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112 , 114 , 118 – 120 Therefore, oxidants will overwhelm cellular antioxidant systems, leading to mitochondrial membrane permeability transition pore opening 121 , 122 and mitochondrial dysfunction that are concurrent with extensive oxidative damage to proteins, DNA, and lipids 123 – 127 (Figure 5)

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Immune checkpoint molecules, tumor-associated macrophages, regulatory T cells, and myeloid-derived suppressor cells can attenuate the efficacy of ferroptosis and cuproptosis inducers, thereby forming a drug-tolerant microenvironment that promotes therapeutic resistance and early recurrence