Beneficial Effects Of Quercetin Research Articles

Beneficial effects of quercetin on titanium dioxide nanoparticles induced spermatogenesis defects in mice.

Many recent studies have demonstrated that most nanoparticles (NPs) have an adverse or toxic action on male germ cells. In present study, protective effect of quercetin (Que) on titanium dioxide nanoparticle (NTiO2)-induced spermatogenesis defects in mice was investigated. Thirty-two Naval Medical Research Institute (NMRI) mice were randomly divided into four groups. Que group received 75mg/kg of Que for 42days. NTiO2 group received 300mg/kg NTiO2 for 35days. NTiO2 + Que group initially received 75mg/kg Que for 7days and was followed by concomitant administration of 300mg/kg NTiO2 for 35days. Control group received only normal saline for 42days. Sperm parameters, testosterone concentration, histological criteria, and apoptotic index were assessed. Product of lipid peroxidation (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were also evaluated for oxidative stress in testicular tissue. Administration of NTiO2 significantly induced histological changes in testicular tissue; increased apoptotic index; and decreased testicular weight, testosterone concentration, and sperm quality (p<0.01). In the testis, NTiO2 increased oxidative stress through an increase in lipid peroxidation and a decrease in SOD and CAT activities (p<0.05). Que pretreatment could significantly attenuate testicular weight; apoptotic index; and histological criteria including vacuolization, detachment, and sloughing of germ cells in seminiferous tubules. Serum and tissue testosterone levels were significantly increased in Que-pretreated mice (p<0.01). Sperm parameters including sperm number, motility, and percentage of abnormality were also effectively improved by Que pretreatment (p<0.01). Pretreatment of Que significantly ameliorated oxidative stress and increased the activities of SOD and CAT in testicular tissue. These results indicate that sperm production can be increased by Que pretreatment in NTiO2-intoxicated mice. The improved sperm quality and reverse testis histology by Que pretreatment may be a consequence of elevation testosterone concentration, reduction in germ cell apoptosis, and suppression of oxidative stress in testicular tissue.

Induction of heme oxygenase-1 with dietary quercetin reduces obesity-induced hepatic inflammation through macrophage phenotype switching.

BACKGROUND/OBJECTIVESObesity-induced steatohepatitis accompanied by activated hepatic macrophages/Kupffer cells facilitates the progression of hepatic fibrinogenesis and exacerbates metabolic derangements such as insulin resistance. Heme oxyganase-1 (HO-1) modulates tissue macrophage phenotypes and thus is implicated in protection against inflammatory diseases. Here, we show that the flavonoid quercetin reduces obesity-induced hepatic inflammation by inducing HO-1, which promotes hepatic macrophage polarization in favor of the M2 phenotype.MATERIALS/METHODSMale C57BL/6 mice were fed a regular diet (RD), high-fat diet (HFD), or HFD supplemented with quercetin (HF+Que, 0.5g/kg diet) for nine weeks. Inflammatory cytokines and macrophage markers were measured by ELISA and RT-PCR, respectively. HO-1 protein was measured by Western blotting.RESULTSQuercetin supplementation decreased levels of inflammatory cytokines (TNFα, IL-6) and increased that of the anti-inflammatory cytokine (IL-10) in the livers of HFD-fed mice. This was accompanied by upregulation of M2 macrophage marker genes (Arg-1, Mrc1) and downregulation of M1 macrophage marker genes (TNFα, NOS2). In co-cultures of lipid-laden hepatocytes and macrophages, treatment with quercetin induced HO-1 in the macrophages, markedly suppressed expression of M1 macrophage marker genes, and reduced release of MCP-1. Moreover, these effects of quercetin were blunted by an HO-1 inhibitor and deficiency of nuclear factor E2-related factor 2 (Nrf2) in macrophages.CONCLUSIONSQuercetin reduces obesity-induced hepatic inflammation by promoting macrophage phenotype switching. The beneficial effect of quercetin is associated with Nrf2-mediated HO-1 induction. Quercetin may be a useful dietary factor for protecting against obesity-induced steatohepatitis.

