This non-specific action can also interfere with the physiological signaling roles of ROS (as discussed in Section 2.2), potentially leading to unintended adverse effects or a lack of targeted efficacy
Iron accumulation, lipid peroxidation, and decreased GPX4 expression, which are characteristic hallmarks of ferroptosis, contribute to inflammation through the induction of oxidative stress and the activation of the high mobility group box-1 protein1-advanced glycosylation end-product-specific receptor signaling pathway and extracellular signal-regulated kinase, respectively [77,78,79]
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Recent reports indicate a more complex mechanism in which wild-type p53 may enhance survival advantage by promoting antioxidation in some cases, and p53-mediated activation of p21 (encoded by CDKN1a) inhibits phospholipid oxidation by protecting intracellular mercaptans (including GSH) (Tarangelo et al., 2018
Excessive ROS can be reduced by cellular antioxidant systems, such as the Nrf2-mediated antioxidant system, GSH, and NADPH [18, 19]
