Acetaminophen (APAP) is the most widely used analgesic in the United States. Its acute overdose causes liver damage by inducing localized centrilobular cell death. Because of widespread use, APAP toxicity has become the most frequent cause of acute liver failure. Many factors have been associated with the susceptibility of APAP-induced liver injuries, however, few of them have been confirmed and used in the clinical setting.
An integrative genomic analysis identifies Bhmt2 as a diet-dependent genetic factor protecting against acetaminophen-induced liver toxicity.
Specimen part, Time
View SamplesA total of 40 female mice 129/SV aged 3-6 months and weighting 18-25 g were used (Janvier, Le Genest-St-Isle, France). NTS was injected in mice (10 l/gBW/day) during three consecutive days. The total number of mice was divided to five treatment groups as followed: 8 mice were injected with PBS and fed with vehicle, 8 mice were injected with NTS and fed with vehicle, 8 mice were injected with NTS and fed with low dose DDR1i, 8 mice were injected with NTS and fed with high dose DDR1i and 8 mice were injected with NTS and fed with Imatinib. All treatments were provided by oral gavage. Treatment was started one day [PM{1}] prior first injection of NTS or PBS. The average food intake was controlled by weighing the food every three days. Mice were found to consume about 4g/day/mouse [PM{2}] which was similar to all groups.
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Sex, Specimen part, Treatment
View Samples