Quercetin inhibits advanced glycation end product formation via chelating metal ions, trapping methylglyoxal, and trapping reactive oxygen species. Issue 5 (4th May 2017)

• Record Type: Journal Article
• Authors: Bhuiyan, Mohammad Nazrul Islam; Mitsuhashi, Shinya; Sigetomi, Kengo; Ubukata, Makoto
• Is Part Of: Bioscience, biotechnology, and biochemistry. Volume 81:Issue 5(2017)
• Page Start: 882
• Page End: 890
• Publication Date: 2017-05-04
• Subjects: advanced glycation end products (AGEs) -- chelation effect -- trapping ROS (reactive oxygen species) -- trapping MGO (methylglyoxal) -- hemiacetal form of di-MGO adduct; Biotechnology -- Periodicals; Biochemistry -- Periodicals; 660.6
• DOI: 10.1080/09168451.2017.1282805
• Languages: English
• ISSNs: 0916-8451

Abstract

Abstract: Physiological concentration of Mg 2+, Cu 2+, and Zn 2+ accelerated AGE formation only in glucose-mediated conditions, which was effectively inhibited by chelating ligands. Only quercetin (10) inhibited MGO-mediated AGE formation as well as glucose- and ribose-mediated AGE formation among 10 polyphenols (1–10 ) tested. We performed an additional structure-activity relationship (SAR) study on flavanols (10, 11, 12, 13, and 14 ). Morin (12 ) and kaempherol (14 ) showed inhibitory activity against MGO-mediated AGE formation, whereas rutin (11 ) and fisetin (13 ) did not. These observations indicate that 3, 5, 7, 4′-tetrahydroxy and 4-keto groups of 10 are important to yield newly revised mono-MGO adducts (16 and 17 ) and di-MGO adduct (18 ) having cyclic hemiacetals, while 3′-hydroxy group is not essential. We propose here a comprehensive inhibitory mechanism of 10 against AGE formation including chelation effect, trapping of MGO, and trapping of reactive oxygen species (ROS), which leads to oxidative degradation of 18 to 3, 4-dihydroxybenzoic acid (15 ) and other fragments. Graphical abstract: : Inhibitory mechanism of quercetin against glucose-, ribose-, and MGO-mediated AGE formation and structures of MGO-quercetin adducts were elucidated.