TL;DR: Efflux transporters Mrp2 and Bcrp1 are shown to compensate for each other and enable the intestinal excretion of flavonoid (i.e., naringenin) glucuronides.
Abstract: The purposes of this study were to investigate how efflux transporters and UDP-glucuronosyltransferases (UGT) affect the disposition of naringenin. A rat intestinal perfusion model with bile duct c...
TL;DR: It was concluded that the glucuronide moiety is linked to the daunosamine sugar at the C4'-OH position and a hypothesis is proposed that this glucuronidation pathway may explain the differences in pharmacokinetics and toxicity between E and A.
TL;DR: The reasons for the lag between the ‘initial hydroxylation’ and the onset of glucuronic acid conjugation of 4-hydroxybiphenyl were investigated and attempts were made to eliminate this lag by prior incubations of the cells with 4-methylumbelliferone in an effort to activate the conjugating enzymes responsible.
TL;DR: The PST oxidation and glucuronidation pathway showed here, is the hepatic conversion of its properly glucuronic-PST synthesized, and the sequential route of PST detoxication in human is shown.
TL;DR: The efficiency of glucuronidation for a series of metabolites derived from the commonly used plasticizer, diethylhexyl phthalate, was measured to determine whether the efficiency of this pathway is compromised in children with ASD.
Abstract: Exposure to environmental chemicals may precipitate autism spectrum disorders (ASD) in genetically susceptible children. Differences in the efficiency of the glucuronidation process may substantially modulate substrate concentrations and effects. To determine whether the efficiency of this pathway is compromised in children with ASD, we measured the efficiency of glucuronidation for a series of metabolites derived from the commonly used plasticizer, diethylhexyl phthalate. Spot urines were collected and analyzed for the fraction of each metabolite conjugated by isotope dilution-liquid chromatography mass spectrometry-mass spectrometry. The degree of glucuronidation was lower with the ASD group. The glucuronidation pathway may differ in some children with ASD.