Antioxidant Effects Of Quercetin Research Articles

Biochemical profiling of metabolomics in heavy metal-intoxicated impaired metabolism and its amelioration using plant-based bioactive compound

Exposure to Pb is widely spreading and has far-reaching negative effects on living systems. This study aimed to investigate the toxic effects of Pb, through biochemical profiling and the ameliorative effects of quercetin against Pb-toxicity. Twenty-five male Wistar albino mice were divided into the following five groups. The CON-group received normal saline; the Pb-group received PbAc; the Pb + Q-CRN group received lead acetate followed by quercetin; the Q-CRN group received quercetin; and the CRN group received corn oil. After 4weeks, the mice were euthanized. It was speculated that Pb significantly increased the levels of serine, threonine, and asparagine and decreased the levels of valine, lysine, and glutamic acid in the plasma of Pb-group, thus impairing amino acid metabolism. However, in the Pb + Q-CRN group, the level of these six amino acids was restored significantly due to the ameliorative effect of quercetin. The presence of lipid metabolites (L-carnitine, sphinganine, phytosphingosine, and lysophosphatidylcholine) in mice serum was confirmed by ESI/MS. The GPx, SOD, GSH, and CAT levels were significantly decreased, and the MDA level was significantly increased, thus confirming the oxidative stress and lipid peroxidation in the Pb group. The antioxidant effect of quercetin was elucidated in the Pb + Q-CRN group. Expression of CPT-I, CPT-II, LCAT, CROT, CACT, and MTR genes was significantly upregulated in the liver of Pb goup mice. Hence, the findings of this study proved that Pb exposure induced oxidative stress, upregulated gene expression, and impaired the lipid and amino acid metabolism in mice.

Quercetin as an inhibitor of hemoglobin-mediated lipid oxidation: Mechanisms of action and use of molecular docking

The antioxidant effect of quercetin on hemoglobin(Hb)-mediated lipid oxidation and the mechanisms involved were investigated. Quercetin strongly inhibited Hb-mediated lipid oxidation in washed muscle. Quercetin showed effective hydroxyl radical scavenging ability similar to butylated hydroxytoluene (BHT). Quercetin reduced metHb resulting in formation of oxyHb. Bound quercetin decreased heme dissociation from metHb. Conversion to oxyHb and decreased heme dissociation represent routes to limit Hb-mediated lipid oxidation. Electrospray ionization mass spectrometry (ESI-MS) indicated one molecule of quercetin was covalently bound to Hb α-chain. Quercetin quinone docked 3.3 Å from the thiol of αCys(H15) but not near any other Cys residues of turkey Hb. At the docking site, hydrogen bonding between quercetin quinone and amino acids of α- and β-chain was demonstrated. This represents a path by which quercetin became covalently bound to α-chain. Molecular docking of heme proteins to polyphenols provides a template to better understand antioxidant interactions in muscle foods.

Quercetin alleviates high-fat diet-induced inflammation in brown adipose tissue

Inflammation in brown adipose tissue (BAT) causes BAT to lose its ability to regulate energy metabolism, which exacerbates obesity development. This study investigated the anti-inflammatory and antioxidant effects of quercetin on BAT in high-fat diet (HFD)-induced obese mice. Quercetin reduced proinflammatory and macrophage genes and increased antioxidant genes in the BAT of HFD-fed mice and in TNFα-induced brown adipocytes. In addition to increasing silent mating type information regulation 2 homolog 1 (SIRT1) levels, quercetin suppressed nuclear translocation and increased deacetylation of the nuclear factor kappa B (NFκB) subunit p65. The effects of quercetin on SIRT1 and NFκB p65 deacetylation disappeared in SIRT1-knockdown brown adipocytes. MicroRNAs that negatively regulate SIRT1 were downregulated in the BAT of HFDQ-fed mice. Taken together, these results suggest that quercetin improves obesity-induced inflammation in BAT by suppressing the NFκB pathway through activation of SIRT1.

