Mechanism of PDT-induced mitochondrial photodamage

David Kessel; Michelle Castelli; John Reiners Jr.

doi:10.1117/12.424448

9 April 2001 Mechanism of PDT-induced mitochondrial photodamage

David Kessel, Michelle Castelli, John Reiners Jr.

Proceedings Volume 4248, Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy X; (2001) https://doi.org/10.1117/12.424448
Event: BiOS 2001 The International Symposium on Biomedical Optics, 2001, San Jose, CA, United States

Abstract

In cell culture, photodamage induced by clinically-effective agents (e.g., Photofrin, SnET2, mTHPC, LuTex, HPPH, NPe6, ALA, Pc-4 or BPD) appears to involve mitochondria and/or lysosomes. When mitochondria are the major PDT target, a rapid apoptotic response is often observed, associated with release of cytochrome c, a trigger for caspase-9 activation. Fluorescence localization studies revealed that many of the 'mitochondrial-targeting' agents do not actually localize in mitochondria, but bind to a variety of intracellular membranes. The initial photodynamic effect involved photodamage to the anti-apoptotic protein Bcl-2, leaving the pro-apoptotic protein Bax unaffected. Subsequent apoptotic interactions between Bax and mitochondria may therefore represent the first step in the mitochondrial apoptotic pathway. We recently reported that certain bile acids can lower the threshold of photodynamic mitochondrial interactions leading to apoptosis. We suggest that this effect derives from the promotion of an interaction between Bax and the mitochondrial membrane interaction leading to cytochrome c release.

Citation Download Citation

David Kessel, Michelle Castelli, and John Reiners Jr. "Mechanism of PDT-induced mitochondrial photodamage", Proc. SPIE 4248, Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy X, (9 April 2001); https://doi.org/10.1117/12.424448

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