Quinone moiety

Redox cycling via a quinone moiety is a biochemical mechanism rather than a specific biological receptor or enzyme. It involves the cyclic reduction of a quinone to a semiquinone radical, followed by its rapid re-oxidation by molecular oxygen, which generates superoxide anion radicals (Bolton et al., 2000). This process is facilitated by various intracellular reductases, such as NADPH-cytochrome P450 reductase and NADH-dehydrogenase (Kappus, 1986). The resulting surge in reactive oxygen species (ROS) leads to significant oxidative stress, causing damage to cellular membranes, proteins, and DNA (Monks et al., 1992). In oncology, this mechanism is leveraged by drugs like anthracyclines (e.g., doxorubicin) to induce apoptosis in malignant cells (Minotti et al., 2004). However, the non-specific nature of ROS generation often leads to severe side effects, particularly permanent cardiomyopathy, which limits the clinical utility of quinone-based therapeutics (Powis, 1989).

Other names

Redox cyclingQuinone-mediated ROS generationSemiquinone radical formationQuinone-mediated free radical formation

The quinone moiety serves as an electron acceptor, undergoing enzymatic one-electron reduction to a semiquinone radical. This radical is then rapidly re-oxidized by molecular oxygen, producing superoxide anions and regenerating the parent quinone to repeat the cycle, resulting in sustained catalytic production of reactive oxygen species (ROS).