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PubMed1998

Supplementation with quercetin markedly increases plasma quercetin concentration without effect on selected risk factors for heart disease in healthy subjects.

The purpose of this double-blind study was to investigate the influence of adding a quercetin-containing supplement to the diet on plasma quercetin status, serum/platelet fatty acid levels and risk factors for heart disease. Healthy men and women with cholesterol levels of 4.0-7.2 mmol/L, consumed four capsules daily of either a quercetin-containing supplement (1.0 g quercetin/d) or rice flour placebo for 28 d. Quercetin intakes were approximately 50-fold greater than the dietary intakes associated with lower coronary heart disease mortality on the basis of epidemiologic studies. Subjects consuming quercetin-containing capsules had plasma quercetin concentrations approximately 23-fold higher than those of subjects consuming the control capsules. Quercetin supplementation did not modify serum total, LDL or HDL cholesterol or triglyceride levels. There were also no alterations of other cardiovascular disease or thrombogenic risk factors, including platelet aggregation, platelet thromboxane B2 production, blood pressure or resting heart rate. Furthermore, there was no effect on the levels of (n-6) or (n-3) polyunsaturated fatty acids in serum or platelet phospholipids. In conclusion, supplementation with quercetin-containing capsules markedly enhanced the plasma quercetin concentration but had no effect on other cardiovascular or thrombogenic risk factors.

Adult↗

PubMed2000

Deglucosidation of quercetin glucosides to the aglycone and formation of antifungal agents by peroxidase-dependent oxidation of quercetin on browning of onion scales.

Outer scales of yellow onion bulbs turn brown during maturing. The brown outer scales contain an antifungal component, 3,4-dihydroxybenzoic acid. An aim of the present study is to elucidate the mechanism of formation of the benzoic acid. In a browning scale, the scale was divided into three areas; fleshy, drying and dried brown areas. Levels of quercetin glucosides in dried brown areas were less than 10% of the glucosides in fleshy and drying areas, whereas levels of quercetin were high in dried brown areas. This result suggests that quercetin was formed by deglucosidation of quercetin glucosides on the border between drying and dried brown areas. Peroxidase (POX) activity of dried brown areas was about 10% of those of fleshy and drying areas. Quercetin was oxidized by autooxidation, and cell-free extracts of drying areas and POX isolated from onion scales enhanced the oxidation even in the absence of externally added hydrogen peroxide. The enhancement of quercetin oxidation was suppressed by catalase. No tyrosinase-like activity was detected in the cell-free extracts and the POX preparation. These results suggest that, during the enhanced oxidation of quercetin, hydrogen peroxide is formed. 3,4-Dihydroxybenzoic acid and 2,4,6-trihydroxyphenylglyoxylic acid, which were the oxidation products of quercetin, were found in dried brown area. These results suggest that an antifungal agent 3,4-dihydroxybenzoic acid is formed by POX-dependent oxidation of quercetin on browning of onion scales.

Antifungal Agents↗

PubMed2004

Anti- and pro-oxidant effects of quercetin in copper-induced low density lipoprotein oxidation. Quercetin as an effective antioxidant against pro-oxidant effects of urate.

We recently reported that, depending on its concentration, urate is either a pro- or an antioxidant in Cu(2+)-induced low-density lipoprotein (LDL) oxidation. We also previously demonstrated an antioxidant synergy between urate and some flavonoids in the Cu(2+)-induced oxidation of diluted serum. As a result, the effect of the flavonoid quercetin on the Cu(2+)-induced oxidation of isolated LDL has been studied either in the presence or absence of urate. We demonstrate that, like urate, quercetin alone, at low concentration, exhibits a pro-oxidant activity. The pro-oxidant behavior depends on the Cu(2+) concentration but it is not observed at high Cu(2+) concentration. When compared with urate, the switch between the pro- and the antioxidant activities occurs at much lower quercetin concentrations. As for urate, the pro-oxidant character of quercetin is related to its ability to reduce Cu(2+) with the formation of semioxidized quercetin and Cu(+) with an expected yield larger than that obtained with urate owing to a more favorable redox potential. It is also shown that the pro-oxidant activity of urate can be inhibited by quercetin. An electron transfer between quercetin and semioxidized urate leading to the repair of urate could account for this observation as suggested by recently published pulse radiolysis data. It is anticipated that the interactions between quercetin-Cu(2+)-LDL and urate, which are tightly controlled by their respective concentration, determine the balance between the pro- and antioxidant behaviors. Moreover, as already observed with other antioxidants, it is demonstrated that quercetin alone behaves as a pro-oxidant towards preoxidized LDL.