Quercetin protects RAW264.7 macrophages from glucosamine-induced apoptosis and lipid accumulation via the endoplasmic reticulum stress pathway.

It is increasingly recognized that macrophages are a key cell in the development of atherosclerosis. Glucosamine, the product of the hexosamine biosynthetic pathway in diabetes mellitus, can disturb lipid metabolism, induce apoptosis and accelerate atherosclerosis via endoplasmic reticulum (ER) stress in various types of cells. Previous studies have indicated that quercetin possesses antidiabetic, anti‑oxidative, anti‑inflammatory and anti‑apoptotic activities as a flavonoid. Studies have also demonstrated its novel pharmacological properties for inhibiting ER stress. The present study focussed on the effects of quercetin on cell injury and ER stress in glucosamine‑induced macrophages. RAW264.7 macrophages were cultured with 15 mM glucosamine, following which the levels of apoptosis, intracellular total and free cholesterol, and apoptosis‑ and ER stress‑associated proteins were measured in the macrophages treated with or without quercetin. Additionally, the ratio of cholestryl ester/total cholesterol was calculated to observe the formation of foam cells. The results demonstrated that apoptosis and abnormal lipid accumulation in the RAW264.7 cells, which was induced by glucosamine, were significantly reversed by quercetin. In addition, quercetin treatment suppressed the increase of C/EBP homologous protein, and inhibited the activation of JNK and caspase‑12, which was induced by glucosamine. Quercetin also increased the expression level of full length activating transcriptional factor 6 and decreased the expression of glucose regulated protein 78. Of note, the beneficial effects of quercetin on the glucosamine‑induced RAW264.7 cells were reversed by treatment with tunicamycin. These findings suggest that quercetin may have properties to prevent glucosamine‑induced apoptosis and lipid accumulation via the ER stress pathway in RAW264.7 macrophages.

Cardiovascular Disease: A Target for the Pharmacological Effects of Quercetin.

Quercetin, a prominent dietary antioxidant present in vegetables, especially onions, fruits, highlighting apples and berries, wine and tea, belongs to a group of plant derived heterocyclic polyphenols. These compounds could be important mediators of the biological actions attributed to healthy diets. Chemically, quercetin is a type of flavonoid that specifically belongs to the flavonols group. It naturally occurs either as glycoside or aglycone, both of which have biological activity. Many of the natural sources of quercetin are included in the Mediterranean diet, a dietary habit associated with a decrease of cardiovascular diseases. During the last years, several researches have reported effects consistent with pharmacological applications of quercetin in cardiovascular diseases, such as atherosclerosis, ischemia-reperfusion injury, cardiotoxicity, and hypertension, among others. In this review, the pathways and molecules involved in the beneficial effects of quercetin are summarized. In addition, a scope of the new insights concerning quercetin pharmacokinetics, pharmacodynamics and bioavailability are presented. The mechanisms whereby quercetin exerts its effects have not been fully elucidated. However, interesting results have been obtained from early clinical studies involving cardioprotection by quercetin, but much knowledge is still lacking in the field of its bioavailability to improve the clinical application of this flavonol. This study presents evidence supporting the point of view that quercetin should be considered a potential therapeutic agent against cardiovascular diseases, giving rise to novel applications in their prevention and treatment.

Beneficial effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin in rats: A histological and biochemical study.

