ABSTRACT
The ability of photodynamic therapy (PDT) to cause cell death depends on a systematic process. This process starts with the accumulation of photosensitizer (PS) in cells followed by its activation (in the presence of oxygen) via light irradiation (of appropriate wavelength, which corresponds to the excitation spectra of that particular PS), all of which combined brings about the production of reactive oxygen species (ROS) within the cellular system (Agostinis et al. 2011). The ROS (or photooxidative stress) have the potential to bring about cell death by reacting with biomolecules, such as lipids or proteins, and activating cell-demise processes. Within the context of a tumor, in addition to the cancer cell-killing potential, PDT also has an ability to destroy tumor vasculature (causing tumor ischemia) as well as to activate the immunological system, thereby assisting in long-term tumor suppression (Agostinis et al. 2004; Garg et al. 2010a). Thus, there are many factors that influence the successful execution and pathways of PDT-based cell killing, for example, oxygen availability, concentration of PS, physicochemical properties and subcellular PS localization, suitable light wavelength and intensity/fluence, and cell type (Castano, Demidova, and Hamblin 2005).
