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Oxidative inactivation of redox sensitive cysteine residues in Keap1, specific phosphorylation of Nrf2, or increased expression of p62, which competes with Nrf2 for Keap 1 binding, disrupts the Keap1/Nrf2 interactions to foster the stabilization and nuclear translocation of Nrf2 where it promotes transcription of a variety of protective antioxidant genes via the antioxidant response element or ARE in their promoter regions

Valence-tailored copper-based nanoparticles for enhanced chemodynamic therapy through prolonged ROS generation and potentiated GSH depletion

[DOI] [PubMed] [Google Scholar] Zaman K, McPherson M, Vaughan J, Hunt J, Mendes F, Gaston B, Palmer LA

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Hence, AOX therapy to enhance fertility by protecting against the harmful effects of ROS is theoretically feasible