Ciprofloxacin is a broad-spectrum quinolone antibiotic commonly used in clinical practice. Quercetin is an antioxidant belongs to flavonoid group. It inhibits the production of superoxide anion. In this study, we aimed to evaluate the effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin. Twenty-eight female Wistar albino rats were divided into four groups: control, quercetin (20 mg kg(-1) day(-1) gavage for 21 days), ciprofloxacin (20 mg kg(-1) twice a day intraperitoneally for 10 days), and ciprofloxacin + quercetin. Samples were processed for histological and biochemical evaluations. Malondialdehyde (MDA) and glutathione (GSH) levels, superoxide dismutase (SOD), and catalase (CAT) activities were measured in kidney tissue. The ciprofloxacin group showed histopathological changes such as infiltration, dilatation in tubules, tubular atrophy, reduction of Bowman's space, congestion, hemorrhage, and necrosis. In the ciprofloxacin + quercetin group, these histopathological changes markedly reduced. MDA levels increased in the ciprofloxacin group and decreased in the ciptofloxacin + quercetin group. SOD and CAT activities and GSH levels significantly decreased in the ciprofloxacin group. On the other hand, in the ciprofloxacin + quercetin group, SOD and CAT activities and GSH levels significantly increased with regard to the ciprofloxacin group. We concluded that quercetin has antioxidative and therapeutic effects on renal injury and oxidative stress caused by ciprofloxacin in rats.

Beneficial effects of quercetin on oxidative stress in liver and kidney induced by titanium dioxide (TiO2) nanoparticles in rats

TiO2 nanoparticles used as vectors for the delivery of drugs have shown greater effectiveness. However, TiO2 nanoparticles can cause oxidative stress in liver and kidney, so we analyzed if a previous or simultaneous quercetin treatment could counteract this in rats. Five groups of male Wistar rats (200–250 g) were included: (1) healthy controls, (2) TiO2 group, (3) quercetin group, (4) preventive group: quercetin for 5 days prior to exposure of TiO2, and (5) therapeutic group: TiO2 (5 mg/kg, i.v.) plus quercetin single dose for 5 days (5 mg/kg/day, i.p.). Hepatic and renal function tests were made. Five animals from each group were sacrificed (0, 14 and 28 days), and liver and kidney tissue were obtained. Malondialdehyde (MDA), reduced/oxidized glutathione, and activity of glutathione peroxidase/reductase were measured, as well as the level of gene expression by q-PCR. There were no significant changes in serum ALT and AST activities. More damage was observed at 14 versus 28 days, because TiO2 was excreted in urine. Quercetin indeed showed a renal protective effect by increasing glutathione reductase and peroxidase levels and reducing MDA levels. On the other hand, TiO2 liver damage was less pronounced with quercetin as therapeutic treatment. TiO2 induces significantly the glutathione reductase expression and it can be down-regulated by quercetin. Biochemical tests in serum and urine showed a better effect of quercetin administered in the therapeutic group. Care should be taken with the dose and time of administration of quercetin, because this antioxidant could also have a pro-oxidant effect.

Beneficial effect of quercetin on cholestatic liver injury

Bile duct obstruction and subsequent cholestasis are associated with hepatocellular injury, cholangiocyte proliferation, stellate cell activation, Kupffer cell activation, oxidative stress, inflammation and fibrosis. Flavonoids have been shown to confer beneficial health effects, including hepatoprotection. However, the molecular mechanism of flavonoid-mediated hepatoprotection is incompletely understood. In this study, we report the protective effect of quercetin on cholestatic liver injury. Cholestasis was produced by bile duct ligation (BDL) in male Sprague–Dawley rats for 3weeks. Daily oral administration of quercetin was started 1week before injury and lasted for 4weeks. In comparison with the control group, the BDL group showed liver injury, as evidenced by histological changes, and elevation in serum biochemicals, ductular reaction, fibrosis, inflammation and oxidative stress. These pathophysiological changes were attenuated by daily quercetin supplementation. Quercetin alleviated BDL-induced transforming growth factor beta-1 (TGF-β1), interleukin-1 beta, connective tissue growth factor and collagen expression. The antifibrotic effect of quercetin was accompanied by reductions in α-smooth muscle actin-positive matrix-producing cells and Smad 2/3 activity critical to the fibrogenic potential of TGF-β1. Quercetin also attenuated BDL-induced oxidative stress, leukocyte accumulation, nuclear factor (NF)-κB activation and proinflammatory cytokine production. Further studies demonstrated an inhibitory effect of quercetin on MyD88 and TGF-β-activated kinase-1 critical for linking toll-like receptor (TLR) and NF-κB. Taken together, the hepatoprotective, anti-inflammatory and antifibrotic effects of quercetin seem to be multifactorial. The beneficial effects of daily quercetin supplementation are associated with antioxidative and anti-inflammatory potential as well as down-regulation of NF-κB and TGF-β/Smad signaling, probably via interference with TLR signaling.

