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Therefore, in this study, we have used human hepatoma HepG2 cancer cells, a commonly used cell culture model, which has been treated with buthionine sulfoximine (BSO), a GSH depleting agent and N-acetylcysteine (NAC), a precursor of GSH synthesis, to study the implications of altered glutathione metabolism in ASA-induced oxidative stress, redox homeostasis and mitochondrial dysfunctions