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Selective photodynamic inactivation of a multidrug transporter by a cationic photosensitising agent

D Kessel1, K Woodburn

  • 1Department of Pharmacology, Wayne State University School of Medicine, Detroit, Michigan 48201.

British Journal of Cancer
|February 1, 1995
PubMed

Insights

Photodamage using tetrabromorhodamine 123 affected P388 cells but only inhibited P-glycoprotein in resistant cells. This suggests limited photo-product migration and P-glycoprotein substrate confinement.

Area of Science:

  • Cell biology
  • Photochemistry
  • Pharmacology

Background:

  • Multidrug resistance (MDR) in cancer is a significant clinical challenge.
  • P-glycoprotein (P-gp) is a key efflux pump contributing to MDR.
  • Rhodamine dyes are fluorescent probes and photosensitizers.

Purpose of the Study:

  • To investigate the cellular sites of photodamage induced by tetrabromorhodamine 123.
  • To determine the effect of this photosensitizer on P-glycoprotein function in drug-resistant cells.
  • To explore the localization and migration of photo-induced cytotoxic products.

Main Methods:

  • Utilized P388 murine leukemia cells and a multidrug-resistant subline (P388/ADR) overexpressing P-glycoprotein.
  • Employed fluorescence emission spectroscopy to determine photosensitizer localization.
  • Assessed cell viability and drug accumulation following photosensitization and irradiation.

Main Results:

  • Tetrabromorhodamine 123 localized in hydrophobic regions of sensitive cells and aqueous loci in resistant cells.
  • Irradiation caused photodamage and loss of viability in sensitive P388 cells.
  • P388/ADR cells showed irreversible P-glycoprotein inhibition, increased daunorubicin accumulation, and enhanced cytotoxicity.

Conclusions:

  • Photodamage is dependent on photosensitizer localization within the cell.
  • P-glycoprotein substrates are confined to membrane sites associated with the transporter.
  • Cytotoxic photo-products exhibit limited migration within the cellular environment.

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