Neuroprotective effect of quercetin against oxidative damage and neuronal apoptosis caused by cadmium in hippocampus

The purpose of the present investigation was to evaluate cadmium (Cd)-induced neurotoxicity in hippocampal tissues and beneficial effect of quercetin (QE) against neuronal damage. A total of 30 male rats were divided into 3 groups: control, Cd-treated, and Cd + QE-treated groups. After the treatment, the animals were killed and hippocampal tissues were removed for biochemical and histopathological investigation. Cd significantly increased tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD) and catalase (CAT) enzyme activities in hippocampal tissue compared with the control. Administration of QE with Cd significantly decreased the levels of MDA and PC and significantly elevated the levels of antioxidant enzymes in hippocampal tissue. In the Cd-treated group, the neurons of both tissues became extensively dark and degenerated with pyknotic nuclei. The morphology of neurons in Cd + QE group was well protected, but not as neurons of the control group. The caspase-3 immunopositivity was increased in degenerating neurons of the Cd-treated group. Treatment of QE markedly reduced the immunoreactivity of degenerating neurons. The results of the present study show that QE therapy causes morphologic improvement in neurodegeneration of hippocampus after Cd exposure in rats.

English

The purpose of this study was to assess the beneficial effect of quercetin, flaxseed and/or in combination as synergetic, in an animal model of metabolic syndrome (MtS), high fructose (HF)-fed rats. Fifty male Sprague-Dawley rats, 3 months old, weighing between 110 to 120 g were randomly divided into 5 groups. Rats were given drinking water (negative (-ve) control rats) or 10% fructose in drinking water (HF; fructose-fed rats) with standard chow for 8 weeks. After 4 weeks of HF feeding, rats were further divided into matched 4 subgroups. Different groups of animals (n = 10, each group) were administered 10% HF (5 mg/kg, +ve control), flaxseed (F; 50 mg/kg), quercetin (Q; 50 mg/kg), flaxseed + quercetin, (FQ; 25 mg/kg each), respectively. All ingredients were given orally, once daily and subsequently for 4 weeks. Serum glucose, insulin, lipids profile, leptin, and adiponectin were estimated. After 4 weeks of feeding, a significant increase in blood glucose level was observed in HF fed rats compared to normal rats, but this was significantly decreased after administration of F, Q and FQ. The serum insulin level in HF fed rats was significantly decreased after administration of F and FQ groups. Significantly, higher concentrations of triacylglycerols (TG), total cholesterol and low density lipoprotein cholesterol (LDL- C) were observed in HF fed rats, and these increases were lower after administration of F, Q and FQ. There was a significant increase in serum high density lipoprotein cholesterol (HDL-C) in FQ group. The increase of serum leptin level was decreased significantly in F, Q and FQ groups. Whereas, the reduction of serum adiponectin level in HF fed rats was increased in F, Q and FQ groups. These data suggests that protective effect of flaxseed and quercetin consumption as functional foods could be less risky for people with decreased insulin sensitivity and increased oxidative stress, such as those with the metabolic syndrome or type 2 diabetes. Key words: Flaxseed, protective effect, quercetin, insulin sensitivity, metabolic syndrome, type 2 diabetes.

