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Since this pathway use NADPH as electron donor, this compromises the availability of this coenzyme to regenerate reduced glutathione, exacerbating the oxidative stress [189]

A shift in mitochondrial substrates and metabolic inflexibility causes DNA mutations, oxidative stress, and apoptosis in PTPMT1 knockout cells

GSH protects cellular mitochondria by clearing environmental toxins and binding to heavy metals as a natural chelator

: Delayed administration of sodium thiosulfate in animal models reduces platinum ototoxicity without reduction of antitumor activity

Huang et al

Cross-talk between energy and redox metabolism in astrocyte-neuron functional cooperation