Electric depolarization of photosensitized cells: lipid vs. protein alterations.

We have monitored several photosensitized reactions in proteins, liposomes and cells under similar conditions. We found that the depolarization of K(+)-diffusion potential of liposomes or the leakage of an entrapped molecule, calcein, progress at a much slower rate than the photosensitized damage to proteins and the photosensitized killing of bacterial and leukemic cells. X-ray microanalysis revealed that upon light exposure of HP-treated leukemic cells and bacteria, they totally lost their cellular potassium. We deduce that the direct photosensitized oxidation of lipid components cannot cause the depolarization of cells, which in turn could be responsible for their death. A photosensitized damage to protein sites in the cell, probably in the membrane, is a more likely reason for the depolarization, the loss of potassium ions and cell death that is caused in light-activated photodynamic processes.