Protection from the negative effects of solar radiation can be achieved by wearing protective clothing, avoiding exposure to sunlight or by the application of topical sunscreens. In this thesis, a number of studies were designed to determine if quercetin is suitable for use as a topical sunscreen.<p> The first objective was to determine if quercetin could protect against UV-induced lipid oxidation. Quercetin is twice as effective at preventing UVB-induced oxidation as preventing UVA-induced oxidation.The difference between UVA- and UVB- induced oxidation is believed to be due to the presence of an excited state form of quercetin in the UVA system. <p> The second objective was to determine the UV photostability of quercetin in solution. Three photoproducts of quercetin form regardless of whether UVA or UVB radiation is used. These photoproducts are 2,4,6-trihydroxybenzaldehyde, quercetin depside and hydroxytyrosol. . The slow rate of formation, less than 20% loss of starting material over 11 hours, and non-toxic nature of the photoproducts indicate that photostability of quercetin is not an obstacle to its use as a sunscreen.<p> The third objective was to determine the ability of quercetin to inhibit photosensitization by ketoprofen. Quercetin was shown to be effective in preventing decomposition of ketoprofen until it was consumed in the formation of the three quercetin photoproducts. This abilty of quercetin to prevent ketoprofen photosensitization indicates a beneficial effect for the use of quercetin as a topical sunscreen.<p> The fourth objective was to determine if quercetin can prevent UV-induced damage in a biological system. Quercetin was found to significantly reduce secretion of matrix metalloprotease 1 (MMP-1) upon UVA or UVB exposure, but had no effect on secretion of tumor necrosis factor á (TNF-á) in HaCaT cells. , Topical application of quercetin to UVA or UVB exposed EpiDerm skin mimics significantly reduced both MMP-1 and TNF-á secretion.<p> These results indicate that quercetin is effective in decreasing or eliminating several harmful effects of UVA and UVB radiation in the skin without major loss of starting material and without formation of toxic photoproducts. As such, quercetin appears to be a good candidate for inclusion into topical sunscreen formulations.

Protection from the negative effects of solar radiation can be achieved by wearing protective clothing, avoiding exposure to sunlight or by the application of topical sunscreens. In this thesis, a number of studies were designed to determine if quercetin is suitable for use as a topical sunscreen.<p> The first objective was to determine if quercetin could protect against UV-induced lipid oxidation. Quercetin is twice as effective at preventing UVB-induced oxidation as preventing UVA-induced oxidation.The difference between UVA- and UVB- induced oxidation is believed to be due to the presence of an excited state form of quercetin in the UVA system. <p> The second objective was to determine the UV photostability of quercetin in solution. Three photoproducts of quercetin form regardless of whether UVA or UVB radiation is used. These photoproducts are 2,4,6-trihydroxybenzaldehyde, quercetin depside and hydroxytyrosol. . The slow rate of formation, less than 20% loss of starting material over 11 hours, and non-toxic nature of the photoproducts indicate that photostability of quercetin is not an obstacle to its use as a sunscreen.<p> The third objective was to determine the ability of quercetin to inhibit photosensitization by ketoprofen. Quercetin was shown to be effective in preventing decomposition of ketoprofen until it was consumed in the formation of the three quercetin photoproducts. This abilty of quercetin to prevent ketoprofen photosensitization indicates a beneficial effect for the use of quercetin as a topical sunscreen.<p> The fourth objective was to determine if quercetin can prevent UV-induced damage in a biological system. Quercetin was found to significantly reduce secretion of matrix metalloprotease 1 (MMP-1) upon UVA or UVB exposure, but had no effect on secretion of tumor necrosis factor á (TNF-á) in HaCaT cells. , Topical application of quercetin to UVA or UVB exposed EpiDerm skin mimics significantly reduced both MMP-1 and TNF-á secretion.<p> These results indicate that quercetin is effective in decreasing or eliminating several harmful effects of UVA and UVB radiation in the skin without major loss of starting material and without formation of toxic photoproducts. As such, quercetin appears to be a good candidate for inclusion into topical sunscreen formulations.

