Reactive Oxygen Species: Role in Pathophysiology, and Mechanism of Endogenous and Dietary Antioxidants during Oxidative Stress.

Abstract

Redox imbalances, which result from excessive production of reactive oxygen species (ROS) or malfunctioning of the antioxidant system, are the source of oxidative stress. ROS affects all structural and functional components of cells, either directly or indirectly. In addition to causing genetic abnormalities, excessive ROS also oxidatively modifies proteins by protein oxidation and peroxidation and alters lipid structure via advanced lipoxidation, decreasing function and promoting damage or cell death. On the other hand, low levels of ROS constitute important redox-signaling molecules in various pathways that maintain cellular homeostasis and regulate key transcription factors. As a result, ROS can affect various cellular processes, such as apoptosis, migration, differentiation, and proliferation. ROS can act as signaling molecules, controlling various normal physiological activities at the cellular level. Furthermore, there is an increasing body of evidence indicating the role of ROS in various clinical conditions. In this review, we will summarize the role of ROS in physiological and pathological processes and antioxidant action during oxidative stress.