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In pregnancies at risk for preterm delivery, high-dose N-acetylcysteine failed to restore glutathione levels but was safe

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In this study, we performed a ChaC1-activity-directed pharmacological screening from FDA-approved drug library to identify GSH-sensitive agents, and found that ChaC1 overexpression mediated glutathione depletion largely enhanced auranofin (AUR)-induced cell death in hepatocellular carcinoma (HCC) cells

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