Reactive oxygen species: friend or foe?

Abstract

Reactive oxygen species (ROS) are an inevitable by-product of cellular metabolism. ROS generation can be associated with the interaction of ionizing radiation with biological molecules, and devoted enzymes in phagocytic cells (NADPH oxidase and myeloperoxidase) or may be the result of an imbalance between radical generating and scavenging systems. Typically ROS have been consider as Pandora’s box, they have several innovative physiological roles in the body. ROS serve as signalling messengers for the activation of transcription factors from cytokine–receptor interactions. This facilitates the evolution and membrane fusion of spermatozoon and oocyte during fertilization. NADPH oxidase enzyme and nitric oxide (NO) function as potent vasodilators and immunity boosters. ROS have been suggested as prevalent regulators of several nuclear factors, including erythroid 2-related factor 2 (Nrf2), nuclear factor kappa-B (NFκB) cells, mitogen-activated protein kinase (MAPK) and p53, which are further associated with several signalling cascades. Under physiological conditions the amount of ROS generated in the body can be counterbalanced by natural antioxidants in the body. However, aberrant augmented levels of ROS predominantly lead to various defined disorders comprising myocardial infarction, autoimmune diseases, atherosclerosis, Alzheimer’s and Parkinson’s diseases and emphysema. Ordinarily, it is observed that the physiological roles of ROS are insubstantial compared with their pathological action. But there is a need to clearly define the line between pathological and physiological functions of ROS. Of particular worth is to reveal the beneficial responsibilities of ROS in different cellular pathways and metabolic functions, over its injurious consequences.