Reactive oxygen species and cellular redox couples (ROS/Redox couples)

Reactive oxygen species (ROS) and cellular redox couples represent a complex network of reactive molecules and their corresponding reduced/oxidized partners that maintain cellular homeostasis (Sies & Jones, 2020). ROS, including superoxide anions, hydrogen peroxide, and hydroxyl radicals, are natural byproducts of mitochondrial metabolism and enzymatic activities like those of NADPH oxidases (Schieber & Chandel, 2014). Cellular redox couples, such as the glutathione (GSH/GSSG) and nicotinamide adenine dinucleotide (NAD+/NADH, NADP+/NADPH) systems, act as buffers to regulate the intracellular oxidative environment (Ursini et al., 2016). While low levels of ROS serve as critical signaling molecules in processes like cell proliferation and differentiation, an imbalance—termed oxidative stress—leads to damage of lipids, proteins, and DNA (Halliwell & Gutteridge, 2015). This imbalance is a hallmark of numerous pathologies, including cancer, where high ROS levels drive genomic instability, and neurodegenerative diseases, where they contribute to neuronal death (Trachootham et al., 2009). Therapeutic strategies involve either scavenging excess ROS with antioxidants like N-acetylcysteine or, conversely, inducing ROS to trigger apoptosis in cancer cells using pro-oxidant agents (Gorrini et al., 2013).

Other names

ROSRedox couplesOxidative stress markersReactive nitrogen speciesRNSThiol-disulfide couples

Direct scavenging of reactive oxygen species, replenishment of intracellular thiol pools (e.g., glutathione), and activation of the Nrf2-Keap1 pathway to induce endogenous antioxidant enzymes.