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Hydrogen peroxide (H 2 O 2 ) is an oxidizing agent that induces cellular damage at inappropriate concentrations and gives rise to an arrest during cell cycle progression, causing cell death. Recent evidence indicates that H 2 O 2 also acts as a promoter for cell cycle progression by oxidizing specific thiol proteins. The intracellular concentration of H 2 O 2 is regulated tightly, enabling its use as a cellular signaling molecule while minimizing its potential to cause cellular damage. Peroxiredoxins (Prxs) have peroxidase activity toward H 2 O 2 , organic hydroperoxides, and peroxynitrite for protecting cells from oxidative stress. They are suggested to work as signaling mediators, allowing the local accumulation of H 2 O 2 by inactivating their peroxidase activity uniquely compared with other antioxidant proteins such as catalase and glutathione peroxidase. Given that Prxs are highly sensitive to oxidation by H 2 O 2 , they act as sensors and transducers of H 2 O 2 signaling via transferring their oxidation state to effector proteins. The concentrations of intracellular H 2 O 2 increase as the cell cycle progresses from G 1 to mitosis. Here, we summarize the roles of Prxs with regard to the regulation of cell cycle-dependent kinase activity and anaphase-promoting complex/cyclosome in terms of changes in H 2 O 2 levels. Protection of the cell from unwanted progression of the cell cycle is suggested to be a role of Prx. We discuss the possible roles of Prxs to control H 2 O 2 levels.

The Role of Hydrogen Peroxide and Peroxiredoxins throughout the Cell Cycle