Alkenes↗

PubMed2001

Inhibition of nitric oxide synthase inhibitors and lipopolysaccharide induced inducible NOS and cyclooxygenase-2 gene expressions by rutin, quercetin, and quercetin pentaacetate in RAW 264.7 macrophages.

Several natural flavonoids have been demonstrated to perform some beneficial biological activities, however, higher-effective concentrations and poor-absorptive efficacy in body of flavonoids blocked their practical applications. In the present study, we provided evidences to demonstrate that flavonoids rutin, quercetin, and its acetylated product quercetin pentaacetate were able to be used with nitric oxide synthase (NOS) inhibitors (N-nitro-L-arginine (NLA) or N-nitro-L-arginine methyl ester (L-NAME)) in treatment of lipopolysaccharide (LPS) induced nitric oxide (NO) and prostaglandin E2 (PGE2) productions, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) gene expressions in a mouse macrophage cell line (RAW 264.7). The results showed that rutin, quercetin, and quercetin pentaacetate-inhibited LPS-induced NO production in a concentration-dependent manner without obvious cytotoxic effect on cells by MTT assay using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide as an indicator. Decrease of NO production by flavonoids was consistent with the inhibition on LPS-induced iNOS gene expression by western blotting. However, these compounds were unable to block iNOS enzyme activity by direct and indirect measurement on iNOS enzyme activity. Quercetin pentaacetate showed the obvious inhibition on LPS-induced PGE2 production and COX-2 gene expression and the inhibition was not result of suppression on COX-2 enzyme activity. Previous study demonstrated that decrease of NO production by L-arginine analogs effectively stimulated LPS-induced iNOS gene expression, and proposed that stimulatory effects on iNOS protein by NOS inhibitors might be harmful in treating sepsis. In this study, NLA or L-NAME treatment stimulated significantly on LPS-induced iNOS (but not COX-2) protein in RAW 264.7 cells which was inhibited by these three compounds. Quercetin pentaacetate, but not quercetin and rutin, showed the strong inhibitory activity on PGE2 production and COX-2 protein expression in NLA/LPS or L-NAME/LPS co-treated RAW 264.7 cells. These results indicated that combinatorial treatment of L-arginine analogs and flavonoid derivates, such as quercetin pentaacetate, effectively inhibited LPS-induced NO and PGE2 productions, at the same time, inhibited enhanced expressions of iNOS and COX-2 genes.

Animals↗

PubMed2006

Quercetin-dependent scavenging of reactive nitrogen species derived from nitric oxide and nitrite in the human oral cavity: interaction of quercetin with salivary redox components.

In the human oral cavity, nitrite is reduced to nitric oxide (NO) by certain bacteria. The NO formed reacts with O2 to generate NO2 and then with NO2 producing N2O3. In this study, N2O3 produced by the reaction between NO and NO2 was detected by fluorescence increase due to the transformation of 4,5-diaminofluorescein to fluorescent triazolfluorescein. Nitrite-induced fluorescence increase in the bacterial fraction of saliva was completely inhibited by 1muM quercetin and the complete inhibition continued until almost all quercetin had been oxidized. Nitrite-induced fluorescence increase was also observed in the saliva which contained salivary redox components. Quercetin effectively inhibited the fluorescence increase. During the inhibition of the fluorescence increases by quercetin, the flavonol was oxidized. NO2 seemed to participate in the oxidation. The main oxidation product was 2-(3,4-dihydroxybenzoyl)-2,4,6-trihydroxy-3(2H)-benzofurane. Thiocyanate inhibited the fluorescence increase in bacterial fraction and duration of the complete inhibition by quercetin was prolonged by SCN-. The inhibition and the prolongation are discussed to be due to SCN--dependent inhibition of oxidation of nitrite to NO2 by salivary peroxidase. Quercetin cooperated with ascorbate to inhibit the fluorescence increase. From the results obtained in this study, it is deduced (1) that quercetin can protect human oral cavity from damages induced by reactive nitrogen species and (2) that the protective function of quercetin may be significant when antioxidant capacity of saliva is decreased by periodontal diseases.

