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Mechanism of mitochondrial membrane permeabilization during apoptosis under photofrin-mediated photodynamic therapy

Shengnan Wu1, Da Xing

  • 1MOE Key Laboratory of Laser Life Science and Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou, Guangdong, China. wushn@scnu.edu.cn

Journal of X-Ray Science and Technology
|September 6, 2012
PubMed

Insights

Photofrin-mediated photodynamic therapy (PF-PDT) triggers apoptosis by damaging mitochondria and causing reactive oxygen species (ROS) generation. This process involves mitochondrial swelling and outer membrane permeabilization, independent of the permeability transition pore.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Photomedicine

Background:

  • Photofrin-mediated photodynamic therapy (PF-PDT) is known to induce apoptosis through the mitochondria/caspase-3 pathway.
  • Understanding the precise mechanisms of PF-PDT-induced mitochondrial damage is crucial for optimizing therapeutic strategies.

Purpose of the Study:

  • To elucidate the detailed mechanism of mitochondrial apoptotic processes initiated by PF-PDT.
  • To investigate the role of reactive oxygen species (ROS) and mitochondrial membrane permeabilization in PF-PDT-induced apoptosis.

Main Methods:

  • Assessment of intracellular ROS generation in mitochondria post-irradiation.
  • Monitoring mitochondrial swelling and transmembrane potential dissipation.
  • Detection of mitochondrial inner and outer membrane permeabilization (MIMP and MOMP) using calcein fluorescence and cytochrome c release.
  • Evaluation of the effect of cyclosporine (CsA) on cytochrome c release.

Main Results:

  • PF-PDT treatment led to immediate, high-level ROS generation in mitochondria, identifying them as primary oxidative damage sites.
  • Mitochondrial swelling and dissipation of transmembrane potential were observed directly after irradiation.
  • PF-PDT induced simultaneous MIMP and MOMP, evidenced by decreased calcein fluorescence and cytochrome c release.
  • Cytochrome c release was not inhibited by CsA, indicating MOMP is independent of the mitochondrial permeability transition (MPT).

Conclusions:

  • PF-PDT induces rapid mitochondrial oxidative damage, characterized by simultaneous MIMP and MOMP, independent of MPT.
  • Inducible mitochondrial ROS generation is a critical factor in PF-PDT-mediated apoptosis.
  • This study provides insights into the initial mitochondrial oxidative damage mechanisms of PF-PDT.

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