Quercetin is a flavonoid found in commonly consumed fruits and vegetables that has exhibited powerful antioxidant and anti-inflammatory properties in rodents and in vitro. In humans, the ergogenic effects of antioxidant supplementation on exercise performance and adaptations are still equivocal and need to be further investigated. A powerful antioxidant such as quercetin may inhibit the high levels of oxidative stress associated with the high volume and intensity of exercise training seen with trained individuals. There have been equivocal findings thus far regarding the ergogenic effect of either acute or chronic supplementation of quercetin on exercise performance. PURPOSE: To determine the effect of 28 days of daily quercetin supplementation on cycling time trial performance and the associated exercise performance variables. METHODS: Thirteen trained cyclists (VO2peak 58.8 ± 3.9 ml/kg/min) were recruited for this study from the University of Texas at Austin and the local Austin, Texas community and participated in this placebo controlled, randomized, crossover designed study. After initial assessment of baseline data (VO2peak, lactate threshold, and two familiarization time trials), participants began daily supplementation of either an antioxidant supplement containing vitamins and quercetin (Q-VIT: 1000mg quercetin, 820mg Vitamin C, 40mg Vitamin B3) or the same vitamin supplement without quercetin (VIT: 820mg Vitamin C, 40mg Vitamin B3). A simulated time trial using an electromagnetically braked cycle ergometer in which subjects had to complete a set amount of work (kJ) as fast as possible was performed on the last day of supplementation. Measured performance variables included: time to completion, average power output, average oxygen consumption (VO2), Respiratory Exchange Ratio (RER), gross mechanical efficiency (GE), heart rate (HR), and rating of perceived exertion (RPE). RESULTS: Quercetin had no effect on HR, RER, power output, or RPE. There was also no difference in time to complete the time trial between treatments. However, an approximately ~2% higher, but not significantly different, VO2 during Q-VIT supplementation significantly lowered the GE compared to VIT (Q-VIT: 20.49 ± 0.26 % and 19.94 ± 0.33 %; VIT: 20.9 ± 0.24 % and 20.37 ± 0.33 %; p < .01) at 15 and 30 min respectively. CONCLUSION: Chronic supplementation for 28 days with a quercetin based antioxidant supplement lowered cycling gross efficiency in well trained cyclists, but it did not affect performance time. The results of the current study suggest that chronic supplementation with quercetin does not influence aerobic exercise performance in well trained athletes. / text

No description available.

Six long chain fatty acid esters of quercetin-3-O-glucoside (Q3G) acylated enzymatically were used for determining their antiproliferative action in comparison to precursor compounds (quercetin, Q3G and six fatty acids namely, stearic acid, oleic acid, linoleic acid, alpha-linolenic acid, eicosapentaenoic and docosahexanoic acids) using HepG2 cells. Long chain fatty acid esters of Q3G showed significant inhibition of cell proliferation (approximately 85% to 90%) compared to the precursor compounds and two prescribed anticancer-drugs (Sorafenib and Cisplatin) after 6 hrs and 24 hrs by inducing cell cycle arrest, apoptosis and DNA topoisomerase II inhibition. Among the six fatty acid esters of Q3G, oleic acid ester (OA-Q3G) displayed the greatest anti-proliferation action and upon further investigation showed significant regulation of expression of genes involved in cell cycle, growth, survival and apoptosis at gene and protein level. Overall, results of the study suggest strong potential of these novel compounds in treatment of liver cancer.

