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In this setting, any perturbation that lowers intracellular GSH to an as yet unknown threshold could eventually induce cell death and, in all likelihood, ferroptosis, but also significantly increase expression and secretion of numerous T2-associated proteins

2024 Mar 18];11(6)

doi: 10.1046/j.1365-2249.1999.00870.x

Research indicates that the DHODH pathway can protect cells from oxidative stress and mitochondrial damage through various mechanisms, including downregulating ROS levels, maintaining mitochondrial membrane potential, and inhibiting cell apoptosis (77, 78)

A conserved dual function of the conserved lysine residue for redox catalysis is also supported by previous studies: Lys19 of human Grx1 and Lys8 of NrdH-redoxin from C
