Protective Effect Of Quercetin Research Articles

Protective effects of quercetin on UVB irradiation‑induced cytotoxicity through ROS clearance in keratinocyte cells.

Human skin is the body's largest organ that protects against diverse environmental injuries. However, ultraviolet(UV) radiation, which induces a transient increase in the intracellular level of reactive oxygen species (ROS) and leads to a variety of injuries and various skin diseases, has deleterious effects on living organisms. Quercetin is a naturally occurring compound with strong antioxidant action and can successfully scavenge free radicals. In the present study, we investigated the effects and the mechanism of quercetin on UVB‑induced cytotoxicity in keratinocyte (HaCaT) cells. The results of this study showed that quercetin (20μM) significantly blocked UVB irradiation (15mJ/cm2)‑induced intracellular ROS generation. In addition, the ROS clearing ability of quercetin prevented cell membrane and mitochondria from ROS attack and inhibited cell membrane fluidity decrease and mitochondrial membrane depolarization. Moreover, the outflow of cytochromec and apoptosis were markedly inhibited. These results suggest that the protective effect of quercetin against UVB irradiation‑induced toxicity is mainly mediated by the ROS scavenging ability. Thus, quercetin is a potential agent against UVB irradiation‑induced skin damage.

Real-time monitoring of oxidative injury of vascular endothelial cells and protective effect of quercetin using quartz crystal microbalance

The adhesion, spreading, and proliferation of human umbilical vein endothelial cell line (HUVEC-C) cells, on a gold electrode were monitored using quartz crystal microbalance (QCM) measurements. The viscodensity effect caused by the normal action of the cells led to a decrease of the resonant frequency and increase of the motional resistance. The oxidative injury of HUVEC-C cells appeared immediately with the addition of H2O2, exhibiting the decline of cellular spreading area and cell coverage on the electrode surface and resulting in inverted QCM responses. The injured extent of the cells was found to be related to the content of H2O2. It is found that 0.05mM quercetin added beforehand in the growth medium could remove completely the oxidative action of 1.0mM H2O2. Quercetin with increased dosage still exerted a partial protective effect on HUVEC-C cells against oxidative injury induced by 2.5mM H2O2. The microscope observations, electrochemical measurements, and MTT analysis validate the QCM assay results, indicating that quercetin is a valuable flavonoid anti-oxidant in the precaution and treatment for the oxidative injury of vascular endothelium. Graphical Abstract Upper part: Microscope images (×400) of 7.5×104 HUVEC-C cells adhered to the substrate at 48 h in the presence of H2O2. Middle part: Real-time Δf 0 and ΔR 1 responses to the addition of 7.5×104 HUVEC-C cells onto QCM gold electrode in the presence of H2O2 added at 24 h after the introduction of the cells. Lower part: Microscope images (×400) of 7.5×104 HUVEC-C cells adhered to the substrate at 48 h in the presence of quercetin added at 18 h and H2O2 added at 24 h after the introduction of the cells.

The protective effects of quercetin on neural cells

Objective To explore the mechanism of quercetin against the toxicity of amyloid β (Aβ) to neuroblastoma cell SK-N-SH. Methods In the experiment, SK-N-SH cells were divided to four groups, control group, Aβ group, Aβ+ quercetin group and quercetin group, and treated for 72h.The proliferation of cells, the concentrations of reactive oxygen species (ROS) and glutathione (GSH) in cells were determined. Results Compared with the control group, Aβ[Aβ grouP=(50.6±2.5)]could significantly suppress the proliferation of neuroblastoma cells (P=0.000). However, Aβ group added with quercetin[Aβ+ quercetin=(88.0±9.1)]showed decreased cellular toxicity induced by Aβ(P=0.001). Additionally, there was no significant difference between the control group and quercetin group.Likely, the concentration of ROS increased in Aβ group (523.3±22.5), which was higher than (190.3±25.7) in the control group and (224.0±56.0) in quercetin group (P=0.000). At last, quercetin could increase GSH level in SK-N-SH cells and higher than Aβ group[(3.0±0.2), P=0.004]and Aβ+ quercetin[(5.6±1.1), P=0.008]. Conclusion Quercetin could attenuate the suppression of proliferation of SK-N-SH cells induced by Aβ, that might be though increased concentration of GSH and decreased level of ROS.These data suggested that quercetin has clinical potentials in neurology. Key words: GSH; Quercetin; Alzheimerś disease; Amyloidβ

Quercetin modulates toll-like receptor-mediated protein kinase signaling pathways in oxLDL-challenged human PBMCs and regulates TLR-activated atherosclerotic inflammation in hypercholesterolemic rats.

