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细胞抗砷性与多药耐药的关系 被引量:3

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出处 《农垦医学》 2008年第3期232-234,共3页 Journal of Nongken Medicine
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参考文献12

  • 1慕晓玲,姜玉峰,李思源,裴学莲,杨磊.骨髓间充质干细胞诱导抗砷细胞[J].中国公共卫生,2005,21(11):1339-1340. 被引量:3
  • 2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
  • 3Elaine M, Anass Haimeur, et al. Arsenic transport by the human multidrug resistance protein 1(MRP1/ABCC1) evidence that a triglutathione conjugate is required. J. Biol. Chem, 2004,279 ( 31 ) : 32700 - 32708
  • 4Liu J, Liu Y, Powell D A, et al. Muhidrug- resistance mdr1a/1b double knockout mice are more sensitive than wild type mice to acute arsenic toxicity, with higher arsenic accumulation in tissues. Toxieology, 2002, 170 (1 -2):55-62
  • 5Chikara Kojima, Wei Qu, et al. Chronic exposure, to methylated arsenicals stimulates arsenic exretion pathways and induces arsenic tolerance in rat liver cells. Jor Sci,2006,90(1) :70 - 81
  • 6Jie Liu, Chengxiu Li, Wei Qu, et al. Nitric oxide prodrugs and metallochemotherapeutics:JS-K and CB - 3 - 100 enhance arsenic and cisplatin cylolethality by increasing cellular accumulation. Molecular Cancer Therapeutics, 2004,3 (6) : 709 - 713
  • 7Olivier Sordet, ZhiYong Liao, Hong Liu, et al. Topoisomerase I-DNA Complexes Contribute to arsenic trioxide-induced apoptosis. The Journal of Biological Chemsity, 2004,279(32) : 33968 - 33975
  • 8Wei Qu, Carl D. Bortner, et ah Acquisition of apototic resistance in arsenic - induced malignant transformation role of the JNK signal transduction pathway. Carcinogenesis, 2002,23(1):151 - 159
  • 9Pi J, He Y, Bortner C, et al. Low lever long-term inorganic arsenite exposure causes generalized resistance to apotosis in cultured human keratinocytes: potential role in skin co - carcinogenesis. Int J Cancer, 2005, 116(1):20-26
  • 10Townsend D M,Tew K D.The role of glutathione- S-transferase in anticancer drug resistance. Oncogene, 2003,22: 7369 - 7375

二级参考文献13

  • 1Rosen BP, Bhattacharjee H, ShiW. Mecnanisms of metal regulation of an anion-translocating ATPase [ J ]. Journal of Bioenergetics and Biomembranes, 1995, 27(1) :85 - 91.
  • 2Aposhian HV. Enzymatic methylation of arsenic species and other new approaches to arsenic toxicity [ J ]. Annu Rev Pharmacol Toxicol,1997, 397:419.
  • 3Liu J, Chen H, Miller DS, et al. Overexpression of glutathione S-transferase and multidrug resistance transport proteins is associated with acquired to inorganic arsenic [ J ]. Mol Pharmacol, 2001, 60: 302 -309.
  • 4Bramblia EM, Achanzar WE, et al. Chronic Aresenic-exposed human prostate epithelial cells exhibit stable arsenic tolerance: mechanistic implications of altered cellular glutathione and glutathione S-transferase[J]. Toxicol Appl Pharmacol, 2002, 183:99 - 107.
  • 5Bernathy CO, Liu Y, Longfellow D. et al. Arsenic: health effects,mechanisms of actions, and research issues [J]. Environ Health Perspect, 1997, 107 : 593-597.
  • 6Teruaki S, Chikara K, Masayuki O, et al. Cellular glutathione prevents cytolethaity of monomethylarsonic acid [J]. Toxicol Pharmacol, 2004,195:129-141.
  • 7Nociari 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.
  • 8Rosen BP. Families of arsenic transporters[J]. Trends Microbiol, 1999,7: 207-212.
  • 9Aposhian HV. Enzymatic methylation of arsenic species and other new approaches to arsenic toxicity[J]. Annu Rev Pharmacol Toxicol, 1997,37: 397-419.
  • 10Maiti 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.

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