The enzymology of human drug and chemical glucosidation

Author: Nuy Chau

Chau, Nuy, 2019 The enzymology of human drug and chemical glucosidation, Flinders University, College of Medicine and Public Health

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Abstract

Accumulating evidence indicates that conjugation with glucose (‘glucosidation’) is a more common metabolic pathway for drugs in humans than previously believed. The studies described in this thesis primarily aimed to characterize the enzymology of drug glucosidation.

Morphine (MOR) is known to be metabolized in humans via glucuronidation and glucosidation at the 3-position, and glucuronidation at the 6-position. Reaction phenotyping studies described in Chapter 3 demonstrated that UDP-glucuronosyltransferase (UGT) 2B7 catalyzes the formation of all three conjugates. Thus, glucuronidation and glucosidation occur as complementary metabolic pathways. Glucuronidation is the dominant pathway because the binding affinity of UDP-glucuronic acid (UDP-GlcUA) to UGT2B7 is higher than that of UDP-glucose (UDP-Glc). Kinetic studies with human liver microsomes (HLM) as the enzyme source showed that the relative formation of the three metabolites observed in humans in vitro was correctly predicted when incubations were performed in the presence of the combined (1:1 UDP-GlcUA/UDP-Glc) cofactors. However, kinetic data generated in the presence of the separated cofactors over-predicted MOR-3-glucoside formation.

Complementary experiments (Chapter 5) investigated the comparative enzymology of mycophenolic acid (MPA) glucuronidation and glucosidation. UGT1A9 and UGT2B7 were confirmed as the respective principle enzymes responsible for MPA phenolic- and acyl-glucuronidation. In contrast to the observations with MOR, multiple hepatic enzymes (UGT2B7, UGT1A1 and UGT1A9) catalyzed MPA phenolic glucosidation. Consistent with plasma and urinary metabolite excretion data in patients treated with MPA, human liver microsomal kinetic data generated in the presence of combined cofactors (1:1 UDP-GlcUA/UDP-Glc) identified phenolic glucosidation as a minor metabolic pathway.

To rationalize the cofactor binding selectivity data, UDP-GlcUA and UDP-Glc were docked in a UGT2B7 protein homology model (Chapter 4). Both cofactors bound within the same C-terminal (CT) domain. Although binding interactions with the UDP-moiety were cofactor independent, residues involved in the binding of the sugar differed; Asp398 and Glu399 interact with glucose -OH groups of UDP-Glc, whereas Asn402 and Tyr33 bind to the carboxylate group of UDP-GlcUA. Site-directed mutagenesis of these residues and enzyme activity studies confirmed a role of these amino acids in cofactor binding.

Following the observation (Chapter 3) that Control SupersomesTM (c-SUP) express a native enzyme that glucosidates MOR, Chapter 6 characterized the glucosidation of c-SUP and membranes from uninfected Spodoptera frugiperda (Sf9) towards a series of aglycones with differing acceptor functional groups. Although both enzyme sources glucosidated phenolic substrates, differences were observed in the selectivities of the native UDP-glycosyltransferases towards aliphatic alcohols, carboxylic acids and amines. The results underscore the need to include control cell membranes in the investigation of drug and chemical glucosidation by UGT enzymes expressed in Trichoplusia ni (SupersomesTM) and Sf9 cells.

Keywords: glucosidation, drug metabolism, UDP-glycosyltransferase (UGT), glucuronidation, morphine, mycophenolic acid, insect cell chemical glucosidation, enzyme kinetics, protein homology modeling, mutagenesis

Subject: Pharmacy thesis

Thesis type: Doctor of Philosophy
Completed: 2019
School: College of Medicine and Public Health
Supervisor: Professor John Miners