Adult↗

PubMed2003

Quercetin-dependent reduction of salivary nitrite to nitric oxide under acidic conditions and interaction between quercetin and ascorbic acid during the reduction.

A salivary component, nitrate, is reduced to nitrite in the oral cavity. Polyphenols in foods are mixed with nitrite in the saliva to be swallowed into the stomach. An objective of the present study is to elucidate reactions between a polyphenol quercetin and a nitrite under acidic conditions. Nitric oxide, which is formed by the reactions between nitrous acid and quercetin or ascorbic acid (AA), can be measured using an oxygen electrode in the saliva as well as a buffer solution. The initial oxidation of quercetin was inhibited by AA, and quercetin enhanced the oxidation of AA, suggesting AA-dependent reduction of quercetin radicals, which might be formed during the oxidation of quercetin by nitrous acid. On the basis of the above results, the usefulness of an oxygen electrode for the measurement of nitrite-dependent nitric oxide formation under acidic conditions is proposed and the possible mechanism of reduction of nitrous acid by quercetin and the interaction between quercetin and AA, which is a normal component in the gastric juice, for the reduction of nitrous acid is discussed.

Ascorbic Acid↗

PubMed2005

A synthetic approach to the generation of quercetin sulfates and the detection of quercetin 3'-O-sulfate as a urinary metabolite in the rat.

To study the biological effects of quercetin, authentic products of quercetin metabolism are required as standards. The synthesis of quercetin sulfate standards is thus described. Quercetin was reacted with a 10-fold molar excess of sulfur trioxide-N-triethylamine, and the products were analyzed by HPLC and mass spectrometry. Four monosulfates and three disulfates were identified, and structural inferences were drawn by 1H NMR spectrometry of HPLC peak isolates. Analysis of the urine of rats that had received quercetin (1.9 g/kg po) yielded a single peak, which by comparison with the products of the reaction between quercetin and sulfur trioxide-N-triethylamine was identified as quercetin 3'-O-sulfate.

Animals↗

PubMed2005

Protection by quercetin and quercetin-rich fruit juice against induction of oxidative DNA damage and formation of BPDE-DNA adducts in human lymphocytes.

Flavonoids are claimed to protect against cardiovascular disease, certain forms of cancer and ageing, possibly by preventing initial DNA damage. Therefore, we investigated the protective effects of the flavonoid quercetin against the formation of oxidative DNA damage and bulky DNA adducts in human lymphocytes, both in vitro and ex vivo. First, human lymphocytes were pre-incubated with various concentrations of quercetin, followed by incubation with hydrogen peroxide; protection against oxidative DNA damage was evaluated by use of the single-cell gel electrophoresis (Comet) assay. Second, quercetin-treated human lymphocytes were challenged by treatment with benzo(a)pyrene (B(a)P), and BPDE-DNA adduct formation was measured by (32)P-postlabelling. Third, in a pilot study, lymphocytes from female volunteers who consumed a quercetin-rich blueberry/apple juice mixture for four weeks, were treated ex vivo with an effective dose of H(2)O(2) and benzo(a)pyrene, respectively, at three different time points, i.e. before (t=0 weeks), during (t=2 weeks) and after (t=4 weeks) the intervention. Results in vitro: a significant dose-dependent protection by quercetin against both the formation of oxidative DNA damage (p<0.01) and of BPDE-DNA adducts (p<0.05) was observed. Results in vivo: four weeks of juice intervention led to a significant increase in the total antioxidant capacity of plasma, as reflected by the increase of the TEAC value from 773 microM trolox equivalent at t=0 to 855 microM at t=4 weeks (p=0.04) and an increase in plasma quercetin content from 5.0 to 10.6 nM (p=0.03). After intervention, the level of oxidative damage upon ex vivo exposure to H(2)O(2) was non-significantly (p=0.07) decreased by 41%, and the BPDE-DNA adduct level induced ex vivo was non-significantly decreased by 11%. The combination of our findings in vitro and ex vivo provides evidence that quercetin is able to protect against chemically induced DNA damage in human lymphocytes, which may underlie its suggested anticarcinogenic properties.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

PubMed2002

Oxidation of quercetin by salivary components. Quercetin-dependent reduction of salivary nitrite under acidic conditions producing nitric oxide.