Investigation of Quercetin interaction behaviors with lipid bilayers: Toward understanding its antioxidative effect within biomembrane

Quercetin (QCT), existing in common dietary sources, is an abundant bioflavonoid with planar structure and exerts multiple pharmacological effects. Herein, four kinds of liposomes were prepared as model biomembranes, and then the partition coefficient, distribution in lipid membrane and influence of the QCT on the membrane properties were evaluated. The partition of QCT to lipid membranes was affected by both membrane phase state and the interference of QCT on membrane properties. The location of QCT in lipid membrane was related to the phase state of lipid membrane. In addition, influence of QCT on the compaction of the hydrocarbon tail in lipid membranes was dependent on the unsaturation degree of lipid molecules. Finally, about its antioxidant activity, from the results of 2,2-diphenyl-1-picrylhydrazyl radical scavenging assay, it can be concluded that the interaction of QCT with lipid membrane greatly influences on QCT reductive activity in lipid membrane. Furthermore, mass spectrometry of DOPC molecule showed no lipid oxidation in the presence of QCT, indicating that in addition to the QCT ability toward radical scavenging, the ordering effect of QCT in unsaturated lipid membrane would be helpful to protect lipid membrane from oxidation by inhibiting radical diffusion (synergy effect). Based on lipid membrane analysis, our study made it clear that the effect of QCT on various lipid membrane and its relation with the antioxidant effect of QCT within lipid membrane. Therefore, our analytical method and findings would be also helpful for understanding the mechanism of other antioxidants effects on biomembrane.

Protective Effect of Quercetin against H2O2-Induced Oxidative Damage in PC-12 Cells: Comprehensive Analysis of a lncRNA-Associated ceRNA Network.

Quercetin is a bioflavonoid with potential antioxidant properties. However, the mechanisms underlying its effects remain unclear. Herein, we focused on integrating long noncoding RNA (lncRNA), microRNA (miRNA), and messenger RNA (mRNA) sequencing of PC-12 cells treated with quercetin. We treated PC-12 cells with hydrogen peroxide to generate a validated oxidative damage model. We evaluated the effects of quercetin on PC-12 cells and established the lncRNA, miRNA, and mRNA profiles of these cells. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses of these RNAs were conducted to identify the key pathways. Quercetin significantly protected PC-12 neuronal cells from hydrogen peroxide-induced death. We identified 297, 194, and 14 significantly dysregulated lncRNAs, miRNAs, and mRNAs, respectively, associated with the antioxidant effect of quercetin. Furthermore, the phosphatidylinositol-3-kinase/protein kinase B pathway was identified as the crucial signalling pathway. Finally, we constructed a lncRNA-associated competing endogenous RNA (ceRNA) network by utilizing oxidative damage mechanism-matched miRNA, lncRNA, and mRNA expression profiles and those changed by quercetin. In conclusion, quercetin exerted a protective effect against oxidative stress-induced damage in PC-12 cells. Our study provides novel insight into ceRNA-mediated gene regulation in the progression of oxidative damage and the action mechanisms of quercetin.

Development of Antioxidant-Loaded Nanoliposomes Employing Lecithins with Different Purity Grades.

This work focused on comparing the ability of lecithins with two purity grades regarding their performance in the development of nanoliposomes, as well as their ability to contain and release polar (trans-aconitic acid) and non-polar (quercetin) antioxidant compounds. First, the chemical characterization of both lecithins was carried out through infrared spectroscopy (FTIR), electrospray ionization mass spectrometry (ESI/MS), and modulated differential scanning calorimetry (mDSC). Second, nanoliposomes were prepared by the ethanol injection method and characterized by means of particle size, polydispersity, and zeta potential measurements. Third, the encapsulation efficiency and in vitro release profiles of antioxidants were evaluated. Finally, the antioxidant effect of quercetin and trans aconitic acid in the presence and absence of nanoliposomes was assessed through the oxygen radical absorbance capacity (ORAC) assay. The results showed that, although there are differences in the chemical composition between the two lecithins, these allow the development of nanoliposomes with very similar physicochemical features. Likewise, nanoliposomes elaborated with low purity grade lecithins favored the encapsulation and release of trans-aconitic acid (TAA), while the nanoliposomes made with high purity lecithins favored the encapsulation of quercetin (QCT) and modified its release. Regarding the antioxidant effect, the vehiculization of TAA and QCT in nanoliposomes led to an increase in the antioxidant capability, where QCT showed a sustained effect over time and TAA exhibited a rapidly decaying effect. Likewise, liposomal systems were also found to have a slight antioxidant effect.

