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Iron-dependent accumulation of reactive oxygen species (ROS) and consumption of polyunsaturated fatty acids (PUFAs) in biofilms are the mechanisms underlying ferroptosis, which is initiated by inhibitors of glutathione biosynthesis or the glutathione-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4)

Long-term inhibition of G6PDH activity and the associated impairment of the NADPH-generating system and glutathione (GSH)-replenishment system significantly increase the vulnerability of the affected cells to apoptosis

Available oral therapies cannot efficiently eliminate large MSU crystal deposits, called tophi, as sUA levels must be maintained well below 6 mg/dL to drive the dissolution of urate crystals 1

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