Ląstelės metabolizme svarbų vaidmenį vaidina oksidacijos – redukcijos reakcijos, kuriose deguonis yra elektronų akceptorius. Įvairių cheminių reakcijų metu gali susidaryti ir aktyviosios deguonies formos – superoksido anijonas, vandenilio peroksidas, hidroksilo radikalas, singletinis deguonis, kurios pažeidžia įvairias biomolekules. Augalai nuo seniausių laikų yra vartojami įvairioms ligoms gydyti. Flavonoidai – tai augalinės kilmės junginiai, randami vaisiuose, daržovėse arbatose, kurie pasižymi antioksidacinėmis savybėmis. Sintetiniai antioksidantai polifenoliai labai plačiai naudojami maisto pramonėje, kaip įvairūs priedai ir konservantai. Vienas jų - kvercetinas. Kvercetino antioksidacinis poveikis priklauso nuo to, kad jis reaguoja su laisvaisiais radikalais, sudarydamas fenoksradikalus, kurie yra ne tokie aktyvūs. Tačiau aukštos kvercetino koncentracijos yra citotoksiškos, o citotoksiškumo mechanizmai, nors ir labai plačiai tyrinėjami visame pasaulyje, lieka neaiškūs. Mūsų darbo tikslas ir buvo ištirti kvercetino ir kitų flavonoidų poveikį Hep 22a linijos ląstelėms. Hep 22a ląstelių linija pasirinkta neatsitiktinai. Tai pelių hepatomos ląstelių kultūra, kuri pasižymi navikinėms ląstelėms būdingomis savybėmis – neribota proliferacija ir ląstelių migracija. Vyrauja epitelinio tipo ląstelės, kurias persėjus po oda susidaro navikai. Ląstelės gerai auga tiek in vivo, tiek in vitro. Ląstelės pailgos, prisitvirtinusios prie substrato, sudaro monosluoksnį. Tirtų flavonoidų... [toliau žr. visą tekstą] / ABSTRACT Flavonoids are widely distributed in edible plants, and considered to be dietary antioxidants. Flavonoids can protect cell from „oxidative stress“, but the same flavonoids compound could behave in two ways as an both antioxidant and prooxidant, depending on the concentration used and free radical source. Among the flavonoids, quercetin is one of the most widely studied flavonoid and has biological, pharmocological, and medicinal properties. Besides the chemopreventive effects, other biological functions of quercetin are believed to improve antioxidant defence systems in living organizms. The aim of this work was to analize the effects of flavonoids (quercetin, myricetin and morin) in Hep 22a cells. Materials and methods: 1. Cell culture cytotoxicity studies; Flavonoids and the other components were obtained from Sigma, and used as received. 2. Study with fluorescence microscope 3. Statistical analysis Results and discusion: Hep 22a cell line is a mouse hepatoma cell line, which posseses the unlimited proliferation and migration features. Quercetin concentration for 50 % death of Hep 22a cells (cL50) was 160 µM, myricetin concentration was 60 µM, and morin concentration was 190 µM,. The citotoxity of flavonoids in Hep 22a cells was partly inhibited by catalase, by the antioxidant N,N‘-diphenyl-p-phenylene diamine DPPD, desferrioxamine and by dicumarol and an inhibitor of DT-diaphorase thus showing its prooxidant character. Inhibitors of cytochromes P-450, &#945... [to full text]

Graduation date: 1961

Quercetin (Q) and chlorogenic acid (CA), two bioactive compounds found in stonefruits, may protect against inflammation and cancer because of anti-cancer, anti-oxidant, and anti-inflammatory properties. Since these compounds reach the colon undigested, they affect the luminal environment before they are metabolized by the microbiota and transported into epithelial cells. We hypothesized that Q and CA may suppress expression of pro-inflammatory molecules, alter the luminal environment, and alter the cell cycle, thereby protecting against injury/colitis. To test this hypothesis, 63 male weanling rats were given one of three diets (basal, 0.45% Q, 0.05% CA). After 3 wk of acclimation, colitis was induced in 11 rats/diet [3% dextran sodium sulfate (DSS), 48 h, 3 treatments, 2 wk separation] and 10 rats/diet served as control (0% DSS). All rats were terminated at wk 9. Measurements included: fecal moisture content, fecal short chain fatty acid (SCFA) concentrations (gas chromatography), epithelial injury and inflammation in the distal colon, proliferation (PCNA), and NF-kappaB activity (ELISA method) and gene expression (real time RT-PCR) in mucosal scrapings. Fecal moisture content was significantly increased by DSS exposure (p<0.05), and never returned to control levels. Fecal SCFA concentrations also increased with DSS (acetate, p<0.05; butyrate, p<0.05). Increased SCFA concentrations could indicate decreased SCFA uptake. Experimental diets were able to mitigate DSS-induced decreases in SLC5A8 (SCFA transporter) expression. DSS significantly increased injury (p<0.0001) and inflammation (p<0.01) scores. Compared to the basal diet, CA decreased NF-kappaB activity in DSS-treated rats (p<0.05). Q and CA may maintain healthy regulation of NF-kappaB through maintaining expression levels of IkappaBalpha and Tollip, molecules that inhibit NF-kappaB activation. Q and CA mitigated DSS-induced increases in pro-inflammatory cytokine expression, specifically IL-1. Q enhanced expression of injury-repair molecule FGF-2 (p<0.01), but neither diet nor DSS treatment altered proliferation. Although Q and CA did not protect against DSS-induced increases in injury and inflammation scores or fecal SCFA concentrations, their influence on expression of injury repair molecules, pro-inflammatory cytokines, SCFA transport proteins, and NF-kappaB inhibitory molecules suggests beneficial influences on major pathways involved in DSS-induced injury/inflammation. The combined benefit of these compounds could have additive/synergistic effects and, therefore, deserve further examination.