Evaluation of Neuroprotective Effects of Quercetin against Aflatoxin B1-Intoxicated Mice.

Simple SummaryAflatoxin B1 (AFB1) is a mycotoxin commonly present in feed, characterized by several toxic effects. AFB1 has been described as being responsible for naturally occurring animal kidney disorders. In addition, AFB1 seems to have a neurotoxical effect that leads to memory impairment behavior. AFB1 toxicity involves the induction of the oxidative stress pathway, rising lipid peroxidation, and it decreases antioxidant enzyme levels. Hence, in our research, we wanted to evaluate the potential protective effects of quercetin in AFB1-mediated toxicity in the brain and the ameliorative effect on behavioral alterations. This antioxidant effect of quercetin in the brains of AFB1-intoxicated mice is reflected in better cognitive and spatial memory capacity, as well as a better profile of anxiety and lethargy disorders. In conclusion, our study suggests that quercetin exerts a preventive role against oxidative stress by promoting antioxidative defense systems and limiting lipid peroxidation.Aflatoxin B1 (AFB1) is a mycotoxin commonly present in feed, characterized by several toxic effects. AFB1 seems to have a neurotoxical effect that leads to memory impairment behavior. AFB1 toxicity involves the induction of the oxidative stress pathway, rising lipid peroxidation, and it decreases antioxidant enzyme levels. Hence, in our research, we wanted to evaluate the potential protective effects of quercetin 30 mg/kg in AFB1-mediated toxicity in the brain and the ameliorative effect on behavioral alterations. Oral supplementation with quercetin increased glutathione peroxidase (GSH) levels, superoxidedismutase (SOD) activity and catalase (CAT) in the brain, and it reduced lipid peroxidation in AFB1-treated mice. This antioxidant effect of quercetin in the brains of AFB1-intoxicated mice is reflected in better cognitive and spatial memory capacity, as well as a better profile of anxiety and lethargy disorders. In conclusion, our study suggests that quercetin exerts a preventive role against oxidative stress by promoting antioxidative defense systems and limiting lipid peroxidation.

Metabolomic profiling reveals similar cytotoxic effects and protective functions of quercetin during deoxynivalenol- and 15-acetyl deoxynivalenol-induced cell apoptosis

Among the family of mycotoxins of deoxynivalenol (DON) detected in nature, high proportions of 15-acetyldeoxynivalenol (15ADON) co-occur with the prototype DON and increase the combined exposure and synergistic health risks. The current study aimed to explore the mechanisms underlying the toxicity of 15ADON and compare them with those of DON. As the natural flavonoid compound quercetin (QUE) possesses antioxidant properties, we also aimed to determine the antioxidant effects of QUE on the tested mycotoxins. First, the global metabolomics approach was applied and showed that the metabolites produced from 15ADON or DON were almost identical, while QUE reversed the changes in the levels of key metabolites. Specifically, both DON and 15ADON activated the cell apoptosis pathway mediated by p38 and JNK, but inhibited the cell survival pathway mediated by ERK1/2 in GES-1 cells. Simultaneously, 15ADON induced FOXO3a nuclear translocation, similar to the results described for DON in our recent report. Furthermore, the addition of QUE appeared to counteract the detrimental effects of 15ADON and DON. We observed the effects of QUE treatment on mutant yeast strains with defects in their antioxidant system. More interestingly, QUE also substantially restored the increased ROS levels and the inhibited the growth rate following exposure to the mycotoxins DON and 15ADON. The data reported here support the hypothesis that QUE rescues the toxic effects of DON or 15ADON due to the similar mechanisms of DON and 15ADON toxicity.

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

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.

