Oxidative stress in human diseases

Oxidative stress is a "privilege" of aerobic organisms. It can be induced by endogenous and exogenous factors. Most often, it is characterized by the production of free radicals and nonradical oxygen and nitrogen products, referred to under a single term "reactive species" (RS). Oxidative stress is a deleterious process that can be an important mediator of damage to cell structures, including lipids and membranes, proteins and DNA. However, reactive oxygen (ROS) and nitrogen species (RNS) are "two-faced" products. Produced in low/moderate concentrations as molecular signals that regulate a series of physiological processes, such as a defence against infectious agents, the maintenance of vascular tone, the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. Many of ROSmediated responses protect cells against oxidative stress and maintain "redox homeostasis". Then, both reactive species are produced by strictly regulated enzymes, such as nitric oxide synthase (NOS), and isoforms of NADPH oxidase, or as by-products from not so well regulated sources, such as the mitochondrial electron-transport chain. An excessive increase in ROS production has been implicated in the pathogenesis of atherosclerosis, cardiovascular diseases, hypertension, ischemia/reperfusion injury, diabetes mellitus, neurodegenerative and immuno-inflammatory diseases. Within the cells, ROS can act as secondary messengers in intracellular signalling cascades, which can induce the oncogenic phenotype of cancer cells, cellular senescence and apoptosis.