Toll-like receptors (TLRs) are pattern recognition receptors that have a unique and essential function in innate immunity. The effect of quercetin on TLR-mediated downstream signaling mechanism and its effect on TLR-mediated MAP kinase and Akt pathways were studied in oxLDL-stimulated hPBMCs using specific inhibitors. The pretreatment of hPBMCs with specific TLR inhibitor, CLI-095, decreased the NF-κB nuclear translocation and TNF-α release by oxLDL. When the cells treated with inhibitor and quercetin together, the inhibition was more effective. The specific inhibitor for p38 MAPK, SB203580, reduced the phosphorylated p38 level and decreased the NF-κB activation and TNF-α release by oxLDL-challenged hPBMCs. This inhibitor showed enhanced inhibition when treated with quercetin together. The inhibitors for ERK1/2, PD98059, and for JNK, SP606125, also showed inhibitory effect on NF-κB activation and TNF-α release by oxLDL-simulated hPBMCs. Quercetin supplementation enhanced the inhibition of nuclear translocation of NF-κB and the release of cytokines. TLR4 inhibition study confirmed the downstream signaling mechanism mediated by NF-κB which is involved in the oxLDL-induced inflammatory response, and quercetin suppresses the cytokine, TNF-α release by modulating TLR-NF-κB signaling pathway. In addition to NF-κB signaling pathway, inflammation induced by oxLDL was also related to the activation of p38MAPK, ERK1/2 and JNK, and Akt pathways, and the protective effect of quercetin may be also related to the inhibition of activation of these pathways. Quercetin significantly downregulated the elevated mRNA expression of TLRs and cytokine TNF-α in HCD-fed atherosclerotic rats in vivo. As quercetin possesses inhibition on both TLR-NF-κB signaling pathway and TLR-mediated MAPK pathway, it is evident that it can be used as a therapeutic agent to ameliorate atherosclerotic inflammation. Since quercetin is the major flavonoid and forms the backbone of many other flavonoids and this study provides strong evidence that it has potent anti-inflammatory effect, quercetin may be a promising agent for the prevention and treatment of atherosclerosis and promote health by reducing harmful vascular inflammation.

Protective effects of quercetin on thioacetamide-induced acute liver damage and its related biochemical and pathological alterations

Acute liver damage may be followed by biochemical, behavioral, and pathological alterations, which can end up in serious complications and even death. The aim of this study was to determine whether quercetin, a flavonoid compound, which is also known to have cell-protective, antioxidant, and anti-inflammatory effects, has any protective impacts against thioacetamide (TAA)-induced liver damage in rats. Thirty-six Sprague–Dawley rats were divided into three groups: group C1, normal rats; group C2, rats that received a single dose of TAA (350 mg/kg) intraperitoneally; and group E, rats that received a single dose of TAA (350 mg/ kg)+300 mg/kg quercetin intraperitoneally. At the end, liver enzymes and plasma ammonia (NH4) were measured, and pathological analysis of the liver carried out. The measured serological markers except for total bilirubin (alanine aminotransferase, aspartate aminotransferase, and NH4) showed a significant decrease in group E compared with group C2. The quercetin-treated group showed a significantly lower clinical grade of encephalopathy. Pathological findings showed a significantly lower piecemeal necrosis in group E compared with group C2. Moreover, there was a nonsignificant decrease in focal necrosis, apoptosis, and focal inflammation in group E compared with group C2. Portal inflammation scores were lower in group E than in group C2. Therefore, quercetin significantly affected the grade of liver damage, as group E had lower grades compared with group C2 (P<0.05). Overall, quercetin showed positive effects on both the liver injury and its related behavioral and biochemical changes.

Molecular and biochemical evidence on the protective effects of quercetin in isoproterenol-induced acute myocardial injury in rats.