Anti-Oxidant Effect of Quercetin in Tris Egg Yolk Citrate Extender on Surti Buck Semen Preserved at Refrigerated Temperature

Anti-Oxidant Effect of Quercetin in Tris Egg Yolk Citrate Extender on Surti Buck Semen Preserved at Refrigerated Temperature

A morphological and biochemical evaluation of the effects of quercetin on experimental sciatic nerve damage in rats.

The present study evaluated the neuroprotective and antioxidant effects of quercetin in a rat model of sciatic nerve crush injury using histopathological, morphometric and biochemical methods. A total of 48 male Sprague Dawley rats, aged 10–12 weeks old were randomly divided into eight groups, consisting of two sham groups (S-7, S-28), three quercetin-treated groups (Q-7, Q-28; 200 mg/kg/7 days), trauma (T-7, T-28; 1 min sciatic nerve crush injury) and three trauma+quercetin groups (T+Q-7, T+Q-28; trauma+quercetin 200 mg/kg/7 days). Rats were sacrificed on day 7 or 28. Oxidant-antioxidant biochemical parameters in nerve tissues from all groups were analyzed using histopathological staining with toluidine blue and Masson's trichrome. DNA fragmentations were identified using terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling in cells from each tissue sample. Degeneration of the axons and myelin sheath, the breakdown of the concentric lamellar structure of the myelin sheath and axonal swelling were observed in groups T-7 and T-28. Myelin sheath thicknesses, nerve fiber diameters and the number of myelinated nerve fibers decreased, while the apoptotic index (AI) increased in the T-7 and T-28 groups. However, it was observed that nerve regeneration began in the T+Q-7 and T+Q-28 groups compared with the sham groups, together with the healing of cellular damage and axonal structure and a decrease in the AI. Malondialdehyde and superoxide dismutase activity did not differ significantly between the T-7 and S-7 groups. However, catalase activity significantly decreased in the T-28 group when compared with the sham 7 day group. Tissue malondialdehyde levels significantly increased, while serum catalase activity increased in the T+Q-7 group compared with the T-7 group. These results suggest that quercetin has beneficial effects on nerve regeneration and may shorten the healing period in crush-type sciatic nerve injuries.

Antioxidant Activity, In Vitro Digestibility and Stability of Flaxseed Oil and Quercetin Co‐Loaded Submicron Emulsions

Flaxseed oil and quercetin have received extensive attention in food industry. However, their poor solubility in water and stability are major limitations for their application in functional foods. In this work, we encapsulated flaxseed oil and quercetin into submicron emulsions by high pressure homogenization method to overcome their shortcomings in application. The loading of flaxseed oil in submicron emulsions was 10% and the solubility of quercetin in water is increased by at least 1300 folds. In vitro antioxidant study indicated that the addition of flaxseed oil could increase the antioxidant activity of quercetin. During in vitro digestion, the smaller the particle size of submicron emulsions, the faster the digestive rate of flaxseed oil and the higher the bio‐accessibility of quercetin. Furthermore, accelerated oxidation study revealed that quercetin could protect flaxseed oil effectively. Besides, metallic ions stability study illustrated that the influence of Na+ on the emulsion stability is smaller than that of Ca2+ and high Ca2+ concentration could lead to stratification of the submicron emulsions. The storage stability shows that the prepared submicron emulsions can be stored for 8 weeks at three different temperatures. Hence, submicron emulsion can be a promising vehicle for delivery of flaxseed oil and quercetin.Practical Applications: Submicron emulsions can be used to improve the water solubility and bioavailability of lipophilic nutrients. The combination of flaxseed oil and quercetin in submicron emulsions can compensate for their individual shortcomings in application and exert synergistic beneficial actions on human health. Furthermore, this technology is easy in operation and can be realized in industry. Flaxseed oil and quercetin co‐loaded submicron emulsions can be applied in milk and liquid beverages in food industry.Submicron emulsions are fabricated to enhance the delivery of flaxseed oil and quercetin. The smaller the particle size of submicron emulsions, the faster the digestive rate of flaxseed oil and the higher the bio‐accessibility of quercetin. Quercetin can protect flaxseed oil against oxidation effectively. The antioxidant effect of quercetin is found to be better than commonly used antioxidants.

