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|Title:||Glutathione-related factors are not correlated with sensitivity of human tumour cells to actinomycin D||Authors:||Zhang, K.
Glutathione conjugate export pump
Human tumour cells
|Issue Date:||28-Feb-2000||Citation:||Zhang, K., Yang, E.B., Zhao, Y.N., Wong, K.P., Mack, P. (2000-02-28). Glutathione-related factors are not correlated with sensitivity of human tumour cells to actinomycin D. Cancer Letters 149 (1-2) : 213-220. ScholarBank@NUS Repository. https://doi.org/10.1016/S0304-3835(99)00364-X||Abstract:||Glutathione (GSH) contents and activities of glutathione S-transferases (GST), glutathione reductase (GSH-RD), glutathione peroxidase (GSHpx) and glutathione conjugate export pump (GS-X pump) were determined in eight human tumour cell lines with different sensitivities to melphalan, a substrate of glutathione conjugation, and actinomycin D which has not been shown to be detoxified by glutathione-related mechanisms. Chang liver cells with highest GSH content and highest activities of GST, GSH-RD, GSHpx and GS-X pump were found to be most resistant to melphalan. Statistical analysis showed significant correlations between sensitivities of the human tumour cells to melphalan and the glutathione-related factors (r = 0.72-0.79; except for GST, r = 0.65, P = 0.08), while there were no significant correlations observed between sensitivities of the human tumour cells to actinomycin D and all the glutathione-related factors tested (r = -0.25-0.14). Significant correlations of the glutathione-related factors to resistance of human tumour cells to melphalan, a substrate of glutathione conjugation, but not to resistance of the human tumour cells to actinomycin D which has not been shown to be detoxified by glutathione-related mechanisms suggested that glutathione- related mechanisms contribute to drug resistance by increased detoxification of the drugs involved. (C) 2000 Elsevier Science Ireland Ltd.||Source Title:||Cancer Letters||URI:||http://scholarbank.nus.edu.sg/handle/10635/107778||ISSN:||03043835||DOI:||10.1016/S0304-3835(99)00364-X|
|Appears in Collections:||Staff Publications|
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