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The PMRS transfers electrons from the intracellular cytosolic RBC compartment to the extracellular medium by oxidizing intracellular electron donors like ascorbate and NADH, acting as a compensatory mechanism against elevated ROS/OS, and may contribute to redox regulation throughout the body [42]

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Compared with WT SOD1, disease-linked mutant SOD1 proteins readily form monomers by reduction of the disulfide bond between Cys-57 and Cys-146 or by demetallation at the dimer interface (Tiwari and Hayward, 2003