It is well known that species derived from oxygen are cytotoxic and are involved in the etiology of cancer. Several carcinogens during metabolism exert their effect by producing reactive oxygen species (ROS). One of the consequences of oxidative damage to cellular DNA is mutated. It plays a vital role in the process of carcinogenesis (especially in the initiation and progression). The alters, including rearrangement of DNA sequence, base modification, DNA miscoding lesions, gene amplification, and the activation of oncogenes, could be implicated in the initiation stage of several cancers. Mitochondrial changes in the cancer cells are well known and as a result are respiratory injured. Mitochondrial dysfunction could lead to a low coupling efficiency of the mitochondrial electron transport chain (mETC), raising electron leakage and increased ROS formation. It has been documented that by reducing and inactivation of antioxidant system, the oxidative stress (OS) in cancer cells is higher. Cancer cells exhibit a higher oxidative stress level compared to normal cells, rendering tumor cells more vulnerable to raise ROS levels. Therefore, increasing ROS levels through redox modulation can be a strategy to selectively kill cancer cells but not normal cells. A promising anti-cancer method named “oxidation therapy” has been developed by causing cytotoxic oxidative stress for cancer therapy. In this chapter, we described the role of ROS as a double-edged sword in cancer development and treatment.
Part of the book: Free Radicals and Diseases