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The key mechanistic concept derived from these mouse studies was that the cellular toxicity was caused by a cytochrome P450-derived reactive metabolite, which was typically detoxified by GSH, but after the depletion of cellular GSH levels during an overdose, the reactive metabolite binds to cellular proteins thereby causing cell death [79]

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Cardiometabolic risk profile was defined as poor glycemic, blood pressure and lipid control, as well as prevalence of left ventricular diastolic dysfunction (LVDD) and carotid atherosclerosis (AS)

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