It can also start lipid peroxidation by taking an electron from polyunsaturated fatty acids. 26,27 Hydroxyl radical is the most reactive of ROS and can damage proteins, lipids, and carbohydrates and DNA. O 2 − itself can also react with H 2O 2 and generate OH −. In a succession of reactions called Haber–Weiss and Fenton reactions, H 2O 2 can breakdown to OH − in the presence of transmission metals like Fe 2+ or Cu 2+. Hydrogen peroxide is also produced by xanthine oxidase, amino acid oxidase, and NAD(P)H oxidase 23,24 and in peroxisomes by consumption of molecular oxygen in metabolic reactions. Hydrogen peroxide easily diffuses across the plasma membrane.
Superoxide is converted into hydrogen peroxide by the action of superoxide dismutases (SODs, EC 1.15.1.1). Upon phagocytosis, these cells produce a burst of superoxide that lead to bactericidal activity. NAD(P)H oxidase is found in polymorphonuclear leukocytes, monocytes, and macrophages. Normally, electrons are transferred through mitochondrial electron transport chain for reduction of oxygen to water, but approximately 1 to 3% of all electrons leak from the system and produce superoxide. The major site for producing superoxide anion is the mitochondria, the machinery of the cell to produce adenosine triphosphate. 22 This process is mediated by nicotine adenine dinucleotide phosphate oxidase or xanthine oxidase or by mitochondrial electron transport system. Superoxide anion is formed by the addition of 1 electron to the molecular oxygen. In this review, we summarize the cellular oxidant and antioxidant systems and regulation of the reducing and oxidizing (redox) state in health and disease states. However, in pathological conditions, the antioxidant systems can be overwhelmed. 16–21 Aerobic organisms have integrated antioxidant systems, which include enzymatic and nonenzymatic antioxidants that are usually effective in blocking harmful effects of ROS. 1–6 The shift in balance between oxidant/antioxidant in favor of oxidants is termed “oxidative stress.” Oxidative stress contributes to many pathological conditions, including cancer, neurological disorders, 7–10 atherosclerosis, hypertension, ischemia/perfusion, 11–14 diabetes, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, 15 and asthma.
At low to moderate concentrations, they function in physiological cell processes, but at high concentrations, they produce adverse modifications to cell components, such as lipids, proteins, and DNA. Reactive oxygen species (ROS) are produced by living organisms as a result of normal cellular metabolism. In this review, we summarize the cellular oxidant and antioxidant systems and discuss the cellular effects and mechanisms of the oxidative stress. Oxidative stress contributes to many pathological conditions and diseases, including cancer, neurological disorders, atherosclerosis, hypertension, ischemia/perfusion, diabetes, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and asthma. Aerobic organisms have integrated antioxidant systems, which include enzymatic and nonenzymatic antioxidants that are usually effective in blocking harmful effects of ROS.
The shift in the balance between oxidants and antioxidants in favor of oxidants is termed “oxidative stress.” Regulation of reducing and oxidizing (redox) state is critical for cell viability, activation, proliferation, and organ function. ROS are highly reactive molecules and can damage cell structures such as carbohydrates, nucleic acids, lipids, and proteins and alter their functions. Reactive oxygen species (ROS) are produced by living organisms as a result of normal cellular metabolism and environmental factors, such as air pollutants or cigarette smoke.