Under acidic conditions, nitrite is protonated to nitrous acid (pK(a) = 3.2-3.4) that can be transformed into nitric oxide by self-decomposition and reduction. When sodium nitrite was mixed with quercetin at pH 1-2, quercetin was oxidized producing nitric oxide. In addition to quercetin, kaempferol and quercetin 4'-glucoside were also oxidized by nitrous acid, but oxidation of apigenin, luteolin, and rutin was slow compared to oxidation of the above flavonols. These results suggested that flavonols, which have a free hydroxyl group at carbon position 3, can readily reduce nitrous acid to nitric oxide. When the pH of saliva was decreased to 1-2, formation of nitric oxide was observed. The nitric oxide formation was enhanced by quercetin, and during this process quercetin was oxidized. These results indicate that there is a possibility of reactions between phenolics and nitrous acid derived from salivary nitrite in the stomach.

Flavonoids↗

PubMed1997

Induction of an adaptive response to quercetin, mitomycin C and hydrogen peroxide by low doses of quercetin in V79 Chinese hamster cells.

The adaptive response is a phenomenon by which cells exposed to low, non-cytotoxic doses of a genotoxicant become significantly resistant to a subsequent higher dose of the same or another genotoxic agent. Induction of the adaptive response has been mainly studied using ionizing radiation and alkylating agents as genotoxic agents. However, other mutagenic agents may warrant further study, since the adaptive response as a whole may be an important general biological mechanism to maintain genetic integrity and thus could prevent carcinogenic initiation of cells. The exposure to mutagenic agents present, or formed, in the diet is considered an important factor in the etiology of human tumors and a considerable number of these agents have not yet been identified or characterized. Flavonoids are a large group of polyphenolic quinoids found in a wide variety of edible fruits and vegetables and a few, such as quercetin, present genotoxic activity in vitro. The mechanisms of mutagenicity of quercetin involve the production of oxygen radicals through an autoxidation process dependent on pH value and the presence of oxygen. Although there are few doubts regarding the mutagenicity of quercetin in vitro, carcinogenicity of flavonoid is still controversial. In view of these conflicting results and the radiomimetic nature of the mutagenicity of flavonoids, we addressed the question of cell exposure to quercetin at the low levels present in the diet leading to adaptation to further exposure to mutagens or carcinogens. The work reported here concerns induction of an adaptive response by low doses of quercetin to challenging doses of quercetin and other compounds, namely hydrogen peroxide and mitomycin C, using induction of chromosomal aberrations in V79 cells as the end point.

Adaptation, Physiological↗

PubMed2005

Liquid chromatography-tandem mass spectroscopy assay for quercetin and conjugated quercetin metabolites in human plasma and urine.

A sensitive and specific method was developed and validated for the quantitation of quercetin in human plasma and urine. The application of liquid chromatography-tandem mass spectrometry (LC/MS/MS) with a TurboIonspray (TIS) interface in negative mode under multiple reactions monitoring was investigated. Chromatographic separation was achieved on a C12 column using a mobile phase of acetonitrile/water with 0.2% formic acid (pH 2.4) (40/60, v/v). The detection limit was 100 pg/ml and the lower limit of quantification was 500 pg/ml for plasma samples; the detection limit was 500 pg/ml and the lower limit of quantification was 1 ng/ml for urine samples. The calibration curve was linear from 1 to 800 ng/ml for plasma samples and was linear from 1 to 200 and 50 to 2000 ng/ml for urine samples. All the intra- and inter-day coefficients of variation were less than 11% and intra- and inter-day accuracies were within +/-15% of the known concentrations. This represents a LC/MS/MS assay with the sensitivity and specificity necessary to determine quercetin in human plasma and urine. This assay was used to determine both parent quercetin and the quercetin after enzymatic hydrolysis with beta-glucuronidase/sulfatase in human plasma and urine samples following the ingestion of quercetin 500 mg capsules.

Calibration↗

PubMed2001

Inhibitory effect of a quercetin metabolite, quercetin 3-O-beta-D-glucuronide, on lipid peroxidation in liposomal membranes.