Cardioprotection represents one of the most important and realistic aspects of preventive therapy today. Quercetin, a naturally occurring dietary flavone, has been studied extensively for its antioxidant properties. The objective of present study is to find out the cardioprotective activity and to explore the underlying mechanisms of quercetin pretreatment (50 mg/kg body weight, orally) for 14 days against isoproterenol (ISO; 100 mg/kg body weight, subcutaneously) induced myocardial infarction in Wistar rats. Cardiac diagnostic markers, oxidative stress, inflammatory cytokines, histopathology along with gene expression analysis of calpain 1 and 2 were carried out in experimental rats. Quercetin pretreatment showed protective effects on heart by significantly attenuating the ISO-induced oxidative stress, inflammation, protecting heart architecture, and by downregulation of the expression of calpain. Overall, these findings revealed the cardio-protective potential of quercetin and its mechanism of action against ISO-induced MI in rats.

Protective effect of quercetin on homocysteine-induced oxidative stress

ObjectiveThe aim of this study was to evaluate whether quercetin (QUER) treatment could have a protective effect against oxidative stress induced by homocysteinemia in rats. Materials and methodsThirty-two male Sprague-Dawley rats (adult) were assigned randomly to four groups: the control group was given physiological saline (PS; 1.5 mL/d); the QUER group was given QUER (50 mg/kg body weight [BW] daily) in distilled water and 0.25 mL PS; the homocysteine (HCY) group was given HCY (1 mg/kg BW daily) in distilled water and 1.25 mL PS; and the QUER + HCY group was given QUER 1 h before the administration of HCY. QUER, HCY, and PS were injected intraperitoneally every other day for 30 d. Plasma malondialdehyde (MDA), carbonyl, erythrocyte-reduced glutathione (GSH), plasma sulphydril (−SH) levels, erythrocyte catalase (CAT), and superoxide dismutase (SOD) activities were determined. ResultsPlasma CAT levels in the QUER group were found to be significantly higher than in the control group, whereas plasma MDA levels in the QUER group significantly decreased compared with the control group. In the HCY group, plasma MDA and carbonyl levels significantly increased and GSH and SOD levels significantly decreased compared with the control group. Plasma MDA levels significantly decreased and GSH and CAT levels significantly increased in the QUER + HCY group compared with the HCY group. Plasma −SH levels were significantly lower in the HCY group than in the control group. Plasma −SH levels were higher in the QUER + HCY group than in the HCY group, but they were not significant. ConclusionThe exposure of rats to HCY leads to oxidative stress reflected in increased MDA and decreased antioxidant enzyme levels. Administration of QUER might attenuate oxidative damage induced by HCY or have a protective effect against it.

Quercetin and Vitamin C Mitigate Cobalt Chloride-Induced Hypertension through Reduction in Oxidative Stress and Nuclear Factor Kappa Beta (NF-Kb) Expression in Experimental Rat Model.

The objective of the present work was to evaluate the toxic effects of cobalt chloride, a potent oxidative stress-inducing chemical, at 650ppm in rats and the protective effect of quercetin and/or vitamin C against the cobalt chloride-induced toxicity. Thirty rats were randomly selected, and assigned to one of five groups: control, cobalt chloride, cobalt chloride + quercetin, cobalt chloride + vitamin C and cobalt chloride + quercetin + vitamin C. The exposure of rats to cobalt chloride led to a significant increase (p<0.05) in malondialdehyde (MDA) and hydrogen peroxide (H2O2) generated, but decreased nitric oxide (NO) bioavailability. Also, significant (p<0.05) reductions were observed in the activity of glutathione peroxidase (GPx) and reduced glutathione (GSH) content in the cardiac and renal tissues. Treatment with quercetin and vitamin C reversed the effect of cobalt chloride on MDA, H2O2 and NO, more potently than with either of the two antioxidants, and increased the antioxidant defence system. Further, treatment of rats with quercetin and vitamin C in combination resulted in significant (p<0.05) decreases in the systolic, diastolic, and mean arterial blood pressure of rats, relative to those exposed to cobalt chloride alone. Immunohistochemical studies revealed a greater expression of nuclear factor kappa beta (NF-kB) in the cobalt chloride group compared with the control- and antioxidants-treated rats. The results of this study suggest a protective role for quercetin and vitamin C in the amelioration of the toxic mechanisms leading to cobalt chloride-induced hypertension and its associated cardiac and renal complications in rats.

