control of Endemic Diseases
基金 辽宁省教育厅课题(L2010705)
关键词 亚砷酸钠(NaAsO2) HaCat细胞株 细胞增殖 细胞凋亡 Sodium arsenite (NaAsO2) HaCat cell Cell proliferation Apoptosis
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  • 1Valenzuela OL,Borja-Aburto VH,Garcia-Vargas GG,et al.Uri-nary trivalent methylated arsenic species in apopulation chronically ex-posed to inorganic arsenic[J].Environ Health Perspect,2005,113(3):250-254.
  • 2International Agency for Research on Cancer.(2004).IARC mono-graphs on the evaluation of carcinogenic risks to humans[J].Vol.84.Some drinking-water disinfectants and contaminants,including arse-nic.WHO,World Health Organization,Geneva.
  • 3Schuhmacher-Wolz U,Dieter HH,Klein D,et al.Oral exposure toinorganic arsenic:evaluation of its carcinogenic and non-carcinogen-ic effects[J].Crit Rev Toxicol,2009,39(4):271-298.
  • 4Druwe IL,Vaillancourt RR.Influence of arsenate and arsenite on sig-nal transduction pathways:an update[J].Arch Toxicol,2010,84(8):585-596.
  • 5Wen G,Hong M,Calaf GM,et al.Phosphoproteomic profiling of ar-senite-treated human small airway epithelial cells[J].Oncol Rep,2010,23(2):405-412.
  • 6Zhang Y,Wang Q,Guo X,et al.Activation and up-regulation oftranslation initiation factor 4B contribute to arsenic-induced transfor-mation[J].Mol Carcinog,2011,50(7):528-538.
  • 7Liu Y,Hock JM,Sullivan C,et al.Activation of the p38 MAPK/Akt/ERK1/2 signal pathways is required for the protein stabilizationof CDC6 and cyclin D1 in low-dose arsenite-induced cell prolifera-tion[J].J Cell Biochem,2010,111(6):1546-1555.
  • 8Tokar EJ,Benbrahim-Tallaa L,Ward JM,et al.Cancer in experi-mental animals exposed to arsenic and arsenic compounds[J].CritRev Toxicol,2010,40(10):912-927.

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