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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
PubMed

Insights

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.

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