To study the antioxidant activity of quercetin 3-O-beta-D-glucuronide (Q3GA), which is one of the quercetin metabolites in the blood after intake of quercetin-rich food, the inhibitory effect of Q3GA on lipid peroxidation was estimated using phosphatidylcholine large unilamellar vesicles (PC LUV) as a biomembrane model. Iron ion, an aqueous peroxyl radical generator, a peroxynitrite generator, or lipoxygenase was used as the inducer of lipid peroxidation. In all cases, Q3GA inhibited lipid peroxidation significantly, although its inhibitory effect was lower than that of quercetin aglycon. The ultrafiltration of PC LUV containing Q3GA revealed that Q3GA has low but significant affinity with the membranes of phospholipid bilayers. It is therefore likely that Q3GA acts as an efficient antioxidant in membranous lipid peroxidation through its localization in the phospholipid bilayer. This conjugated quercetin metabolite seems to retain the ability to protect cellular and subcellular membranes from peroxidative attack by reactive oxygen species and peroxidative enzymes.

Arachidonate 15-Lipoxygenase↗

PubMed2004

Quercetin-4'-glucoside is more potent than quercetin-3-glucoside in protection of rat intestinal mucosa homogenates against iron ion-induced lipid peroxidation.

Quercetin is a typical antioxidative flavonoid found in vegetables, which is more commonly present as its glucosides, quercetin-3-glucoside (Q3G) and quercetin-4'-glucoside (Q4'G). The main aim of this study was to estimate the antioxidant activity of Q3G and Q4'G on iron ion-driven lipid peroxidation of the gastrointestinal mucosa. Q4'G markedly suppressed the lipid peroxidation when rat gastrointestinal mucosa homogenates were incubated with Fe(NO3)3 and ascorbic acid. Its effectiveness was greater as compared to that of Q3G and comparable to that of quercetin aglycone. Furthermore, Q4'G yielded higher amounts of quercetin aglycone than Q3G on incubation with the homogenates. However, Q4'G showed a lower chelating activity in comparison to Q3G. These results indicate that Q4'G, even though it has a low chelating activity, because of its efficient conversion to antioxidative aglycone on exposure to the mucosa, can act as a powerful antioxidant on iron ion driven lipid peroxidation in the intestinal mucosa. Thus, vegetables rich in Q4'G, such as onion, are likely to serve as favorable antioxidant sources for suppressing iron-induced oxidative stress in the intestinal tract.

Animals↗

PubMed2005

Quercetin-dependent inhibition of nitration induced by peroxidase/H2O2/nitrite systems in human saliva and characterization of an oxidation product of quercetin formed during the inhibition.

Local pH in the oral cavity can decrease to below 7 at the site where acid-producing bacteria are proliferating. Effects of pH on nitration of 4-hydroxyphenylacetic acid were studied using dialyzed human saliva. Dialyzed saliva nitrated 4-hydroxyphenylacetic acid to 4-hydroxy-3-nitrophenylacetic acid in the presence of nitrite and H(2)O(2). The rate of the nitration was dependent on pH, and the maximal rate was observed between pH 5.5 and 7.2. The optimum pH seemed to reflect rates of formation of nitrogen dioxide and 4-hydroxyphenylacetic acid radicals. Quercetin inhibited the nitration. The quercetin-dependent inhibition might be due to scavenging of nitrogen dioxide and 4-hydroxyphenylacetic acid radicals, which were formed by salivary peroxidase-dependent oxidation of nitrite and 4-hydroxyphenylacetic acid, respectively, and competition with nitrite and 4-hydroxyphenylacetic acid for peroxidase in saliva. An oxidation product of quercetin was formed during inhibition of the nitration by quercetin. The oxidation product was identified as 2-(3,4-dihydroxybenzoyl)-2,4,6-trihydroxy-3(2H)-benzofuranone. This component could also be oxidized by salivary peroxidase and nitrogen dioxide radicals. The oxidation products were 2,4,6-trihydroxyphenylglyoxylic and 3,4-dihydroxybenzoic acids. On the basis of the results, the significance of quercetin for inhibition of nitrogen dioxide formation and for scavenging of nitrogen dioxide radicals in the oral cavity is discussed.

Humans↗

PubMed2006

In vitro degradation of the flavonol quercetin and of quercetin glycosides in the porcine hindgut.

