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85 KhalafS.AhmadA

K., & Morozov, V

Yu, J., Carroll, T
It was well established that the hepatotoxicity of APAP begins with the metabolic conversion of APAP to its reactive metabolite (N/-acetyl-p-benzoquinone imine, or NAPQI) (Wallace, 2004)
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Compared with a low-Se diet (0.05 mg/kg), a high-Se diet (1.5 mg/kg) maintained postischemic plasma GSH levels and GPX activity and improved myocardial infarct size and postischemic mean arterial blood pressure in rats [115]