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Delayed oxidative photodamage induced by photodynamic therapy
1Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA. DHKESSEL@med.wayne.edu
Photochemistry and Photobiology
|September 1, 1996
Summary
Photodynamic therapy induces cell death through DNA fragmentation. Radical scavengers prevent this effect, suggesting long-lasting photoproducts initiate apoptosis post-irradiation.
Area of Science:
- Cell Biology
- Photochemistry
- Cancer Research
Background:
- Photodynamic therapy (PDT) utilizes photosensitizers to induce cell death.
- Lysosomal targeting photosensitizers are employed in PDT.
- Apoptosis is a key mechanism of cell death in PDT.
Purpose of the Study:
- To investigate the role of radical scavengers in PDT-induced apoptosis.
- To elucidate the mechanism and timeline of photoproducts mediating apoptosis.
Main Methods:
- Murine leukemia cells were treated with PDT using lysosomal-targeting photosensitizers.
- Radical scavengers (trolox, alpha-tocopherol succinate) were administered before, during, and after irradiation.
- Apoptotic DNA fragmentation and phototoxicity were assessed.
Main Results:
- Apoptotic DNA fragmentation was observed 60 minutes post-PDT.
- Radical scavengers present during irradiation prevented apoptosis and phototoxicity.
- Scavenger addition after irradiation provided only partial protection, abolished if delayed by 10 minutes.
Conclusions:
- Long-persisting photoproducts initiate apoptosis for approximately 10 minutes after PDT.
- Radical oxygen species generated during PDT play a critical role in initiating apoptosis.
- The timing of scavenger intervention is crucial for mitigating PDT-induced cell death.