期刊文献+

谷胱甘肽耗竭与微囊藻毒素-LR细胞毒性的关系初探 被引量:2

Relationship between glutathione depletion and cytotoxicity of microcystin-LR
下载PDF
导出
摘要 目的探讨谷胱甘肽耗竭与微囊藻毒素-LR(MCLR)细胞毒性的关系。方法不同剂量的MCLR作用人肝癌细胞HepG2后,采用四甲基偶氮噻唑蓝法检测细胞毒性,并用二硫硝基苯甲酸法测定细胞内还原型谷胱甘肽(GSH)的含量。结果细胞存活率随处理剂量的增加而降低,抗氧化剂N-乙酰半胱氨酸明显减轻MCLR诱导的细胞毒性。细胞内GSH含量显著降低,处理剂量与GSH水平之间呈现剂量-反应和时间-反应关系。结论谷胱甘肽耗竭可能是微囊藻毒素-LR引起细胞毒性的原因之一。 Objective To study the relationship between glutathione depletion and the cytotoxicity of microcystin- LR(MCLR). Methods Human hepatoma cell lines HepG2 were treated with MCLR, then the cytotoxicity was measured by the MTT assay and the level of intracellular glutathione (GSH) was measured by the colofimetfic 5,5' - dithio - bis (2- nitrobenzoic acid) (DTNB) assay. Results MCLR dose - dependently decreased the cell viability, which were inhibited by N - acetyl - cysteine. In MCLR - treated HepG2 cells, GSH levels decreased in a dose - and time - dependent manner. Conclusion Glutathione depletion is playing important roles in MCLR- induced cytotoxicity.
出处 《应用预防医学》 2008年第3期129-131,共3页 Applied Preventive Medicine
基金 国家留学基金委资助项目(No.20845014)
关键词 微囊藻毒素-LR 谷胱甘肽耗竭 细胞毒性 Microcystin - LR Glutathione depletion Cytotoxicity
  • 相关文献

参考文献5

  • 1[1]Gehringer MM.Microcystin-LR and okadaic acid-induced cellular effects:a dualistic response[J].FEBS Lett,2004,557(3):1-8.
  • 2[2]Nong QQ,Komatsu M,Izumo K,et al.Involvement of reactive oxygen species in Microcystin-LR-induced cytogenotoxicity.Free Radical Research,2007,41(12):1326-1337.
  • 3孙鲜策,刘珊,孙贵范,高颖.细胞内谷胱甘肽对砷细胞毒性的保护作用[J].环境与健康杂志,2006,23(1):28-30. 被引量:8
  • 4李悦,郑云亭.N-乙酰半胱氨酸对镉致人胚肾细胞凋亡拮抗作用[J].中国公共卫生,2007,23(5):543-544. 被引量:8
  • 5[5]Pflugmacher S,Wiegand C,Oberemm A,et al.Identification of an enzymatically formed glutathione conjugate of the cyanobacterial hepatotoxin microcystin-LR:the first step of detoxication[J].Biochim Biophys Acta,1998,1425(3):527-533.

二级参考文献16

  • 1任香梅,蔡云清,吴小丽.镉诱导LLC-PK_1细胞凋亡对基因表达的影响[J].中国公共卫生,2006,22(6):682-683. 被引量:5
  • 2Bernathy CO, Liu Y, Longfellow D. et al. Arsenic: health effects,mechanisms of actions, and research issues [J]. Environ Health Perspect, 1997, 107 : 593-597.
  • 3Teruaki S, Chikara K, Masayuki O, et al. Cellular glutathione prevents cytolethaity of monomethylarsonic acid [J]. Toxicol Pharmacol, 2004,195:129-141.
  • 4Nociari 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.
  • 5Rosen BP. Families of arsenic transporters[J]. Trends Microbiol, 1999,7: 207-212.
  • 6Aposhian HV. Enzymatic methylation of arsenic species and other new approaches to arsenic toxicity[J]. Annu Rev Pharmacol Toxicol, 1997,37: 397-419.
  • 7Maiti 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.
  • 8Keays 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.
  • 9Konstantinos N T,Gerorgios I P,Maria D,et al.The hepatoprotective effect of putrescine against cadmium-induced acute liver injury[J].Archives of Toxicology,2004,6(78):321-329.
  • 10Vestergeard P,Shaikh ZA.The nephrotoxicity of intravenously administration and preexisting renal cadmium burden[J].Toxical Apl Pharmacol,2003,126:240-247.

共引文献14

同被引文献37

引证文献2

二级引证文献2

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