Supplementation With Quercetin Attenuates 4‐Nitrophenol‐Induced Testicular Toxicity in Adult Male Mice

The beneficial effects of quercetin on reproductive damage elicited by 4-nitrophenol (PNP) were studied in adult male mice. A six-week treatment of weekly intraperitoneal injections of PNP (50 mg/kg) resulted in severe damage to the seminiferous tubules, a remarkable increase in both hydroxyl radical and malondiadehyde production, and notably decreased glutathione peroxidase and superoxide dismutase activities. Moreover, PNP treatment induced germ cell apoptosis, inhibited Bcl-xl expression, and then activated Bax expression and the caspase-3 enzyme. Exposure to PNP also increased XBP-1 and HO-1 mRNAs levels. However, simultaneous supplementation with quercetin (75 mg/kg) attenuated the toxicity induced by PNP through renewal of the antioxidant enzyme's status, alleviating apoptosis by regulating the expressions of Bax and Bcl-xl, XBP-1 and HO-1mRNAs, and the regulation of caspase-3 activity. Taken together, these findings indicated that the antioxidant quercetin displays a potential preventive effect on PNP-induced oxidative damage in mouse testes and may represent an efficient supplement to attenuate reproductive toxicity from environmental toxicants in order to ensure reproductive health and sperm production.

Abstract P426: Quercetin Intake Differentially Affects the Plasma Lipid Levels and Lipoproteins Associated Gene Expression in Normal C57bl Female Mice

Background: Quercetin is a member of the bioflavonoids family known to have antiatherogenic, antiinflammatory, and antihypertensive properties; and reported to have cardiovascular protective role. Quercetin through its antioxidant action may protect against oxidative stress induced by free radicals consequently decreasing the potential for modification of low density lipoprotein cholesterol (LDL); however it is not clear if the intake of quercetin during exercise may have beneficial effect on plasma lipids. Goals and hypothesis: We hypothesized that the intake of quercetin with exercise will affect plasma lipids. The goal of this study is to investigate the beneficial effect of Quercetin on normal female mice. Study Design and Methods: We investigated the possible beneficial effects of the combined exercise and quercetin on plasma lipids in C57BL6 normal female mice fed normal mouse chow. Mice (N=29) were divided into four groups. These groups are as follows: Control mice, left untreated; control quercetin group, orally supplied with 100 μg/day of quercetin without exercising; exercise group without quercetin, and exercise group with quercetin supplements. The exercise groups were run on a treadmill for 30 minutes, 15m/m/ 5 days/week for 30 days. At the end of the month of the treatment, mice were sacrificed liver gene expressions for genes associated with lipoprotein metabolism were analyzed, and plasma lipids levels were analyzed. Results and Discussion: Our data interestingly showed that Quercetin differentially influences the levels of lipoprotein, oxidative stress and inflammatory markers gene expression during exercise in normal female mice; however plasma lipids, specifically TG plasma levels have elevated among mice consuming quercetin alone or with exercise significantly (P&lt;0.5). Conclusion: This study have demonstrated that Quercetin intake with exercise may differentially affects the plasma lipid levels and lipoproteins associated gene expression in normal C57BL female mice.

Quercetin improves the postthaw characteristics of cryopreserved sex-sorted and nonsorted stallion sperm

