Abstract

Photodynamic therapy (PDT) is a promising, minimally invasive cancer therapy. This clinically approved treatment is usually carried out in two stages. In the first step, the photosensitizer (PS) is administered into the body of the patient and allowed to localize at neoplastic regions. Subsequently, in the second step, the neoplastic area is irradiated with specific wavelength of light from a laser source. Upon irradiation the photosensitizer (PS) gets excited and takes part in photochemical reactions by producing free radicals and/or singlet oxygen molecules that induce oxidative stress in cancer cells. These reactive oxygen species (ROS) target many cellular macromolecules like nucleic acids, lipids, proteins, and vitamins. PDT activates many signaling pathways that results in activation of caspases leading to apoptosis. Further, necrosis is the mode of cell death when high doses of PDT were used. PDT generated singlet oxygen molecules activate RIP-mediated necrotic pathway. PDT exerts anticancer activity directly by killing the cancer cells and indirectly by damaging the tumor vasculature and by activating antitumor immunity. In this chapter, the mechanism of PDT-induced oxidative damage of cellular components and cell death through multiple signaling pathways is discussed in detail. Understanding the chemical and biological processes involved in PDT will help in devising ways to increase photodynamic therapeutic efficiency against cancer. The measures to make PDT an efficient cancer therapeutic modality by overcoming cancer cell survival pathways that operate after PDT are also discussed.KeywordsOxidative stressPhotodynamic therapyCancerSinglet oxygenROS

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