Targeting the Antioxidant Enzymes for the Treatment of Reactive Oxygen Species (ROS)-Induced Cancer

Abstract

An increase in the free radicals or reactive oxygen species (ROS) production and/or reduced scavenging through impaired endogenous antioxidant enzymes could result in oxidative stress (OS). The elevated level of OS in the cells may result in extensive cellular damage to molecules with double bond, viz., membrane phospholipid and nucleic acids such as DNA, RNA, and other macromolecules, that ultimately leads to apoptosis or necrosis. Exposure to environmental contaminants and virus could augment the production of ROS and result in the development of cancer. The increase of ROS levels is reported during various physiological and pathological conditions, such as aging, stress, inflammation, rheumatoid arthritis, respiratory disorders, diabetes, myocardial infarction, and cancer. This book chapter is focused to discuss several aspects of endogenous antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), their relevance in the initiation of oncogenesis, epithelialmesenchymal transition (EMT), and carcinogenesis. Several drugs, which primarily utilize antioxidant enzymes to mediate anticancer activities, are also discussed in this chapter. Further, the chapter also collates the information regarding antioxidant enzyme mimics to circumvent several cancer types.