The present study investigated the microbial degradation of the plant flavonol quercetin and its naturally occurring glycosides isoquercitrin and rutin in the porcine hindgut. The experiments were carried out with the semicontinuous colon-simulation technique. The fluid and particle phase of pig hindgut contents from freshly slaughtered animals were used for the in vitro incubations. Following a five-day equilibration period, quercetin, isoquercitrin or rutin were administered to fermentation vessels and their turnover rate was determined. None of the flavonols affected parameters of microbial fermentation like pH, redox potential or VFA production. The turnover rate for isoquercitrin was seven times higher than the turnover for the fermentation fluid. The turnover rates for quercetin and rutin were four and twofold higher than fluid turnover, respectively. After administration of isoquercitrin or rutin, their aglycone quercetin was detected as an intermediary metabolite. Under sterile conditions using autoclaved incubation fluids and hindgut contents, turnover rates for quercetin and rutin were still higher than the fluid turnover in the fermentation vessels. This indicates a certain chemical instability of the flavonols and/or adsorption to ingesta particles. Thus, flavonols are subjected to microbial metabolism in the porcine hindgut. The glycosidic structure strongly influences the rate of metabolism.

Adsorption↗

PubMed2005

The reversibility of the glutathionyl-quercetin adduct spreads oxidized quercetin-induced toxicity.

Quercetin is one of the most prominent dietary antioxidants. During its antioxidant activity, quercetin becomes oxidized into its o-quinone/quinone methide QQ. QQ is toxic since it instantaneously reacts with thiols of, e.g., proteins. In cells, QQ will initially form an adduct with glutathione (GSH), giving GSQ. We have found that GSQ is not stable; it dissociates continuously into GSH and QQ with a half life of 2min. Surprisingly, GSQ incubated with 2-mercapto-ethanol (MSH), a far less reactive thiol, results in the conversion of GSQ into the MSH-adduct MSQ. A similar conversion of GSQ into relatively stable protein thiol-quercetin adducts is expected. With the dithiol dihydrolipoic acid (L(SH)(2)), quercetin is formed out of GSQ. These results indicate that GSQ acts as transport and storage of QQ. In that way, the initially highly focussed toxicity of QQ is dispersed by the formation of GSQ that finally spreads QQ-induced toxicity, probably even over cells.

Glutathione↗

PubMed2004

Molecular imaging of the biological effects of quercetin and quercetin-rich foods.

The human diet contains several thousands of organic plant molecules (i.e. phytochemicals), many of which have significant bioactivities. The specific physiological effects of these compounds are impossible to predict from in vitro studies using cell cultures and cell-free model systems. Nutrigenomics, which may be defined as the application of genomic tools to study the integrated effects of nutrients on gene regulation, however, holds great promise in increasing the understanding of how nutrients affect molecular events in an organism. Quercetin, a phytochemical belonging to the flavonoids, has antioxidant activities, inhibit protein kinases, inhibit DNA topoisomerases and regulate gene expression. The aim of the present review is to describe some of the many effects of quercetin, and how molecular imaging using transgenic reporter mice may serve as a tool to study the integrated influence of quercetin and other dietary phytochemicals on gene expression in vivo. We are using the bioluminescence emitted from firefly luciferase as the reporter since light originating from the inside of a cell or organism can be detected externally in an intact living organism. Molecular imaging using reporter models is therefore a unique technology to study the integrated effects of environmental insults and dietary substances on the influence of gene expression in disease development. We utilize these in vivo models to elucidate the role of various flavonoids, such as quercetin, for modulating gene expression related to oxidative stress and the antioxidant defence system.

Animals↗

PubMed2003

Oxidized quercetin reacts with thiols rather than with ascorbate: implication for quercetin supplementation.

When an antioxidant scavenges a reactive species, i.e., when it exerts its antioxidant activity, the antioxidant is converted into potentially harmful oxidation products. In this way, the antioxidant quercetin might yield an ortho-quinone, denoted as QQ, which has four tautomeric forms, i.e., the ortho-quinone and three quinonmethides. We evaluated the interaction of QQ with ascorbate or glutathione (GSH). Ascorbate recycles QQ to the parent compound quercetin, while GSH forms two adducts with QQ, i.e., 6-GSQ and 8-GSQ. When both GSH and ascorbate are present, QQ is converted exclusively into GSQ. In the absence of GSH, protein thiols will be arylated by QQ. This protein arylation is not prevented by ascorbate. Thiol arylation by quinones and quinonmethides can impair several vital enzymes. This implies that the product formed when quercetin displays its antioxidant scavenging effect is toxic in the absence of GSH. Therefore, an adequate GSH level should be maintained when quercetin is supplemented.

Antioxidants↗