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FIGURE 3 A newly identified GPX4-independent mitochondria-localized ferroptosis defense system, the DHODHCoQH2 system can compensate for GPX4 loss and detoxify mitochondrial lipid peroxides ( Recent studies revealed that the GCH1-BH4 system is another critical inhibitor of ferroptosis ( The mitochondrion is the major organelle to produce ROS ( 2 O 2 ) through superoxide dismutase mediated dismutation ( 2 O 2 can react with ferrous ion (Fe 2+ ) to generate hydroxyl radicals (OH), which then abstract the bis-allylic hydrogen in PUFAs to generate PUFA radicals (PUFA) (Zheng and Conrad, 2020)

Taba M, Kinney J, Kim AS, Giannobile WV

Updated 2016

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