期刊文献+

细胞内谷胱甘肽对砷细胞毒性的保护作用 被引量:8

Effect of Intracellular Glutathione in Relieving the Cytotoxicity Induced by Arsenic
暂未订购
导出
摘要 目的研究细胞内谷胱甘肽(GSH)对砷致人永生化角质形成细胞系(HaCaT)毒性的保护作用。方法HaCaT细胞用N-乙酰半胱氨酸(N-acetylcysteine,NAC)和丁硫氨酸亚矾胺(L-buthionine-眼S’R演-sulfoximine,BSO)预处理后,加入亚砷酸钠(sodiumarsenite,NaAsO2)继续作用,用Alamarblue摄入法检测细胞活力,每组4个复孔。结果单独用NaAsO2作用细胞24h后,0.001~10.000μmol/L组Alamarblue还原率增高(P<0.05),大于10.000μmol/L时Alamarblue还原率下降(P<0.01);用NAC预处理24h后再加入NaAsO2,15μmol/L组Alamarblue还原率比NaAsO2单独作用增加(P<0.05);用BSO预处理24h后再加入NaAsO2,15μmol/L组的Alamarblue还原率均下降(P<0.05)。结论低浓度NaAsO2刺激细胞增殖,高浓度具有细胞毒性;NAC可减轻砷的细胞毒性,而BSO则加重其细胞毒性。 Objective To study the effect of cellular glutathione (GSH) in relieving the cytotoxicity induced by arsenic on HaCaT. Methods The HaCaT ceils were pre-treated with N-acetylcysteine (NAC) and L-buthionine-[S' R]-sulfoximine (BSO) for 24 h, then treated with sodium arsenite (NaAsO2) by adding it into the medium for 24 h. Alarmarblue assay was used to detect the proliferation of the cells. Results The reduction rate of Alarmarblue increased when the HaCaT cells were treated with 0.001-10.000 μmol/L of NaAsO2 alone (P〈0.05), when pre-treated with NAC for 24 hours, the reduction rate in the 15 ixmoVL group increased (P〈0.05), while pre-treated with BSO for 24 hours, the reduction rate decreased markedly (P〈0.05). Conclusion Low level NaAsO2 stimulates the proliferation of HaCaT cells, but at high levels it shows an inhibitive effect. NAC can relieve the cytotoxicity of arsenic while BSO may aggravate it. The results of the present paper indicate that the intracellular GSH may play an important role in relief of the cytotoxicity induced by arsenic.
出处 《环境与健康杂志》 CAS CSCD 北大核心 2006年第1期28-30,共3页 Journal of Environment and Health
关键词 亚砷酸钠 角质形成细胞 谷胱甘肽 Sodium arsenite HaCaT Glutathione
  • 相关文献

参考文献8

  • 1Bernathy CO, Liu Y, Longfellow D. et al. Arsenic: health effects,mechanisms of actions, and research issues [J]. Environ Health Perspect, 1997, 107 : 593-597.
  • 2Teruaki S, Chikara K, Masayuki O, et al. Cellular glutathione prevents cytolethaity of monomethylarsonic acid [J]. Toxicol Pharmacol, 2004,195:129-141.
  • 3Nociari MM, Shalev A, Venias P, et al. A novel one-step highly sensitive fluorometric assay to evaluate cell-mediated cytotoxicity[J]. J Immunol Meth, 1998, 213:157-167.
  • 4Rosen BP. Families of arsenic transporters[J]. Trends Microbiol, 1999,7: 207-212.
  • 5Aposhian HV. Enzymatic methylation of arsenic species and other new approaches to arsenic toxicity[J]. Annu Rev Pharmacol Toxicol, 1997,37: 397-419.
  • 6Maiti S, Chanerjee AK. Effects on levels of glutathione and some related enzymes in tissues after an acute arsenic exposure in rats and their relationship to dietary protein deficiency [J]. Arch Toxicol, 2001,75:531-537.
  • 7Keays R, Harrison PM, Wendon JA, et al. Intravenous acetyleysteine in paracetamol induced fulminant hepatic failure: a prospective controlled trial[J]. BMJ, 1991, 303: 1026-1029.
  • 8程时,丁海勤.谷胱甘肽及其抗氧化作用今日谈[J].生理科学进展,2002,33(1):85-90. 被引量:82

二级参考文献1

  • 1程时.生物膜与疾病[M].北京:北京医科大学出版社,2000.44-79.

共引文献81

同被引文献59

引证文献8

二级引证文献29

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