Protective Effects of Quercetin on Selected Oxidative Biomarkers in Bovine Spermatozoa Subjected to Ferrous Ascorbate.

Quercetin (QUE) is a natural flavonol-type flavonoid with antibacterial, anti-inflammatory and anti-aggregatory properties. It is also a powerful reactive oxygen species (ROS) scavenger and chelating agent. The aim of this study was to assess the effectiveness of QUE to reverse ROS-mediated alterations to the motility, viability and intracellular antioxidant profile of bovine spermatozoa. Spermatozoa were washed out of fresh bovine semen, suspended in 2.9% sodium citrate and subjected to QUE treatment (7.5, 25, 50 and 100μmol/l) in the presence or absence of a pro-oxidant, that is ferrous ascorbate (FeAA; 150μmol/l FeSO4 and 750μmol/l ascorbic acid) during a 6-h invitro culture. Spermatozoa motion characteristics were assessed using the SpermVision computer-aided sperm analysis (CASA) system. Cell viability was examined with the metabolic activity (MTT) assay, ROS generation was quantified via luminometry, and the nitroblue tetrazolium (NBT) test was applied to quantify the intracellular superoxide formation. Cell lysates were prepared at the end of the invitro culture to investigate the intracellular activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) as well as the concentrations of glutathione (GSH) and malondialdehyde (MDA). FeAA treatment led to a reduced sperm motility (p<0.001), viability (p<0.001) and decreased the antioxidant parameters of the sperm samples (p<0.001) but increased the ROS generation (p<0.001), superoxide production (p<0.001) and lipid peroxidation (p<0.001). QUE administration resulted in a preservation of the spermatozoa vitality and antioxidant characteristics (p<0.01 with respect to the enzymatic antioxidants, p<0.001 in relation to GSH) with a concentration range of 50-100μmol/l QUE revealing to be the most effective. Our results suggest that QUE exhibits significant ROS-scavenging and metal-chelating properties which may prevent spermatozoa alterations caused by ROS, and preserve the functionality of male reproductive cells.

Quercetin Impacts Expression of Metabolism- and Obesity-Associated Genes in SGBS Adipocytes.

Obesity is characterized by the rapid expansion of visceral adipose tissue, resulting in a hypoxic environment in adipose tissue which leads to a profound change of gene expression in adipocytes. As a consequence, there is a dysregulation of metabolism and adipokine secretion in adipose tissue leading to the development of systemic inflammation and finally resulting in the onset of metabolic diseases. The flavonoid quercetin as well as other secondary plant metabolites also referred to as phytochemicals have anti-oxidant, anti-inflammatory, and anti-diabetic effects known to be protective in view of obesity-related-diseases. Nevertheless, its underlying molecular mechanism is still obscure and thus the focus of this study was to explore the influence of quercetin on human SGBS (Simpson Golabi Behmel Syndrome) adipocytes’ gene expression. We revealed for the first time that quercetin significantly changed expression of adipokine (Angptl4, adipsin, irisin and PAI-1) and glycolysis-involved (ENO2, PFKP and PFKFB4) genes, and that this effect not only antagonized but in part even overcompensated the effect mediated by hypoxia in adipocytes. Thus, these results are explained by the recently proposed hypothesis that the protective effect of quercetin is not solely due to its free radical-scavenging activity but also to a direct effect on mitochondrial processes, and they demonstrate that quercetin might have the potential to counteract the development of obesity-associated complications.

Protective Effect of Quercetin against Visible Light‐Induced Retinal Degeneration in Vivo

Quercetin is a major polyphenols in fruits and vegetables and a potential nutritional supplement for preventing retinal degeneration. The protective effects of quercetin against retinal photooxidative damage in vivo are investigated in this study. Pigmented rabbits were orally administered quercetin at the dose of 0.11 mmol/kg/day for 3 weeks. Electroretinography, histological analysis, and TUNEL assay were performed 7 days after light exposure (18000 lx for 2 h), which showed that quercetin attenuated retinal cell apoptosis. The expression of oxidative stress markers (4‐hydroxynonenal, 3‐nitrotyrosine and 8‐hydroxydeoxyguanosine) were up‐regulated after light exposure but attenuated by quercetin. Quercetin attenuated the expression of proinflammatory cytokines (cyclooxygenase 2, tumor necrosis factor‐alpha, interleukin‐1 β and monocyte chemoattractant protein 1). Quercetin also attenuated the visible light‐induced changes on certain apoptotic proteins (caspase‐3, Bax and Bcl‐2) and the expression of angiogenesis‐related cytokines (vascular endothelial growth factor, interleukine‐8 and hypoxia‐inducible factor‐1α). The results suggest that quercetin exhibited protective effects against light‐induced retinal degeneration by reducing oxidative stress and inflammation. Quercetin also attenuated the photooxidation‐induced apoptosis and angiogenesis in the retina.

