Reactive oxygen species-mediated cytotoxicity

Reactive oxygen species-mediated cytotoxicity is a process by which elevated levels of reactive oxygen species (ROS)—such as superoxide, hydrogen peroxide, hydroxyl radical, and singlet oxygen—induce cellular damage and death. ROS are byproducts of normal cellular metabolism but can accumulate to toxic levels during cellular stress or exposure to certain drugs. This oxidative stress leads to damage of DNA, proteins, and lipids, resulting in apoptosis, necrosis, or autophagy[1][3]. Multiple anti-cancer drugs work in part by increasing intracellular ROS, pushing cancer cells beyond their antioxidant capacity, thereby inducing programmed or unregulated cell death. While this process can be therapeutically beneficial for eliminating cancerous or infected cells, excessive ROS can also damage healthy tissue and contribute to a wide range of pathological conditions, including cancer, cardiovascular, neurodegenerative, and inflammatory diseases[1][3][4]. In summary, "reactive oxygen species-mediated cytotoxicity" is *not* a molecular target but a cytotoxic mechanism involving numerous molecules and pathways; as such, it does not map to a canonical target required by drug discovery databases.

Other names

ROS-mediated cytotoxicityoxidative stress-induced cell deathROS-induced cytotoxicity

Induction of oxidative stress leading to apoptosis or necrosis; Disruption of mitochondrial membrane potential; DNA damage via ROS; Lipid peroxidation; Protein oxidation (These mechanisms outline how drugs exploit ROS-mediated cytotoxicity[1][4].)