Reactive oxygen species generation via redox cycling

Reactive oxygen species generation via redox cycling" does not refer to a specific, canonical single molecule or receptor, but rather to a biochemical process by which certain molecules (often drugs, environmental toxins, or endogenous metabolites) repeatedly undergo reduction and oxidation to catalytically generate reactive oxygen species (ROS) such as superoxide, hydrogen peroxide, and hydroxyl radicals[2][4][5]. Redox cycling agents accept electrons from biological reductants and transfer them to oxygen, leading to sustained ROS production. These species play dual roles as both signaling molecules and agents of cellular damage via oxidative stress, influencing biological functions such as signal transduction, apoptosis, and immune modulation[2][3][4]. Excessive ROS production via redox cycling is implicated in various pathological processes, including tissue injury, inflammation, cancer, and neurodegeneration[2][3][4]. Several drugs (e.g., doxorubicin, paraquat, menadione) exert their toxic or therapeutic effects through ROS generation via redox cycling. However, this process is not itself a distinct therapeutic "target" such as a receptor or enzyme; it is a complex mechanism or pathway involving multiple molecular species and cellular systems. Caveats: - The term refers to a molecular process rather than a single entity, so it is not a "canonical" drug target, and not suitable as a structured therapeutic target entry. - If you require information on a specific enzyme (e.g., NADPH oxidase), transporter, or drug that mediates ROS generation via redox cycling, please clarify for a more precise mapping.

Other names

ROS generation via redox cyclingROS redox cyclingRedox cycling ROS production

Induction of oxidative stress by promoting ROS generation through redox cycling. Disruption of cellular redox homeostasis leading to cellular damage or death. Modulation of redox-sensitive signaling pathways.