The Role of Subcellular Localization in Initiation of Apoptosis by Photodynamic Therapy

TLDR

Rapid initiation of apoptosis can be induced by photodynamic therapy, depending on cell line and sensitizer. The study evaluated the photodynamic responses of two structurally related photosensitizing agents in the P388 murine leukemia cell line. The authors assessed these responses by culturing P388 cells and applying the agents, measuring photodynamic effects. Tin etiopurpurin caused rapid apoptosis via lysosomal and mitochondrial damage within 60 min, whereas tin octaethylpurpurin amidine targeted lysosomes, mitochondria, and membranes, delaying apoptosis until 24 h, supporting the hypothesis that membrane photodamage can delay or prevent apoptosis.

Abstract

Rapid initiation of apoptosis can be induced by photodynamic therapy, depending on the cell line and sensitizer employed. In this study, we evaluated the photodynamic responses to two structurally related photosensitizing agents, using the P388 murine leukemia cell line in culture. Photodamage mediated by tin etiopurpurin involved lysosomes and mitochondria and yielded a rapid apoptotic response; apoptotic nuclei were observed within 60 min after PDT. A drug analog, tin octaethylpurpurin amidine, targeted lysosomes, mitochondria and cell membranes; apoptotic nuclei were not observed until 24 h after PDT. These results, together with other recent reports, are consistent with the hypothesis that membrane photodamage can delay or prevent an apoptotic response to PDT.