Targeting Redox Signaling and ROS Metabolism in Cancer Treatment

Reactive oxygen species (ROS) are reactive chemical and/or biochemical intermediates or fragments containing oxygen as peroxides, superoxide (O2●−), hydrogen peroxide (H2O2), hydroxyl radical (●OH), hydroxyl ion (−OH), singlet oxygen, and nitric oxide (NO). At optimal concentration ROS have been implicated to serve varieties of important physiological functions in different types of cells under normal physiological conditions. On the other hand, excessive amounts of ROS are one of the main determinants in the pathogenesis of different types of diseases including cancer, metabolic syndromes, cardiovascular, and neurodegeneration. The mechanism of the generation of ROS and its concentration decides the fate of cells in different types and conditions; excessive ROS can cause detrimental effects on normal cells, deregulate cellular homeostasis, and induce carcinogenic changes. In order to continue their growth and proliferation, cancer cells increase ROS production rate compared with normal cells, and to maintain their ROS homeostasis, they simultaneously increase their antioxidant capacity. It is now evident that this unique and altered redox environment of cancer cells upturns or increases their vulnerability to ROS-metabolism therapies. This chapter aims to discuss a current scenario of ROS in physiological and pathological contributions with emphasis on cellular and molecular mechanistic ways. In addition, it discusses the role of oxidative stress in initiation and progression of different types of cancers as well as current and new strategies targeting ROS for the development of therapeutic interventions of ROS-induced cancers.