Antioxidant effect of quercetin in an extender containing DMA or glycerol on freezing capacity of goat semen

This study was performed to evaluate the effectiveness of quercetin as a non-enzymatic antioxidant in combination with glycerol or Dimethylacetamide (DMA), on freezability of goat semen. Ejaculates from four healthy mature Mahabadi goats were collected using an artificial vagina. After primary processing, semen was pooled and extended by egg yolk based extender supplemented with different concentrations of quercetin (10 or 20 μM) along with 5% glycerol or DMA. The extended semen was frozen and sperm motility parameters, viability, abnormality, membrane integrity and lipid peroxidation were assessed after thawing. Results showed that sperm viability, total motility, progressive motility, straightness (STR) and linearity (LIN) were higher (P < 0.05), and abnormality percentage and MDA concentration were lower (P < 0.05) in extender containing DMA. Similarly, higher (P < 0.05) total motility, progressive motility, viability and membrane integrity along with lower (P < 0.05) MDA level were noted in Q10 group. The lowest (P < 0.05) MDA level was observed in DMA extender containing moderate level of quercetin (Q10D). Also the STR was higher (P < 0.05) in Q10D compared to Q10G and Q20G groups. In conclusion, supplementation of extender with 10 μM quercetin in combination with DMA improves the goat sperm motion kinetics and suppresses lipid peroxidation after freezing and thawing. Furthermore, DMA is more effective cryoprotectant for the freezing of goat sperm.

Antidepressant-like effect of quercetin in bulbectomized mice and involvement of the antioxidant defenses, and the glutamatergic and oxidonitrergic pathways

Olfactory bulbectomy (OB) is an animal model of depression that can mimic symptoms that are characteristic of depressive patients, such as behavioral, neurochemical and neuromorphological changes. Quercetin decreased the immobility time in the forced swimming test and tail suspension test. With the open field test, quercetin did not alter the locomotor activity of mice and in the splash test, quercetin increased the time spent grooming. The repeated treatment with quercetin (25mg/kg, for 14days) reversed the behavioral hyperactivity induced by OB in the open field test and was able to prevent depressant-like effects in the forced swimming test and tail suspension test. Regarding oxidative stress, OB reduced the levels of glutathione and increase the activity of superoxide dismutase and lipid hydroperoxide content (LOOH) in the hippocampus. Only the increase in LOOH levels was reversed by treatment with quercetin. In a further series of experiments with non-bulbectomized mice, the antidepressant effect of quercetin in the tail suspension test was reversed by the pretreatment of mice with NMDA, l-arginine or sildenafil. The administration of methylene blue and 7-nitroindazole, in combination with an underactive dose of quercetin (5mg/kg, p.o.), decreased the immobility time in the tail suspension test compared with the use of drug alone. There was no significant change in locomotor activity in the open field test. Our results suggest that the antidepressant effect of quercetin is dependent on the inhibition of the NMDA receptors and/or synthesis of nitric oxide. In addition, considering the reduction of LOOH levels on the hippocampus, we verify that the antioxidant effects of quercetin also contribute to its antidepressive potential. These data contribute to the understanding of the mechanisms involved in the antidepressant effect of quercetin and reinforce the involvement of the NMDA receptors and the nitric oxide on the pathophysiology of depression.

Quercetin and Resveratrol Decrease the Inflammatory and Oxidative Responses in Human Ocular Surface Epithelial Cells.

