Circadian rhythm in acetaminophen toxicity: Role of nonprotein sulfhydryls
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Drug Hepatotoxicity: Environmental Factors
2017, Clinics in Liver DiseaseCitation Excerpt :Deletion of circadian gene Per1 has been shown to change the hepatotoxic risk from alcohol,62 whereas mPer2 has a role in the diurnal variation of APAP toxicity, both in mice.64 Patients taking APAP may also be predisposed due to hepatotoxicity due to 24-hour circadian variation.59,68 This may be due in part to the normal pattern of intermittent fasting states over a 24-hour period because during times of fasting,68 glutathione levels are known to drop,69,70 thus potentially decreasing a protective mechanism that normally prevents toxicity from APAP.
A role of the circadian system and circadian proteins in aging
2007, Ageing Research ReviewsPrevention of acetaminophen-induced liver toxicity by 2(R,S)-n-propylthiazolidine-4(R)-carboxylic acid in mice
2001, Biochemical PharmacologyCitation Excerpt :The apparent Cys concentration was increased at 4 hr (0.18 ± 0.04 μmol/g, N = 3; 198% of vehicle control; P < 0.05) but not at 24 hr (0.15 ± 0.07 μmol/g, N = 5; 83% of vehicle control). The observation that hepatic concentrations of sulfhydryl and disulfide compounds 4 hr after the administration of the APAP vehicle (50% propylene glycol) were lower than the concentrations at time zero in untreated animals (Fig. 1) is consistent with the diurnal variation in hepatic non-protein sulfhydryl levels in mice and rats [23, 24]. Some other possible explanations include a response to the stress of i.p. injection or an effect of propylene glycol.
Metabolism and hepatotoxicity of acetaminophen in mice fed on a liquid glucose diet
1999, Nutrition ResearchDiurnal variability of cysteine and glutathione content in the pancreas and liver of the mouse
1996, Comparative Biochemistry and Physiology - B Biochemistry and Molecular Biology