ABSTRACT:
The term ‘‘oxidative stress” is defined as a disturbance in the equilibrium between free radicals (FR), reactive oxygen species (ROS), and endogenous antioxidant defense mechanisms. Cells continuously produce free radicals as a part of their normal metabolic processes. Under normal metabolic conditions, 2–5% of the O2 consumed by mitochondria is converted to reactive oxygen species (ROS) which has been implicated in diverse processes in various cancers. The increased ROS in cancer cells is known to play an important role in the initiation and progression of cancer. Lipid peroxidation and DNA damage are two major factors responsible for cancer. Lipid peroxidation is one of the forms of oxidative damage in cell membranes which leads to formation of lipid hydroperoxides (LOOH) that may cause permanent structural changes in DNA such as base-pair mutations, deletions, insertions, rearrangements and sequence amplification. Hence, the prevention of excess free radical formation is a vital step for cell survival. This review article emphasises on the relationship between the increase in cellular reactive oxygen radicals and the pathogenesis of cancer.