Protective effects of quercetin against arsenic-induced testicular damage in rats.

This study investigated the effect of quercetin on changes in testes due to arsenic exposure. Twenty-seven male rats were divided into three groups: control (10mlkg-1 day-1 saline), arsenic (10mgkg-1 day-1 sodium arsenite) and arsenic+quercetin (arsenic+50mgkg-1 day-1 quercetin). The rats were sacrificed at the end of 15-day experiment. There was no difference between control group and arsenic group in body weight gain, testicular weight and serum total testosterone level. Quercetin treatment did not cause a significant difference in these parameters. In the arsenic group rats, we determined deterioration in the structure of seminiferous tubules, a decrease in the number of spermatogenic cells, an increase in the number of apoptotic cells, a decrease in the number of PCNA-positive cells, a decrease in SOD, CAT and GSH-Px activities, and an increase in the MDA level in testicular tissue. In all these changes, arsenic+quercetin group showed an improved compared to arsenic group. The amount of arsenic increased in the arsenic group was compared to the control group, and there was no difference between arsenic group and arsenic+quercetin group in the amount of arsenic. In conclusion, quercetin prevented arsenic-induced testicular damage with its anti-apoptotic and antioxidant effects.

Enhanced therapeutic efficacy and amelioration of cisplatin-induced nephrotoxicity by quercetin in 1,2-dimethyl hydrazine-induced colon cancer in rats.

Objective:The aim of quercetin treatment in combination of cisplatin (CP)-induced nephrotoxicity as well on 1,2-dimethyl hydrazine (DMH)-induced colon cancer.Materials and Methods:In this study, animals are exposed to DMH hydrochloride to induce colon cancer. In these groups, nephrotoxicity was assessed with the help of blood urea nitrogen, urea, and creatinine. The antitumor activity of quercetin and CP assessed with the help of number of aberrant crypts and foci formation. Tumor size in different treatment group determined with the help of vernier caliper.Results:CP is one of the most widely used antineoplastic drugs against colon cancer, but it has a major dose-limiting drawbacks of causing nephrotoxicity. Therefore, there is a need for a novel therapeutic regimen which will reduce the nephrotoxicity and enhance the anticancer activity of CP. The protective effect of quercetin on CP-induced nephrotoxicity is well-known. Moreover, quercetin is proven to have antitumor activity in colon cancer. Keeping all the facts in view, this study was conceived to evaluate the role of quercetin on therapeutic efficacy and nephrotoxicity of CP in DMH-induced colon cancer in male Sprague–Dawley rats. Treatment of quercetin with CP (7.5 mg/kg) prevents the CP-induced nephrotoxicity along with enhance the anticancer activity confirmed by the reduction of aberrant crypt foci number. Treatment of CP and quercetin alone leads to significant increase in the anticancer activity as compared to control colon tumor rats.Conclusion:In DMH-induced colon cancer model, combination of quercetin and CP ameliorates CP-induced nephrotoxicity as well as enhanced antitumor activity.

Protective effect of quercetin on pig intestinal integrity after transport stress is associated with regulation oxidative status and inflammation.

This experiment was conducted to evaluate the effects of quercetin supplementation on intestinal integrity, intestinal reactive oxygen species (ROS) levels and intestinal inflammation in pigs under transport stress. A total of 170 finishing pigs were randomly assigned into two groups. Animals in the control group consumed a basal diet, while those in the treatment group consumed the same diet supplemented with 25 mg quercetin per kg feed. After a 4-week period, pigs were transported for 5 hr. The quercetin-supplemented pigs showed decreased serum levels of endotoxin (P<0.05), increased height of jejunum villi (P<0.05), and increased occludin and zonula occudens-1 (ZO-1) mRNA expression in the jejunum (P<0.05). These parameters are associated with intestinal health and were markedly improved by quercetin supplementation. Pigs consuming the quercetin-supplemented diet had lower intestinal levels of ROS and malondialdehyde (MDA) compared with the control group (P<0.05). This finding coincided with greater inhibition of the innate immune system (P<0.05), including mitogen-activated protein kinase (MAPK), protein kinase B (Akt) and nuclear factor κB (NF-κB) signaling pathways, as well as decreased expression of inflammatory cytokines in the jejunum. These results indicate that quercetin alleviates intestinal injury in pigs during transport, probably through modulation of intestinal oxidative status and inflammation.