To determine the anti-inflammatory and antioxidant effects of quercetin (QCT) and/or resveratrol (RES) on human conjunctival (IOBA-NHC) and corneal (HCE) epithelial cell lines. IOBA-NHC and HCE cells were treated with QCT (0.5-25 μM), RES (0.5-50 μM) and a low-dose mixture of QCT (0.5 μM) and RES (5 μM) (QCT+RES) and stimulated with either TNF-α or ultraviolet (UV)-B radiation. Cytokine production (IL-6, IL-8, IP-10, and VEGF) was analyzed by an immune bead-based array, and intracellular reactive oxygen species (ROS) production was determined by a H2DCF-DA dye assay. Stimulation of IOBA-NHC and HCE cells with TNF-α induced an increase of IL-6, IL-8, and IP-10 secretion in both cell lines. Quercetin and RES decreased IL-6 and IP-10 secretion in a dose-dependent manner in both cell lines. Interleukin-8 secretion was also inhibited in a dose-dependent manner by QCT in HCE, but only at 20 and 25 μM QCT and 50 μM RES in IOBA-NHC and at 50 μM RES in HCE. QCT+RES decreased IL-6 and IL-8 secretion (P < 0.01 and P < 0.05, respectively) in IOBA-NHC cells. Ultraviolet-B induced a significant increase of ROS in both cell lines (P < 0.01 and P < 0.001 for IOBA-NHC and HCE cells, respectively), which was significantly decreased in a dose-dependent manner by QCT and RES in HCE cells. Reactive oxygen species production in IOBA-NHC cells was inhibited (P < 0.05) by 50 μM RES. Quercetin and RES have anti-inflammatory and antioxidant effects on IOBA-NHC and HCE cells. These in vitro data suggest that both polyphenols may have a therapeutic potential in the treatment of inflammatory ocular surface diseases.

Antioxidant effect of quercetin against acute spinal cord injury in rats and its correlation with the p38MAPK/iNOS signaling pathway

AimsThe present study aimed to investigate the correlation between quercetin (Que) and the p38 mitogen-activated protein kinase (p38MAPK)/inducible nitric oxide synthase (iNOS) signaling pathway and to explore its regulating effect on secondary oxidative stress following acute spinal cord injury (SCI), so as to elucidate the protective effects and mechanism associated with Que treatment during acute SCI. Main methodsSprague–Dawley rats were randomly divided into sham-surgery, SCI, Que, methylprednisolone (MP), and specific p38MAPK inhibitor SB203580 treatment groups. Acute SCI models were established in rats by a modified Allen's method. Real-time PCR analysis, western blot assay and immunohistochemistry for molecular changes in the p38MAPK/iNOS signaling pathway, determination of malondialdehyde (MDA) content and superoxide dismutase (SOD) activity, reflecting the levels of secondary oxidative stress, and functional or behavioral data, reflecting changes induced by Que and control treatments post-SCI were performed. Key findingsQue significantly increased Basso, Beattie and Bresnahan scores and inclined plane test scores in SCI rats similar to the positive control drug, MP. Que significantly inhibited increases in phosphorylated-p38MAPK (p-p38MAPK) and iNOS expression and reduced the rate of iNOS-positive cells in rats with SCI, similar to the effects of SB203580. In addition, both Que and SB203580 reduced MDA content and enhanced SOD activity in SCI rats, with Que effects being stronger. SignificanceThese experimental findings indicate that in SCI rats, Que has protective effects on the spinal cord by the potential mechanism of inhibiting the activation of p38MAPK/iNOS signaling pathway and thus regulating secondary oxidative stress.

Antioxidant effects of quercetin and naringenin are associated with impaired neutrophil microbicidal activity.

Naringenin and quercetin are considered antioxidant compounds with promising activity against oxidative damage in human cells. However, no reports have described their effects on reactive oxygen species (ROS) production by phagocytes during microbicidal activity. Thus, the present study evaluated the effects of naringenin and quercetin on ROS production, specifically hypochlorous acid (HOCl), and their involvement in the microbicidal activity of neutrophils. Naringenin and quercetin inhibited HOCl production through different systems, but this inhibition was more pronounced for quercetin, even in the cell-free systems. With regard to the microbicidal activity of neutrophils, both naringenin and quercetin completely inhibited the killing of Staphylococcus aureus. Altogether, these data indicate that the decrease in the oxidant activity of neutrophils induced by these compounds directly impaired the microbicidal activity of neutrophils. Naringenin and quercetin exerted their effects by controlling the effector mechanisms of ROS production, with both positive and negative effects of these antioxidant agents in oxidative stress conditions and on ROS in the microbicidal activity of phagocytes. The present results challenge the traditional view of antioxidants as improvers of pathological conditions.

