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After GPx consumes part of the initial H 2 O 2 substrate, the remaining H 2 O 2 interacts with ferrous ions (Fe 2+ ), proceeding through a classic Fenton-type redox reaction that oxidizes Fe 2+ ions to ferric ions (Fe + )

demonstrated that oxidative stress and H 2 O 2 treatment led to a marked increase in senescence-associated -galactosidase activity but only to minimal apoptotic cell death in CSCs, suggesting that ROS triggered the induction of senescence and exhibited therapeutic potential in the eradication of drug-resistant CSCs [8]