Iron-Mediated Lysosomal Membrane Permeabilization in Ethanol-Induced Hepatic Oxidative Damage and Apoptosis: Protective Effects of Quercetin.

Iron, in its free ferrous states, can catalyze Fenton reaction to produce OH∙, which is recognized as a crucial role in the pathogenesis of alcoholic liver diseases (ALD). As a result of continuous decomposition of iron-containing compounds, lysosomes contain a pool of redox-active iron. To investigate the important role of intralysosomal iron in alcoholic liver injury and the potential protection of quercetin, male C57BL/6J mice fed by Lieber De Carli diets containing ethanol (30% of total calories) were cotreated by quercetin or deferoxamine (DFO) for 15 weeks and ethanol-incubated mice primary hepatocytes were pretreated with FeCl3, DFO, and bafilomycin A1 at their optimal concentrations and exposure times. Chronic ethanol consumption caused an evident increase in lysosomal redox-active iron accompanying sustained oxidative damage. Iron-mediated ROS could trigger lysosomal membrane permeabilization (LMP) and subsequent mitochondria apoptosis. The hepatotoxicity was attenuated by reducing lysosomal iron while being exacerbated by escalating lysosomal iron. Quercetin substantially alleviated the alcoholic liver oxidative damage and apoptosis by decreasing lysosome iron and ameliorating iron-mediated LMP, which provided a new prospective of the use of quercetin against ALD.

Antioxidant Agent Quercetin Prevents Impairment of Bladder Tissue Contractility and Apoptosis in a Rat Model of Ischemia/Reperfusion Injury.

To examine the possible protective effect of quercetin (QT), which is well known for its antioxidant and protective effects in circumstances of oxidative stress, on urinary bladder tissue in a rat model of ischemia/reperfusion (I/R) injury, which is a known factor for the development of lower urinary tract dysfunction partly mediated by the generation of free radicals causing oxidative damage. Thirty male Sprague-Dawley rats were subjected to I/R injury through clamping the abdominal aorta for 30 min and then allowing reperfusion for the next 60 min. Quercetin (20 mg/kg; subcutaneously) or vehicle were given before ischemia and just before reperfusion. Findings of the isometric contraction studies in the organ bath and of the histological examinations along with oxidative stress markers were evaluated in bladder tissues. Increased malondialdehyde (MDA) levels and myeloperoxidase (MPO) activities and decreased glutathione (GSH) levels and superoxide dismutase (SOD) activities in the I/R group were reduced by QT treatment. In the I/R group, pro-apoptotic marker caspase-3 was increased and anti-apoptotic bcl-2 protein was decreased, while QT treatment significantly reversed these parameters. In the I/R group contractile responses of the bladder strips to carbachol were significantly lower than those of the control group, which were reversed by QT treatment. Quercetin treatment protects bladder tissue contractility against acute I/R injury by decreasing oxidative stress and apoptosis induced by I/R.

Ameliorative effect of quercetin against arsenic-induced sperm DNA damage and daily sperm production in adult male rats

In this study, the protective effect of quercetin was evaluated against arsenic induced reproductive ailments in male rats. For this purpose, male rats (n = 5/group) weighing 180–250 g were used. First group served as control, second group received arsenic (50 ppm) in drinking water. Third group was treated with quercetin (50 mg/kg) alone, while fourth group received arsenic + quercetin. All treatments were carried out for 49 days. After treatment, animals were killed by decapitation; testis and epididymis were dissected out. Right epididymis was minced immediately for comet assay, while left epididymis was processed for histology. Similarly, right testis was homogenized for estimation of daily sperm production (DSP) and detection of metal concentration. The results of our research revealed that arsenic treatment did not cause any significant change in body weight and testicular volume. Quercetin treatment significantly prevented tissue deposition of arsenic within the testis. Arsenic treatment caused a significant reduction in DSP, however, in the arsenic + quercetin-treated group and quercetin alone-treated group, DSP was significantly high as compared to the arsenic-treated group. Histological study of epididymis showed empty lumen in arsenic-treated group while in arsenic + quercetin-treated group and quercetin alone-treated group, lumen were filled with sperm and were comparable to control. Sperm DNA damage, induced by arsenic, was significantly reversed toward control levels by supplementation of quercetin. These results suggest that quercetin not only prevents deposition of arsenic in tissues, but can also protect the sperm DNA damage.

