MITOCHONDRIAL PHOTOSENSITIZATION BY PHOTOFRIN II

Abstract V‐79 Chinese hamster cells grown as monolayers or as multicell spheroids were treated with Photofrin II (10 μ.g m−1 for 16 h) and various doses of red light irradiation. The resulting biochemical and functional damage to cell mitochondria was studied. The activities of both succinic dehydrogenese and cytochrome c oxidase were found to decrease in a light dose‐dependent manner. The respiratory control quotient (RC) decreased in parallel with a decrease in the activities of the respiratory chain proteins. Our data also showed a distinct temporal difference in the relative progression of mitochondrial damage and cell death as assessed by loss of discrete Rhodamine‐123 (Rh‐123) localization and trypan blue infiltration, respectively. Mitochondrial damage was detected immediately, as seen by derealization of Rh‐123 resulting from dissipation of the electrochemical gradient in damaged mitochondria. Trypan blue infiltration occurs with a distinct time lag. These findings are consistent with the hypothesis that, at least for long Photofrin II incubation times, the mitochondrion is a primary target of photosensitization. The subsequent changes in cell membrane permeability may be a delayed result of decreased bioenergetics of the Photofrin II photosensitized cell.

MITOCHONDRIAL PHOTOSENSITIZATION BY PHOTOFRIN II Journal Articles