Reactive Oxygen Species and Oxidative Stress Mediators (ROS/Oxidative Stress)

Broad cellular free radicals and oxidative/inflammatory processes refer to the systemic accumulation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) that overwhelm cellular antioxidant defenses, leading to oxidative stress (Pizzino et al., 2017) [1]. These reactive species, including superoxide anions and hydroxyl radicals, are produced during mitochondrial respiration and by enzymes like NADPH oxidase, playing dual roles as both damaging agents and essential signaling molecules (NIH/NCI) [2]. When unregulated, they cause oxidative damage to DNA, proteins, and lipids, which in turn triggers pro-inflammatory signaling pathways such as the NF-κB cascade (Reuter et al., 2010) [3]. This interplay between oxidative stress and inflammation is a central driver in the progression of chronic diseases, including neurodegeneration, atherosclerosis, and various cancers (Halliwell, 2006) [4]. Pharmacological intervention typically involves the use of radical scavengers like Edaravone or antioxidants like N-acetylcysteine to neutralize these species or enhance endogenous defense mechanisms (Watanabe et al., 2018) [5]. However, the lack of specificity in targeting these broad processes remains a significant challenge, as ROS are also required for normal physiological functions like immune defense and cellular adaptation (Forman & Zhang, 2021) [6].

Other names

Free radicalsReactive Oxygen SpeciesROSReactive Nitrogen SpeciesRNSOxidative stressCellular oxidative damagePro-inflammatory oxidative processes

Direct scavenging of reactive oxygen and nitrogen species, and induction of endogenous antioxidant enzyme systems (e.g., via Nrf2 activation).