Structure–Activity Relationship and Prediction of the Electron‐Transfer Potential of the Xanthones Series

Li, Xican; Jiang, Qian; Chen, Dong Feng; Luo, Xin

doi:10.1002/open.201800108

Cited by 11 publications

(8 citation statements)

References 59 publications

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“…Besides the 3- O -galactosylation process, other structural factors may also affect the antioxidant activity of phytophenols, such as C -glycosidation, glucuronidation, isoprenylation, methylation, geometrical configuration, and p -coumaroylation [32,52,53,54,55,56]. However, the effects of all these structural factors were thought to be concentrated in the propagation step.…”

Section: Resultsmentioning

confidence: 99%

Comparative Analysis of Radical Adduct Formation (RAF) Products and Antioxidant Pathways between Myricetin-3-O-Galactoside and Myricetin Aglycone

Ouyang

Liang

et al. 2019

Molecules

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The biological process, 3-O-galactosylation, is important in plant cells. To understand the mechanism of the reduction of flavonol antioxidative activity by 3-O-galactosylation, myricetin-3-O-galactoside (M3OGa) and myricetin aglycone were each incubated with 2 mol α,α-diphenyl-β-picrylhydrazyl radical (DPPH•) and subsequently comparatively analyzed for radical adduct formation (RAF) products using ultra-performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight tandem mass spectrometry (UPLC-ESI-Q-TOF-MS) technology. The analyses revealed that M3OGa afforded an M3OGa–DPPH adduct (m/z 873.1573) and an M3OGa–M3OGa dimer (m/z 958.1620). Similarly, myricetin yielded a myricetin–DPPH adduct (m/z 711.1039) and a myricetin–myricetin dimer (m/z 634.0544). Subsequently, M3OGa and myricetin were compared using three redox-dependent antioxidant analyses, including DPPH•-trapping analysis, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide radical (PTIO•)-trapping analysis, and •O2 inhibition analysis. In the three analyses, M3OGa always possessed higher IC50 values than those of myricetin. Conclusively, M3OGa and its myricetin aglycone could trap the free radical via a chain reaction comprising of a propagation step and a termination step. At the propagation step, both M3OGa and myricetin could trap radicals through redox-dependent antioxidant pathways. The 3-O-galactosylation process, however, could limit these pathways; thus, M3OGa is an inferior antioxidant compared to its myricetin aglycone. Nevertheless, 3-O-galactosylation has a negligible effect on the termination step. This 3-O-galactosylation effect has provided novel evidence that the difference in the antioxidative activities of phytophenols exists at the propagation step rather than the termination step.

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Section: Resultsmentioning

confidence: 99%

Comparative Analysis of Radical Adduct Formation (RAF) Products and Antioxidant Pathways between Myricetin-3-O-Galactoside and Myricetin Aglycone

Ouyang

Liang

et al. 2019

Molecules

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“…From the perspective of redox chemistry, quercetin ortho-quinone is virtually an oxidized form of quercetin. The ortho-quinone moiety can be achieved through catechol oxidation by multiple pathways, including electron-transfer (ET) plus proton-transfer (PT) [75][76][77][78], hydrogen-abstraction [79][80][81], the ET pathway alone [82][83][84], or even enzymatic oxidation [25,26]. Therefore, it is very difficult for quercetin ortho-quinone to be further oxidized, suggesting that quercetin ortho-quinone is a weak antioxidant [79].…”

Section: Resultsmentioning

confidence: 99%

“…The co-existence and high relevance between catecholic flavonols and the Diels-Alder dimers have further indicated that the Diels-Alder dimers were the metabolites of catecholic flavonols in plants. During plant metabolism, quite a few factors can oxidize catecholic moieties to orthoquinone, including bio-enzymes (e.g., catechol oxidase and aurone synthase) [25,26,85], iron [83,86], LPO [86], and free radicals [75]. Of these, iron and LPO are relevant to ferroptosis.…”

Section: Resultsmentioning

confidence: 99%

“…Undoubtedly, the formation of ortho-quinone with π-π conjugation has facilitated Diels-Alder dimerization reactions [22][23][24]27,70,71,72]. During plant metabolism, quite a few factors can oxidize catecholic moieties to ortho-quinone, including bio-enzymes (e.g., catechol oxidase and aurone synthase) [25,26,85], iron [83,86], LPO [86], and free radicals [75]. Of these, iron and LPO are relevant to ferroptosis.…”

Section: Resultsmentioning

confidence: 99%

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Inhibitory Effect and Mechanism of Action of Quercetin and Quercetin Diels-Alder anti-Dimer on Erastin-Induced Ferroptosis in Bone Marrow-Derived Mesenchymal Stem Cells

