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Direct current decreases cell viability but not P-glycoprotein expression and function in human multidrug resistant
C Holandino1, V F Veiga, M L Rodrigues
1Departamento de Medicamentos-Faculdade de Farmácia, Instituto de Biofisica Carlos Chagas Filho, Rio de Janeiro, Brazil.
Bioelectromagnetics
|September 25, 2001
Summary
Direct current (DC) treatment effectively reduces human leukemic cell viability through direct cellular damage. This cancer therapy approach does not impact P-glycoprotein (P-gp) function, a key factor in multidrug resistance.
Area of Science:
- Oncology
- Cell Biology
- Biophysics
Background:
- Direct current (DC) therapy shows promise for inhibiting tumor growth.
- Multidrug resistance (MDR) is a significant challenge in cancer chemotherapy, often mediated by P-glycoprotein (P-gp).
Purpose of the Study:
- To investigate the cellular effects of DC treatment on human leukemic K562 cells and their vincristine-resistant counterpart, K562-Lucena 1.
- To determine if DC treatment affects P-glycoprotein (P-gp) expression and function in these cells.
Main Methods:
- Cell viability was assessed using trypan blue staining.
- Cellular morphology and ultrastructure were examined via transmission electron microscopy.
- P-glycoprotein (P-gp) expression and function were analyzed using reverse transcription polymerase chain reaction, flow cytometry, and Rhodamine 123 extrusion assays.
Main Results:
- DC treatment induced significant cellular effects, including lysis, shape alteration, membrane discontinuity, and vacuolization, leading to decreased cell viability.
- The expression of the mdr1 gene, which encodes P-gp, remained unchanged after DC treatment.
- P-gp surface expression and efflux function were unaltered by DC treatment in K562-Lucena 1 cells.
Conclusions:
- DC treatment effectively reduces leukemic cell viability through direct cellular damage, independent of P-gp modulation.
- The findings suggest that DC therapy targets leukemic cells via mechanisms distinct from P-gp activity, offering a potential strategy against MDR cancers.