Oxidative and nitrosative stress

Oxidative and nitrosative stress describe interrelated cellular states characterized by excess production of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS), which overwhelm antioxidant defenses and lead to biochemical damage of proteins, lipids, and nucleic acids[1][2]. These stress conditions are implicated in the pathogenesis of numerous diseases, including cardiovascular disease, diabetes, neurodegeneration, and chronic inflammation. While many drugs aim to modulate the consequences of oxidative/nitrosative stress or affect the generating pathways (such as using antioxidants or NOS inhibitors), these states are *not molecular drug targets* themselves but rather conditions resulting from altered cellular redox balance[1][2]. Specific molecules produced during oxidative/nitrosative stress, such as 3-nitrotyrosine or malondialdehyde, serve as biomarkers, but “oxidative/nitrosative stress” should not be listed as a canonical drug target. Note: The entry “Oxidative/nitrosative stress” is not a valid molecular target; it refers to a general redox pathological phenomenon rather than a distinct protein, receptor, or other druggable entity. For structured drug target information, focus instead on specific enzymes (like NADPH oxidase or inducible nitric oxide synthase), receptors, or signaling proteins involved in redox regulation[1][2].

Other names

Oxidative stressNitrosative stressReactive oxygen species (ROS)/Reactive nitrogen species (RNS) imbalance