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Further simulations showed that over a wide range of doxorubicin (050 M), the model can be used to suggest the specific concentration and exposure duration required to deplete cytosolic GSH by 70%, the threshold by which antioxidant defence is impaired, protein binding occurs, and cell death is possible

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For instance, animal studies have demonstrated that administering glutathione precursors leads to increased cell proliferation and improved recovery outcomes after hepatic injury

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Enzymes like glutathione reductase, ascorbate peroxidase, glutathione peroxidase and glutathioneS-transferase also showed altered activities in the affected tissues