rutin and isoquercitrin

Flavonols play key roles in many plant defense mechanisms, consequently they are frequently investigated as stress sensitive factors in relation to several oxidative processes. It is well known that grapevine (Vitis vinifera L.) can synthesize various flavonol glycosides in the leaves, however, very little information is available regarding their distribution along the cane at different leaf levels. In this work, taking into consideration of leaf position, the main flavonol glycosides of a red grapevine cultivar (Cabernet Sauvignon) were profiled and quantified by HPLC-DAD analysis. It was found that amount of four flavonol glycosides, namely, quercetin-3-O-galactoside, quercetin-3-O-glucoside, kaempferol-3-O-glucoside and kaempferol-3-O-glucuronide decreased towards the shoot tip. Since leaf age also decreases towards the shoot tip, the obtained results suggest that these compounds continuously formed by leaf aging, resulting in their accumulation in the older leaves. In contrast, quercetin-3-O-glucuronide (predominant form) and quercetin-3-O-rutinoside were not accumulated significantly by aging. We also pointed out that grapevine boosted the flavonol biosynthesis in September, and flavonol profile differed significantly in the two seasons. Our results contribute to the better understanding of the role of flavonols in the antioxidant defense system of grapevine.

Topics: Chromatography, High Pressure Liquid; Flavonols; Fruit; Glucosides; Glucuronides; Glycosides; Kaempferols; Monosaccharides; Plant Leaves; Quercetin; Seasons; Vitis

The natural flavonoid quercetin is a low affinity ligand of the aryl hydrocarbon receptor (AhR), a transcription factor regulating the expression of cytochrome P450 (CYP) 1A enzymes. This study examined the ability of quercetin, isoquercitrin (quercetin-3-O-glucoside), rutin (quercetin-3-O-rutinoside) and taxifolin (dihydroquercetin) to activate AhR and to induce CYP1A1 expression in human hepatoma HepG2 cells. Gene reporter assays showed that quercetin significantly activated AhR and triggered CYP1A1 transcription after 24 h exposure. These effects were, however, much lower than those of 2,3,7,8-tetrachlorodibenzo-p-dioxin, a prototypical AhR ligand. Quercetin also induced a significant increase in CYP1A1 mRNA levels together with a moderate increase in the level of CYP1A1 activity. In contrast, isoquercitrin and rutin had negligible effects on AhR activity and CYP1A1 expression. Taxifolin at the highest concentration tested (50 µm) produced a mild non-significant increase in AhR activity and CYP1A1 transcription. Taxifolin also significantly increased CYP1A1 mRNA expression, but this effect was approximately 15 times weaker than that of quercetin and was not accompanied by induction of CYP1A1 activity. It is concluded that quercetin, but not its 3-O-glycosides isoquercitrin and rutin, induces AhR activation and CYP1A1 expression in HepG2 cells and that the CYP1A1-inducing activity of taxifolin has a low toxicological potential.

Topics: Cytochrome P-450 CYP1A1; Glucosides; Hep G2 Cells; Humans; Quercetin; Receptors, Aryl Hydrocarbon; Rutin