Reactive oxygen species and oxidative damage intermediates (ROS)

Reactive oxygen species (ROS) and oxidative damage intermediates represent a broad class of oxygen-containing chemically reactive molecules and their downstream products that play dual roles in human physiology [1.4.1, 1.5.1]. Under normal conditions, ROS such as superoxide, hydrogen peroxide, and hydroxyl radicals function as critical second messengers in redox signaling, regulating gene expression, cell proliferation, and immune responses [1.1.2, 1.2.1]. However, an imbalance between ROS production and antioxidant defenses leads to oxidative stress, causing irreversible damage to DNA, lipids, and proteins [1.2.4, 1.5.1]. This damage results in the formation of intermediates like 8-hydroxydeoxyguanosine and malondialdehyde, which are key biomarkers and drivers of diseases such as cancer, neurodegeneration, and cardiovascular disorders [1.2.2, 1.3.2]. Therapeutic interventions include antioxidants that scavenge ROS directly, inhibitors of ROS-producing enzymes like NADPH oxidase, and pro-oxidant drugs that exploit ROS to induce apoptosis in malignant cells [1.3.1, 1.3.3].

Other names

Reactive oxygen speciesROSOxidative stress intermediatesReactive oxygen metabolitesFree radicalsPro-oxidantsReactive species

Drugs targeting reactive oxygen species primarily act through direct chemical scavenging and neutralization of radicals, inhibition of ROS-generating enzymes such as NADPH oxidase and xanthine oxidase, or induction of endogenous antioxidant defense systems via the Nrf2 pathway [1.3.1, 1.4.2]. Conversely, pro-oxidant chemotherapeutics intentionally elevate ROS levels to exceed the toxic threshold in cancer cells, triggering apoptosis or ferroptosis [1.3.2].