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Researchers have observed this protective effect through glutathiones activation of the Nrf2/HO-1 signaling pathway [4]

one with a point mutation where the selenocysteine residue was replaced by a cysteine and the other with a premature stop codon, showed resistance during development when exposed to the chemotherapeutic agent, cisplatin [167]

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To maintain a steady, endogenous supply of cysteine for glutathione production, the body relies heavily on the transsulfuration pathway