FAT对K562/A02细胞内GSH含量的影响  

Effect of FAT on K562/A02 intracellular GSH concentration

作　　者：张玉霞[1] 雍国新[1] 梁琼[2] 

机构地区：[1]海南工商职业学院应用技术系,海南海口570203 [2]海口经济学院工程技术学院,海南海口570203

出　　处：《中国当代医药》2012年第2期5-6,共2页China Modern Medicine

摘　　要：目的:探讨FAT对K562/A02细胞内谷胱甘肽(GSH)含量的影响,及其对白血病细胞代谢解毒系统介导的多药耐药(MDR)的逆转效果。方法:采用生化DTNB法测定细胞内谷胱甘肽水平。结果:K562/A02细胞内GSH含量(231.54μmol/106细胞)高于K562细胞内GSH含量(58.03μmol/106细胞),为K562细胞的3.99倍;VRP(10μmol/L)、FAT(0.01、0.02、0.04、0.08mg/ml)作用48h后,K562/A02细胞内GSH含量从231.54μmol/106细胞分别减少到96.95μmol/106细胞、212.89μmol/106细胞、161.00μmol/106细胞、122.35μmol/106细胞。结论:细胞内GSH含量增加是K562/A02细胞产生MDR的机制之一;FAT降低K562/A02细胞内GSH的含量是FAT逆转MDR的机制之一。Objective： To investigate the impact of FAT on K562/A02 intracellular glutathione （GSH） concentration, and leukemia cell metabolism system of detoxification mediated drug-resistant （MDR） reversal effect. Methods： Intracellular GSH concentration was examined by biochemical DTNB method. Results： Intracellular GSH concentration in K562/A02 cell line （231.54 μmol/106 cells） was higher than that in K562 cell line （58.03 μmol/106 cells）, and 3.99-fold greater in K562/A02 cell line compared with in K562 cell line. Intracellular GSH levels in K562/A02 cell line treated with VRP （10 μmol/L）, FAT （0.02, 0.04, 0.08 mg/ml） for 48 hours （96.95 μmol/106 cells, 212.89 μmol/106 cells, 161.00 μmol/106 cells,122.35 μmol/106 cells respectively） was decreased than that in K562/A02 cell line without FAT （231.54 μmol/106 cells）. The intracellular GSH concentration in K562/A02 cell line was higher than that in K562 cell line. Conclusion： The intracellular GSH content increase in K562/A02 cells to produce MDR mechanism of K562/A02. One of the mechanisms of MDR reversal by FAT is decrease of intracellular GSH levels on K562/A02.

关 键 词：白血病 多药耐药 FAT 谷胱甘肽 

分 类 号：R-33[医药卫生]