Abstract: A main feature of cancer cells, when compared to normal ones, is a persistent pro-oxidative state that leads to an intrinsic oxidative stress. Cancer cells have higher levels of reactive oxygen species (ROS) than normal cells, and ROS are, in turn, responsible for the maintenance of the cancer phenotype. Persistent ROS stress may induce adaptive stress responses, enabling cancer cells to survive with high levels of ROS and maintain cellular viability. However, excessive ROS levels render cancer cells highly susceptible to quercetin, one of the main dietary flavonoids. Quercetin depletes intracellular glutathione and increases intracellular ROS to a level that can cause cell death.
Keywords: cancer; reactive oxygen species; redox homeostasis; flavonoids; quercetin
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Gibellini, L.; Pinti, M.; Nasi, M.; De Biasi, S.; Roat, E.; Bertoncelli, L.; Cossarizza, A. Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin. Cancers 2010, 2, 1288-1311.
Gibellini L, Pinti M, Nasi M, De Biasi S, Roat E, Bertoncelli L, Cossarizza A. Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin. Cancers. 2010; 2(2):1288-1311.
Gibellini, Lara; Pinti, Marcello; Nasi, Milena; De Biasi, Sara; Roat, Erika; Bertoncelli, Linda; Cossarizza, Andrea. 2010. "Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin." Cancers 2, no. 2: 1288-1311.