目的：了解多药耐药基因（ｍｄｒ１）机制以外导致人白血病细胞耐药的因素。方法：采用生化方法，对Ｋ５６２和ＨＬ６０敏感和耐药细胞株谷胱甘肽（ＧＳＨ）含量、谷胱甘肽Ｓ转移酶（ＧＳＴ）活力进行测定；用Ｎｏｒｔｈｅｒｎ杂交对ＧＳＴα、π、μ和多药耐药相关蛋白（ＭＲＰ）ｍＲＮＡ表达进行检测；用Ｗｅｓｔｅｒｎ杂交对ＧＳＴα、π、μ蛋白表达进行检测。结果：与敏感株相比，Ｋ５６２／Ｈ２０和Ｋ５６２／ＶＣＲ的ＧＳＨ含量、ＧＳＴ活力明显增高，ＨＬ６０／Ａｄｒ的ＧＳＨ含量和ＧＳＴ活力无明显增高，Ｎｏｒｔｈｅｒｎ和Ｗｅｓｔｅｒｎ杂交可见ＧＳＴα、π和ＧＳＴπ、μ在Ｋ５６２／Ｈ２０和Ｋ５６２／ＶＣＲ过度表达，ＨＬ６０／Ａｄｒ无ＧＳＴ同工酶过度表达，ＭＲＰ在三种耐药株均有过度表达。结论：ＧＳＨ、ＧＳＴ和ＭＲＰ参与了Ｋ５６２／Ｈ２０和Ｋ５６２／ＶＣＲ耐药，ＨＬ６０／Ａｄｒ耐药与ＧＳＨ、ＧＳＴ无关，与ＭＲＰ有关。在实际应用中，应对多种耐药指标同时进行检测 OBJECTIVE: To understand the factors that lead to the resistance of human leukemia cells beyond the mechanism of multidrug resistance gene (mdr1). METHODS: Biochemical methods were used to determine the levels of glutathione (GSH) and glutathione S transferase (GST) in K562 and HL60 sensitive and resistant cell lines; GSTα, π, and μ were used in Northern hybridization. The expression of MRP mRNA was detected. Western blot was used to detect the expression of GSTα, π, and μ proteins. Results: The GSH content and GST activity of K562/H20 and K562/VCR were significantly higher than those of sensitive strains. GSH content and GST activity of HL60/Adr were not significantly increased. GSTα, π, and GSTπ were observed in Northern and Western hybridizations. μ was over-expressed in K562/H20 and K562/VCR. There was no GST isoenzyme overexpression in HL60/Adr, and MRP was over-expressed in the three drug-resistant strains. CONCLUSION: GSH, GST and MRP are involved in K562/H20 and K562/VCR resistance. HL-60/Adr resistance is not related to GSH and GST, but also to MRP. In practical applications, simultaneous detection of multiple resistance indicators