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A synergistic depletion of glutathione has been suggested to be one critical factor in the hepatic injury in mice induced by non-toxic doses of paracetamol (APAP) when co-administered with α-adrenergic agonists. Prazosin (an α-adrenergic antagonist) could confer hepatoprotection following a toxic APAP dose (530mg/kg) by increasing glutathione levels and enhancing bioinactivation by glucuronidation...
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