Excessive reactive oxygen species generation during sex sorting and cryopreservation of stallion sperm leads to DNA fragmentation, lipid peroxidation, and motility loss. In this study we investigated whether antioxidant supplementation during sex sorting and cryopreservation could ameliorate the effects of reactive oxygen species on stallion sperm. In experiment 1, the postthaw characteristics of stallion sperm (N = 9) cryopreserved in the presence or absence of catalase (200 U/mL), cysteine (0.2 mg/mL), or quercetin (0.15 mM) was examined. Motility and acrosome integrity were assessed at 0, 1, and 3 hours after thawing. The sperm chromatin structure assay (SCSA; detectable DNA fragmentation index [DFI], mean DFI, and DFI) was used to assess DNA integrity immediately after thawing. Quercetin increased the total postthaw motility (25.3% vs. 20.9%; P < 0.05), but there was no beneficial effect of catalase or cysteine. Based on these results, the effect of quercetin during cryopreservation on the postthaw zona binding ability of sperm was assessed using a heterologous (bovine) zona binding assay. Quercetin increased the number of sperm bound per oocyte (13.6 vs. 9.2; P < 0.05) compared with the control. In experiment 2, the effect of quercetin (0.15 mM) in the media used during semen storage and transport, Hoechst 33342 staining and cryopreservation of stallion sperm (N = 9) was investigated. Motility, acrosome integrity, and viability were assessed at 0, 1, and 3 hours after thawing and SCSA was performed at 0 hours after thawing. Quercetin supplementation during sex sorting and cryopreservation improved DNA integrity (SCSA; detectable DFI of 54.9% vs. 74.6%, P < 0.05; mean DFI of 270.2 vs. 288.1, P < 0.05; and DFI of 26.3% vs. 28.5%, P < 0.05) compared with control sex-sorted sperm. There was no beneficial effect of quercetin on the motility, acrosome integrity, or viability of sex-sorted sperm. In conclusion, quercetin significantly improved the motility and zona binding ability of cryopreserved stallion sperm, and reduced DNA fragmentation in sex-sorted, cryopreserved stallion sperm.

Quercetin Induces Mitochondrial Biogenesis through Activation of HO-1 in HepG2 Cells

The regeneration of mitochondria by regulated biogenesis plays an important homeostatic role in cells and tissues and furthermore may provide an adaptive mechanism in certain diseases such as sepsis. The heme oxygenase (HO-1)/carbon monoxide (CO) system is an inducible cytoprotective mechanism in mammalian cells. Natural antioxidants can provide therapeutic benefit, in part, by inducing the HO-1/CO system. This study focused on the mechanism by which the natural antioxidant quercetin can induce mitochondrial biogenesis in HepG2 cells. We found that quercetin treatment induced expression of mitochondrial biogenesis activators (PGC-1α, NRF-1, TFAM), mitochondrial DNA (mtDNA), and proteins (COX IV) in HepG2 cells. The HO inhibitor SnPP and the CO scavenger hemoglobin reversed the effects of quercetin on mitochondrial biogenesis in HepG2 cells. The stimulatory effects of quercetin on mitochondrial biogenesis could be recapitulated in vivo in liver tissue and antagonized by SnPP. Finally, quercetin conferred an anti-inflammatory effect in the liver of mice treated with LPS and prevented impairment of mitochondrial biogenesis by LPS in vivo. These salutary effects of quercetin in vivo were also antagonized by SnPP. Thus, our results suggest that quercetin enhances mitochondrial biogenesis mainly via the HO-1/CO system in vitro and in vivo. The beneficial effects of quercetin may provide a therapeutic basis in inflammatory diseases and sepsis.

Quercetin and its metabolites improve vessel function by inducing eNOS activity via phosphorylation of AMPK

Quercetin is a major flavonoid in a wide range of fruits and vegetables. Consumption of quercetin may contribute to a reduction in risk of cardiovascular disease (CVD). Following ingestion, flavonoids are metabolized rapidly by methylation or glucuronidation, which can alter their biological activity. Certain dietary flavonoids have been shown to upregulate the expression of adenosine monophosphate-activated protein kinase (AMPK). AMPK is a conserved key enzyme in cellular energy homeostasis that affects fatty acid oxidation. The aim of the present study was to investigate the effects of supraphysiological concentrations of quercetin and its methyl and glucuronide metabolites (3′-O-methyl-quercetin and quercetin-3-O-glucuronide) on activation of AMPK and eNOS in human aortic endothelial cells (HAECs) and endothelial function in isolated aortic rings from C57BL mice. We found that 5 and 10μM quercetin and its metabolites, and pretreatment of arteries with quercetin and its metabolites can protect vessels against hypochlorous acid-induced endothelial dysfunction in isolated arteries (P<0.05). Inhibition of AMPK blocked these protective effects. We also found that 5 and 10μM quercetin and its metabolites can induce activation of AMPK and eNOS in human aortic endothelial cells, and lead to an increase in the concentrations of S-nitrosothiols and nitrite in cell culture media (P<0.05). These results provide further support for the cardioprotective effects of certain dietary flavonoids. They suggest that beneficial effects of quercetin on endothelial cell functions are in part mediated via AMPK pathway.

