Reactive oxygen species and cellular thiols (ROS/Thiols)

Reactive oxygen species (ROS) and cellular thiols constitute a fundamental redox system that maintains cellular homeostasis and regulates signaling pathways [1, 6]. ROS, including superoxide, hydrogen peroxide, and hydroxyl radicals, are produced as byproducts of aerobic metabolism and by specific enzymes like NADPH oxidases [3, 15]. Cellular thiols, such as glutathione (GSH) and thioredoxin, act as the primary antioxidant defense and redox buffers, neutralizing ROS to prevent oxidative damage to lipids, proteins, and DNA [8, 11]. In many diseases, including cancer, neurodegeneration, and cardiovascular disorders, this balance is disrupted, leading to oxidative stress or maladaptive redox remodeling [1, 4, 18]. Therapeutic strategies target this system either by scavenging excessive ROS with antioxidants, replenishing thiol pools with prodrugs like N-acetylcysteine, or deliberately inducing ROS to trigger apoptosis in cancer cells [2, 9, 13]. However, the dual role of ROS as both damaging agents and essential signaling molecules presents a significant challenge for clinical intervention, as non-specific modulation can interfere with vital physiological processes [1, 5]. Furthermore, excessive suppression of ROS can lead to reductive stress, which may impair normal cellular functions and promote disease progression in certain contexts [1, 19]. Consequently, modern drug development focuses on precision redox modulation rather than global antioxidant supplementation [1, 4].

Other names

Oxidative stress mediatorsRedox environmentReactive oxygen speciesReactive nitrogen speciesCellular thiol poolRedox homeostasis

Mechanisms include direct scavenging of reactive oxygen species, replenishment of intracellular thiol pools (e.g., glutathione), and induction of antioxidant defenses to restore redox homeostasis or selectively induce cell death in pathological contexts [1, 9, 13].