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CHAC1 further exacerbates cellular stress by degrading GSH, intensifying oxidative damage and ultimately driving ferroptotic cell death (Figure 5) ( FIGURE 5 While the eIF2K3/PERK-eIF2-ATF4 cascade, another branch of the ISR, can modulate ferroptosis in the context of ER stress, cysteine deprivation selectively activates GCN2 rather than PERK, highlighting distinct regulatory mechanisms ( Cysteine starvation triggers mitochondrial fragmentation, impairs mitochondrial function and leads to the accumulation of ROS ( CHAC1 is upregulated through the ATF4-dependent ISR pathway, where it degrades GSH to liberate cysteine needed for the synthesis of Fe-S cluster proteins (Ward et al., 2024)

The search for new endpoints is necessary, given the complexity of skin irritation mechanism

GSH, also known as glutathione, possesses the ability to undergo oxidation, thereby contributing to the maintenance of redox homeostasis

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The mechanism leading to 5-oxoprolinuria is the following: decreased activity of 5-oxoprolinase leads to decreased conversion of 5-oxoproline to glutamate