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A specific oxidoreductase, previously known as apoptosis-inducing-factor mitochondrial-2 (AIFM2), capable of recycling reduced ubiquinol (Co-enzymeQ 10 H 2 ) from ubiquinone at the expense of NAD(P)H, has been presented as a potential ferroptosis inhibitor due to the fact that its overexpression complements the loss of GPx4 in PFA1 and human fibrosarcoma (Figure 2)
Transitory glutathione deficit during brain development induces cognitive impairment in juvenile and adult rats: relevance to schizophrenia
W.ChoiA
Both oxidative damage to cells and a decrease in antioxidant ability contribute to this disease
2.7.10a 108
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