Beneficial Effects of Quercetin on Obesity and Diabetes

Scientific research is constantly looking for new molecules that could be used as dietary functional ingredients in the fight against obesity and diabetes, two pathologies highly prevalent in Western societies. In this context, flavonoids represent a group of molecules of increasing interest. The major flavonoid is Quercetin, which belongs to the class called flavonols and is mainly found in apples, tea, onions, nuts, berries, cauliflower, cabbage and many other foods. It exhibits a wide range of biological functions including anticarcenogenic, anti-inflammatory and antiviral; it also inhibits lipid peroxidation, platelet aggregation and capillary permeability. This review focuses on the main effects of Quercetin on obesity and diabetes. The mechanisms of action explaining the effects of Quercetin on these two metabolic disturbances are also considered. Good perspectives have been opened for Quercetin, according to the results obtained either in cell cultures or in animal models. Nevertheless, further studies are needed to better characterize the mechanisms of action underlying the beneficial effects of this flavonoid on these pathologies. Moreover, the body fat-lowering effect and the improvement of glucose homeostasis need to be confirmed in humans. Animal studies have consistently failed to demonstrate adverse effects caused by Quercetin. In contrast, due to inhibitory effect of Quercetin in cytochrome P450, interactions with drugs can be taken into account when they are administered at the same time than Quercetin.

Beneficial effects of quercetin on sperm parameters in streptozotocin‐induced diabetic male rats

Quercetin (QR) is a strong antioxidant and has been shown to reduce oxidative stress in the long-term treatment of streptozotocin (STZ)-induced diabetes in animal models. Antioxidants have significant effects on spermatogenesis, sperm biology and oxidative stress, and changes in antioxidant capacity are considered to be involved in the pathogenesis of chronic diabetes mellitus. The present study aims to examine the influence of QR on spermatogenesis in STZ-induced diabetes in male Wistar rats. Animals (n = 50) were allocated into five groups: Group 1: Control rats given 0.5 ml of 20% glycerol in 0.9% normal saline. Group 2: Control rats given buffer (pH4.0).Group 3: diabetic controls. Group 4: rats given QR 15 mg/kg/day (i.p.). Group 5: STZ + QR rats. Animals were kept in standard conditions. At the end of the experiment (28th day), blood samples were taken for determination of testosterone, total antioxidant capacity, and levels of malondialdehyde and oxidized low-density lipoprotein. All rats were euthanized, testes were dissected out and spermatozoa were collected from the epididymis for analysis. Sperm numbers, percentages of sperm viability and motility, and total serum testosterone increased significantly in QR-treated diabetic rats (P < 0.05) compared with control groups. In histopathology, degeneration and inflammation in testes cells associated with diabetes were improved and testes weights in the QR-treated diabetic group decreased significantly in comparison with controls (P < 0.05). We conclude that QR has significant beneficial effects on the sperm viability, motility, and serum total testosterone and could be effective for maintaining healthy sperm parameters and male reproductive function in diabetic rats.

Acute treatment with polyphenol quercetin improves postischemic recovery of isolated perfused rat hearts after global ischemia