Zeng

Liu

et al. 2020

Antioxidants

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In this study, the anti-ferroptosis effects of catecholic flavonol quercetin and its metabolite quercetin Diels-Alder anti-dimer (QDAD) were studied using an erastin-treated bone marrow-derived mesenchymal stem cell (bmMSCs) model. Quercetin exhibited higher anti-ferroptosis levels than QDAD, as indicated by 4,4-difluoro-5-(4-phenyl-1,3-butadienyl)-4-bora-3a,4a-diaza-s-indacene-3-undecanoic acid (C11-BODIPY), 2′,7′-dichlorodihydrofluoroscein diacetate (H2DCFDA), lactate dehydrogenase (LDH) release, cell counting kit-8 (CCK-8), and flow cytometric assays. To understand the possible pathways involved, the reaction product of quercetin with the 1,1-diphenyl-2-picrylhydrazyl radical (DPPH●) was measured using ultra-performance liquid-chromatography coupled with electrospray-ionization quadrupole time-of-flight tandem mass spectrometry (UHPLC-ESI-Q-TOF-MS). Quercetin was found to produce the same clusters of molecular ion peaks and fragments as standard QDAD. Furthermore, the antioxidant effects of quercetin and QDAD were compared by determining their 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide radical-scavenging, Cu2+-reducing, Fe3+-reducing, lipid peroxidation-scavenging, and DPPH●-scavenging activities. Quercetin consistently showed lower IC50 values than QDAD. These findings indicate that quercetin and QDAD can protect bmMSCs from erastin-induced ferroptosis, possibly through the antioxidant pathway. The antioxidant pathway can convert quercetin into QDAD—an inferior ferroptosis-inhibitor and antioxidant. The weakening has highlighted a rule for predicting the relative anti-ferroptosis and antioxidant effects of catecholic flavonols and their Diels-Alder dimer metabolites.

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“…A hydrogen atom is abstracted from the butein-4-O-radical by excess DPPH • to form butein quinone ( Figure 4A). Finally, the catechol moiety is easily oxidized to quinone [65][66][67][68][69]. However, some of the butein-4-O-radicals can produce a butein dimer, through radical resonance, radical adduct formation, and subsequent keto-enol tautomerization [8] ( Figure 5A).…”

Section: Resultsmentioning

confidence: 99%

Simultaneous Study of Anti-Ferroptosis and Antioxidant Mechanisms of Butein and (S)-Butin

Liu

Cai

et al. 2020

Molecules

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To elucidate the mechanism of anti-ferroptosis and examine structural optimization in natural phenolics, cellular and chemical assays were performed with 2′-hydroxy chalcone butein and dihydroflavone (S)-butin. C11-BODIPY staining and flow cytometric assays suggest that butein more effectively inhibits ferroptosis in erastin-treated bone marrow-derived mesenchymal stem cells than (S)-butin. Butein also exhibited higher antioxidant percentages than (S)-butin in five antioxidant assays: linoleic acid emulsion assay, Fe3+-reducing antioxidant power assay, Cu2+-reducing antioxidant power assay, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide radical (PTIO•)-trapping assay, and α,α-diphenyl-β-picrylhydrazyl radical (DPPH•)-trapping assay. Their reaction products with DPPH• were further analyzed using ultra-performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight tandem mass spectrometry (UPLC-ESI-Q-TOF-MS). Butein and (S)-butin produced a butein 5,5-dimer (m/z 542, 271, 253, 225, 135, and 91) and a (S)-butin 5′,5′-dimer (m/z 542, 389, 269, 253, and 151), respectively. Interestingly, butein forms a cross dimer with (S)-butin (m/z 542, 523, 433, 419, 415, 406, and 375). Therefore, we conclude that butein and (S)-butin exert anti-ferroptotic action via an antioxidant pathway (especially the hydrogen atom transfer pathway). Following this pathway, butein and (S)-butin yield both self-dimers and cross dimers. Butein displays superior antioxidant or anti-ferroptosis action to (S)-butin. This can be attributed the decrease in π-π conjugation in butein due to saturation of its α,β-double bond and loss of its 2′-hydroxy group upon biocatalytical isomerization.

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Structure–Activity Relationship and Prediction of the Electron‐Transfer Potential of the Xanthones Series

Cited by 11 publications

References 59 publications

Comparative Analysis of Radical Adduct Formation (RAF) Products and Antioxidant Pathways between Myricetin-3-O-Galactoside and Myricetin Aglycone

Comparative Analysis of Radical Adduct Formation (RAF) Products and Antioxidant Pathways between Myricetin-3-O-Galactoside and Myricetin Aglycone

Inhibitory Effect and Mechanism of Action of Quercetin and Quercetin Diels-Alder anti-Dimer on Erastin-Induced Ferroptosis in Bone Marrow-Derived Mesenchymal Stem Cells

Simultaneous Study of Anti-Ferroptosis and Antioxidant Mechanisms of Butein and (S)-Butin

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