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It serves as a model compound for investigating peptide-driven cellular responses, copper-mediated biological signaling, metalloprotein interactions, and tissue-remodeling biochemistry under controlled experimental conditions
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There are various agents acting as inhibitors or inducers of ferroptosis: Iron chelators, lipophilic antioxidants, inhibitors of lipid peroxidation and depletion of PUFAs inhibit ferroptosis, whereas ferroptosis is induced by the accumulation of iron or PUFA-phospholipids and by the depletion of endogenous inhibitors such as GSH, NADPH, GPX4 or vitamin E (178)
Lowering GSH levels also triggers ferroptosis through deactivation of GPX4, leading to accumulation of lipid peroxides [87] In some cases, GSH depletion alone can induce therapeutic effects without relying on Fenton chemistry, which typically involves HO reacting with Fe 2 to form hydroxyl radicals (OH) that damage critical biomolecules such as DNA, proteins, and lipids