Quercetin is a plant-derived bioflavonoid with potentially beneficial effects on the cardiovascular system. Studies focused on the efficiency of flavonoids against ischemia-reperfusion (I/R) injury have demonstrated that quercetin exerts robust protective effects in renal, cerebral, and hepatic I/R models. However, there is only limited evidence about the effect of quercetin on myocardial I/R injury. Therefore, the aim of the current study was to examine the effect of quercetin on isolated rat heart during ischemia and reperfusion. Rat hearts perfused according to Langendorff at 37 degrees C were examined during 25 min global ischemia followed by 120 min reperfusion. Quercetin (15 micromol/L) was administered either 15 min before ischemia (group Q1), or during the entire reperfusion period (group Q2). Changes in functional parameters of the hearts were measured during the initial 40 min of reperfusion. At the end of the experiment, the hearts were stained with tetrazolium to estimate the size of infarction (IS). Our study showed that quercetin improved postischemic recovery of functional parameters of isolated hearts in both treated groups. This improvement was manifested by significantly higher values of left ventricular developed pressure (LVDP) and the maximal rates of pressure development and fall (+(dP/dt)max and -(dP/dt)max) and by significantly lower increase of end-diastolic pressure. Coronary flow was not significantly changed during reperfusion in the group treated before ischemia, but was significantly increased in the group treated during reperfusion. Quercetin also significantly reduced IS in both groups, more markedly in postischemically treated group. We conclude that acute quercetin treatment exerts significant positive effects on isolated hearts during I/R injury. These results are consistent with the beneficial effects of quercetin and other flavonoids on the cardiovascular system.

Improvement of renal blood flow underlies the beneficial effect of quercetin on cisplatin nephrotoxicity

Improvement of renal blood flow underlies the beneficial effect of quercetin on cisplatin nephrotoxicity

Food Content, Processing, Absorption and Metabolism of Onion Flavonoids

The question as to how far the development of chronic diseases in humans depends on diet still remains open. Simultaneously, epidemiological studies suggest the consumption of a flavonoids rich diet might decrease the risk of degenerative changes and certain diseases. The intake of this group of compounds as to quality and quantity depends on dietary habits and a widespread presence of quercetin in the diet makes this compound one of the key factors. Onion, one of the richest and most common quercetin sources, was particularly often studied in different aspects. Quercetin is present in onion mainly as glycosides, of which the distribution within the onion bulb changes in onion processing, and biological activities attracted a lot of attention. Especially antioxidative activity demonstrated in vitro was initially associated with most of the beneficial effects of quercetin on the human body. However, after ingestion quercetin undergoes extensive metabolism and microbial action resulting in its altered or degraded structure; therefore, most of the effects shown in in vitro experiments with the pure compound cannot be directly extrapolated to in vivo systems. Yet, this does not mean that quercetin simultaneously loses its positive impact on consumer health. Even after being metabolized it may still affect the redox balance by inducing antioxidative and detoxifying enzymes or compounds which may be involved in sustaining homeostasis.

Effect of quercetin on altered vascular reactivity in aortas isolated from streptozotocin-induced diabetic rats

The present work examined ex vivo the acute effect of quercetin on diabetic rat aortic ring reactivity in response to endothelium-dependent (acetylcholine, ACh) and endothelium-independent (sodium nitroprusside, SNP) relaxants, and to the α 1-adrenergic agonist phenylephrine (PE). Responses were compared to those of aortic rings from age- and sex-matched euglycemic rats. Compared to euglycemic rat aortic rings, diabetic rings showed less relaxation in response to ACh and SNP, and greater contraction in response to PE. Pretreatment with quercetin (10 μM, 20 min) increased ACh-induced relaxation and decreased PE-induced contraction in diabetic, but did not affect euglycemic rat aortic ring responses. Following pretreatment with the nitric oxide synthase inhibitor Nω-nitro- l-arginine methyl ester ( l-NAME, 10 μM), quercetin reduced PE-induced contractions in both aortic ring types, although l-NAME attenuated the reduction in the diabetic rings. Quercetin did not alter SNP vasodilatory effects in either ring type compared to their respective controls. These findings indicate that quercetin acutely improved vascular responsiveness in blood vessels from diabetic rats, and that these effects were mediated, at least in part, by enhanced endothelial nitric oxide bioavailability. These effects of quercetin suggest the possible beneficial effects of quercetin in vivo in experimental diabetes and possibly in other cardiovascular diseases.