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Spring Symposium on UR and Community Engagement has ended
Tuesday, April 24 • 12:00pm - 1:30pm
Glucuronidation Of Mono(ethylhexyl)-phthalate, Mono(ethyl-hydroxy-hexyl) phthalate, And Uridine-5'-diphospho-glucuronosyltransferase-1A1 Inhibition Via Over-The-Counter Drugs

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Phthalates, a di-substituted benzylic family of chemicals with various industrial applications, is a known androgen disrupter that causes severe defects in sexual development when a fetus is exposed in utero. Despite being regulated in many countries, excluding the United States, most people have a base level of phthalate contamination despite the fact that it is not a naturally occurring chemical. Elimination of phthalates requires a Phase II metabolic pathway called glucuronidation, which varies both in an individual and between individuals. This pathway is aided by enzymes from the family of uridine 5'-diphospho-glucuronosyltransferases (UGTs), specifically UGT1A1 and UGT2B7, that allow the environmental toxicants to be excreted via urination. If glucuronidation is inhibited by the common over-the-counter drugs (OTCs) investigated in this study, phthalates would remain in the system for extended periods of time as the primary and more toxic metabolite, exacerbating any harmful side effects of this compound in vivo. Though there are several phthalate derivatives, mono(2-ethylhexyl) phthalate (MEHP), mono(ethyl-hydro-hexyl) phthalate (MEHHP) and mono(butyl) phthalate (MbP) and their interactions with UGT2B7 were targeted specifically. Enzyme kinetics were determined using the Michaelis-Menten model (Vmax, Km apparent, and Ki) for UGT2B7. Enzyme activity and inhibition was evaluated via biochemical assays using UGT Corning Supersomes™ and UGT Reaction Mix Solutions A & B. The resulting solutions were then analyzed via Liquid Chromatography Tandem Mass Spectrometry (LC/MS/MS) to determine the levels of glucuronide and substrate.

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Tuesday April 24, 2018 12:00pm - 1:30pm
Sherrill Center Concourse