Development of resistance to toxic effects of acetaminophen (APAP) was reported in rodents and humans, though the mechanism is only partially understood. We examined in rats the effect of administration with subtoxic daily doses (0.2, 0.3, and 0.6g/kg, i.p.) of
Journal of pediatric gastroenterology and nutrition, 52(2), 198-202 (2011-01-18)
: The aim of the study was to evaluate UDP-glucuronyltransferase activity and the pharmacokinetics of a single oral dose of acetaminophen (APAP) in children with nonalcoholic fatty liver disease (NAFLD). : Twelve boys 10 to 17 years old with biopsy-proven
In this work, we developed a microfluidic device for the imitation of drug metabolism in human liver and its cytotoxicity on cells. The integrated microfluidic device consists of three sections: (1) bioreactors containing poly(ethylene) glycol (PEG) hydrogel encapsulated human liver
Journal of clinical pharmacology, 53(4), 413-420 (2013-02-26)
Acetaminophen poisoning is the most frequent cause of acute hepatic failure in the US. Toxicity requires reductive metabolism of acetaminophen, primarily via CYP2E1. Liquid acetaminophen preparations contain propylene glycol, a common excipient that has been shown to reduce hepatocellular injury
Drug metabolism and disposition: the biological fate of chemicals, 35(11), 2060-2066 (2007-08-10)
The effect of spironolactone (SL) administration on 17alpha-ethynylestradiol (EE)-induced cholestasis was studied, with emphasis on expression and activity of Mrps. Adult male Wistar rats were divided into the following groups: EE (5 mg/kg daily for 5 days, s.c.), SL (200