Antioxidant Effects of Quercetin and Catechin Encapsulated into PLGA Nanoparticles

Polymeric nanoparticles (PLGA) have been developed for the encapsulation and controlled release of quercetin and catechin. Nanoparticles were fabricated using a solvent displacement method. Physicochemical properties were measured by light scattering, scanning electron microscopy andζ-potential, X-ray diffraction, infrared spectroscopy and differential scanning calorimetry. Encapsulation efficiency andin vitrorelease profiles were obtained from differential pulse voltammetry experiments. Antioxidant properties of free and encapsulated flavonoids were determined by TBARS, fluorescence spectroscopy and standard chelating activity methods. Relatively small (d≈ 400 nm) polymeric nanoparticles were obtained containing quercetin or catechin in a non-crystalline form (EE≈79%) and the main interactions between the polymer and each flavonoid were found to consist of hydrogen bonds.In vitrorelease profiles were pH-dependant, the more acidic pH, the faster release of each flavonoid from the polymeric nanoparticles. The inhibition of the action of free radicals and chelating properties, were also enhanced when quercetin and catechin were encapsulated within PLGA nanoparticles. The information obtained from this study will facilitate the design and fabrication of polymeric nanoparticles as possible oral delivery systems for encapsulation, protection and controlled release of flavonoids aimed to prevent oxidative stress in human body or food products.

Protective effect of quercetin, a polyphenolic compound, on mouse corpus cavernosum

Flavonoids are plant-based phenolic compounds, and quercetin is the most abundant dietary member of this family. One of the most important characteristics of quercetin is its antioxidant property. The aim of this study was to investigate antioxidant effects of quercetin on corpora cavernosa of mice. Corpora cavernosa were isolated in organ baths, precontracted with phenylephrine (0.5 microm) and relaxant responses were mediated by acetylcholine (0.1-1 microm), electrical field stimulation (EFS, 1-16 Hz, 0.5 ms, 30 V) or acidified sodium nitrite (a NaNO(2), 0.5 mm). Superoxide anion generators; pyrogallol (50 microm), hydroquinone (100 microm), LY 83583 (6-Anilinoquinolin-5,8-quinone, 10 microm) and superoxide dismutase (SOD) inhibitor; diethyldithiocarbamic acid (DETCA, 8 mm) were used in order to expose corpus cavernosa to oxidant stress. Acetylcholine (0.1-1 microm) induced relaxant responses were significantly inhibited in LY 83583 (10 microm) and DETCA + LY 83583 applicated trials. EFS-induced relaxant responses were significantly inhibited in DETCA (8 mm) and DETCA + LY 83583 administrated trials. On the other hand, acidified sodium nitrite-induced responses were inhibited by all of the superoxide anion generators tested. Quercetin (10 microm) failed to improve the inhibitions on endothelium and electrically stimulated responses. Acidified sodium nitrite (0.5 mm) mediated relaxant responses were significantly restored by quercetin except the groups in which LY 83583 were used. The data suggest that quercetin acts as a protective agent in mouse corpus cavernosum, increasing the bioavailability of exogenous nitric oxide by protecting it from superoxide anion (O(2)(-)).

Biological activity of quercetin-3-O-glucoside, a known plant flavonoid

Cytotoxic, phytotoxic, antimicrobial and antioxidant effects of quercetin 3-O-glucoside (Q3G) isolated by HPLC from aerial parts of Prangos ferulaceae was studied by MTT assay, lettuce germination assay, disk diffusion and DPPH method. Our results showed that Q3G exhibits high antioxidant effect with RC(50) of 22 microg/mL, it has low cytotoxicity and no antibacterial effects. Q3G exhibits high phytotoxic effect with IC(50) value of 282.7 microg/ml, as well. It is assumed that Q3G does not play a defense role in plants and it may act as an allelopatic agent.