P 220 - The intracellular metabolites of quercetin derivatives correlate with oxidative stress in hypertrophied 3T3-L1 adipocytes

Quercetin (Q) is one of the most abundant flavonoids in human dietary sources and has demonstrated that might ameliorate obesity-related pathologies. Quercetin-3-glucuronide (Q3GA) is supposed to be the main metabolite in blood circulation, but the intracellular final effectors for its activity are...

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Published inFree radical biology & medicine Vol. 108; p. S94
Main Authors Herranz-López, Maria, Olivares-Vicente, Mariló, Borrás-Linares, Isabel, Barrajón-Catalán, Enrique, Segura-Carretero, Antonio, Micol-Molina, Vicente
Format Journal Article
LanguageEnglish
Published Elsevier Inc 01.07.2017
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Summary:Quercetin (Q) is one of the most abundant flavonoids in human dietary sources and has demonstrated that might ameliorate obesity-related pathologies. Quercetin-3-glucuronide (Q3GA) is supposed to be the main metabolite in blood circulation, but the intracellular final effectors for its activity are still unknown. Here we investigate the uptake and metabolism of quercetin and its metabolite quercetin-3-glucuronide by hypertrophied 3T3-L1 adipocytes and their effect on oxidative stress. Cytoplasmic fractions were obtained and quercetin metabolites were determined by liquid chromatography coupled to a time-of-flight mass detector with electrospray ionization (HPLC-DAD-ESI-TOF). Intracellular ROS generation was measured by a ROS-sensitive fluorescent probe. Both Q and Q3GA were efficiently absorbed by hypertrophied adipocytes and metabolized to some extent to Q3GA and Q, respectively, but Q absorption was more efficient (1.92 ±0.03μg/μg protein) and faster than that of Q3GA (0.12 ±0.0015μg/μg protein), leading to a higher intracellular concentration of the aglycone. The intracellular decrease of ROS in a hypertrophied adipocyte model treated with Q or Q3GA is correlated with the intracellular metabolite for the first time. Both compounds might be able to reach other intracellular targets, thus contributing to their bioactivity.
ISSN:0891-5849
1873-4596
DOI:10.1016/j.freeradbiomed.2017.04.305