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- W2092199434 abstract "Using the human erythroleukaemic cell line K562 cl.6 and its daunorubicin-resistant subline KDAU600, and the human T-lymphoblastic leukaemic cell line CCRF-CEM and its vinblastine-resistant subline CEMVLB100, we have shown that the drug-resistant cell lines were more sensitive to cytotoxicity induced by tumour necrosis factor-alpha (TNFα). Drug-resistant cell lines showed increased activities of copper/zinc superoxide dismutase (CuZnSOD) and catalase compared with their parental drug-sensitive cell lines. However, the greater susceptibility of drug-resistant cells to TNFα cytotoxicity was, in part, related to their decreased activities of manganese superoxide dismutase (MnSOD). Persistence of this differential sensitivity when MnSOD is inhibited by sodium nitroprusside (SNP) suggests that the greater susceptibility of drug-resistant cells to TNFα was not entirely due to their decreased level of MnSOD activity. K562 cl.6 and KDAU600, which were more resistant to TNFα, both expressed greater levels of endogenous plasma membrane-bound TNFα than the CCRF-CEM cell line. All cell lines examined were (more or less) equal in susceptibility to the cytolytic effect of exogenous O2.− generated by xanthine/xanthine oxidase. These results demonstrate that both MnSOD and endogenous TNFα play a role in protecting leukaemic cells against TNFα cytotoxicity, but there is an unknown mechanism that causes drug-resistant cells to be more susceptible to TNFα cytotoxicity." @default.
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- W2092199434 date "1995-03-01" @default.
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- W2092199434 title "TNF-mediated killing of human leukaemic cells: Effects of endogenous antioxidant levels and TNFα expression in leukaemic cell lines" @default.
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- W2092199434 doi "https://doi.org/10.1016/0145-2126(94)00149-5" @default.
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