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However, reactive oxygen species, which are central players in the APAP-induced signaling cascade, have been shown to be involved in RIP3-induced necroptosis in the cardiomyocyte [135] and several studies have also implicated RIP1 in APAP-induced liver injury [57,73,74,136] further confirming that the mode of cell death after APAP is regulated necrosis

Group 4: pristane - treated animals were treated intravenously with liposomal-glutathione in a dose of 5 mg/kg daily for 30 days [15]

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