Quercetin protects HCT116 cells from Dichlorvos-induced oxidative stress and apoptosis.

The present study was designed to assess the possible protective effects of Quercetin (QUER), a flavonoid with well-known pharmacological effects, against Dichlorvos (DDVP)-induced toxicity in vitro using HCT116 cells. The cytotoxicity was monitored by cell viability, reactive oxygen species (ROS) generation, anti-oxidant enzyme activities, malondialdehyde (MDA) production, and DNA fragmentation. The apoptosis was assessed through the measurement of the mitochondrial transmembrane potential (ΔΨm) and caspase activation. The results indicated that pretreatment of HCT116 cells with QUER, 2 h prior to DDVP exposure, significantly decreased the DDVP-induced cell death, inhibited the ROS generation, modulated the activities of catalase (CAT) and superoxide dismutase (SOD), and reduced the MDA level. The reductions in mitochondrial membrane potential, DNA fragmentation, and caspase activation were also attenuated by QUER. These findings suggest that dietary QUER can protect HCT116 cells against DDVP-induced oxidative stress and apoptosis.

Possible Protective Effects of Quercetin and Sodium Gluconate Against Colon Cancer Induction by Dimethylhydrazine in Mice.

Micronutrients in food have been found to have chemopreventive effects, supporting the conclusions from epidemiologie studies that consumption of fresh fruits and vegetables reduces cancer risk. The present study was carried out to evaluate the role of querctin (Q) and sodium gluconate (GNA) supplementation separately or in combination in ameliorating promotion of colon tumor development by dimethyl-hydrazine (DMH) in mice. Histopathological observation of colons in mice treated with DMH showed goblet cell dysplasia with inflammatory cell infiltration. This pathological finding was associated with significant alteration in oxidative stress markers in colon tissues and carcinoembryonic antigen (CEA) levels in plasma. Mice co-treated with GNA and Q showed mild changes of absorptive and goblet cells and inflammatory cell infiltration in lamina properia, with improvement in oxidative stress markers. In conclusion, findings of the present study indicate significant roles for reactive oxygen species (ROS) in pathogenesis of DMH-induced colon toxicity and initiation of colon cancer. Also, they suggest that Q, GNA or the combination of both have a positive beneficial effect against DMH induced colonic cancer induction in mice.

Effect of quercetin against mixture of four organophosphate pesticides induced nephrotoxicity in rats

1. It has been demonstrated that the ingestion of foods containing quercetin protects against the toxicity of single pesticides. The aim of this study is to make a comprehensive elaboration about the protective effect of quercetin against multi-organophosphorous pesticides induced nephrotoxicity by measuring indices in rat kidney, urine and serum. Rats were divided into six groups (n = 10/group): control, two different doses of quercetin, pesticide mixture (PM), and different doses of quercetin plus PM-treated groups.2. The following parameters were significantly changed in PM-treated groups compared with the control (p < 0.01). In kidney, malondialdehyde level raised; catalase, superoxide dismutase activities and glutathione levels were decreased. Comet assay of nephrocytes showed that the proportion of DNA in the tail and tail length increased. In urine, β2-microglobulin, retinol-conjugated protein levels and N-acetyl-β-d-glucosaminidase activity showed increasing response; meanwhile uric acid level was decreased. In serum, creatinine and urea nitrogen levels were increased. However, the anomaly changes of indexes mentioned above in PM-treated group were alleviated when simultaneously administrated with 50 mg/kg body weight/day quercetin (p < 0.05).3. From the present findings, it can be evaluated that quercetin may protect against adverse effects resulted from multi-organophosphorous pesticides with significant high levels of uptake in man provided.