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However, this preservation of mitochondrial function creates a paradox: by maintaining the electron transport chain, CHAC1 inadvertently supplies the ROS that propagate iron-dependent lipid peroxidation ( via two convergent mechanisms: the direct depletion of glutathione and the indirect facilitation of mitochondrial ROS production, thereby coupling sustained metabolic activity to ferroptotic cell death under cysteine limitation

doi: 10.1111/j.1600-079X.2008.00555.x 73 SatiL

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Corresponding monomers show a root-mean-square deviation (r.m.s.d of all Cs) of 0.116 to 0.212