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Sporadic studies have suggested mitochondrial dysfunction, enhanced oxidative stress, and specific defects in other metabolic pathways can promote dysregulation of innate and adaptive immune responses in vitiligo

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Animal model research demonstrated that depleting GSH via inhibition of GCL triggered a cascade of lipid peroxidation and cell death in mesencephalic cultures, identifying oxidative stress from glutathione insufficiency as a likely initiating mechanism in neurodegeneration