Abstract
Role of the calmodulin inhibitor trifluoperazine on the induction and expression of cell cycle traverse perturbations and cytotoxicity of daunorubicin and doxorubicin (adriamycin) in doxorubicin-resistant P388 mouse leukaemia cells
Highlights
Strong and weak DNA-binding anthracyclines in DOX-resistant cells is possibly different
Since the cellular pharmacokinetics of anthracyclines and the effect of TFP on the cytotoxicity of anthracylines have been extensively studied in P388/DOX cells, it represents a model system wherein a clearer understanding of the mechanism(s) of anthracycline resistance and scope for modulation, may be possible
In P388/DOX cells treated with 5 UM TFP alone for 24h, survival was 100% of control, and calmodulin inhibitors affect cell cycle traverse (Chafouleas et al, 1982) no changes in cell cycle phase distribution were apparent at the concentration of TFP used in this study
Summary
Role of the calmodulin inhibitor trifluoperazine on the induction and expression of cell cycle traverse perturbations and cytotoxicity of daunorubicin and doxorubicin (Adriamycin) in doxorubicin-resistant P388 mouse leukaemia cells. In the present study, using the P388/DOX cells, we demonstrate that similar cellular DOX and DAU levels in the absence and presence of TFP can be achieved, perturbations in cell cycle traverse and cytotoxicity occur only with TFP treatment. Data on cellular DAU and DOX fluorescence, cell cycle phase distribution and survival in soft agar of P388/DOX cells treated with DAU and DOX in the absence and presence of TFP for 3 h,. These perturbations in cell cycle traverse were accompanied by reductions in colony formation of
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