In den letzten Jahrzehnten haben Inzidenz und Prävalenz von GEP NET deutlich zugenommen (Yao et al. 2008). Den SSTR kommt eine entscheidende Rolle bei zahlreichen etablierten Therapieverfahren zu. Allerdings stoßen die meisten Therapien bei G3 Tumoren oder bei langfristigem Einsatz an ihre Grenzen, was die Etablierung neuer, molekular zielgerichteter Therapien notwendig macht. Die Inhibition des Wnt-Signalweges stellt einen möglichen Ansatzpunkt für Therapien dar. Ziel dieser Arbeit war es die Wirkung der Wnt-Modulatoren Quercetin und Lithiumchlorid auf die Wnt-Aktivität sowie die Expression von Somatostatinrezeptoren und CXCR4 in den neuroendokrinen Tumorzelllinien QGP-1 und BON-1 zu untersuchen. Durch Real-Time PCR, Western Blots und Immunhistochemie wurden die Effekte auf RNA-, und Proteinebene sowie morphologisch analysiert und ausgewertet. An den verwendeten Zelllinien konnte gezeigt werden, dass Quercetin die Wnt-Signalgebung inhibierte, die SSTR-Expression steigerte und die CXCR4-Expression senkte. Lithiumchlorid bewirkte eine Wnt-Aktivierung und konnte über diesen Weg eine gesteigerte Expression von CXCR4 erzielen. Es konnte gezeigt werden, dass ein Zusammenhang zwischen der Aktivität des Wnt- Signalwegs und der Befähigung der GEP-NET Zelllinien zur SSTR- und CXCR4-Expression bestand. Die Wnt-Inhibierung kann über den Effekt der Steigerung von SSTR Teil neuer Therapiestrategien sein. So ist z.B. eine „add-on“ Therapie von Wnt-Inhibitoren wie Quercetin zusammen mit der PRRT denkbar. / In the last few centuries there is a rising incidence and prevalence on GEP NET noticed (Yao et al. 2008). SSTR are important for established therapy procedures. But there is limitation for most therapies among G3 tumors and in long-term use. So new therapy strategies are needed. Wnt-signaling inhibitors are a potential agent. Aim of this work was to investigate the influence of wnt-signaling modulators quercetin and lithiumchloride on the expression of SSTR and CXCR4 in neuroendocrine tumor cell lines QGP-1 and BON-1. A real-time PCR, western blot and immunohistochemistry were performed. The used cell lines showed that quercetin inhibits wnt-signaling, increases SSTR expression and decreases CXCR4 expression. Lithiumchloride activated Wnt signalling and increased CXCR4 expression. It was shown that there is an association between activated wnt-signaling and the ability of GEP NET cell lines to express SSTR and CXCR4. Wnt inhibition could be part of new strategies for therapy by the effect of increased SSTR expression. For example, an “add on” therapy with wnt inhibitor quercetin in PRRT is a opportunity.

"December 2004." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (p. 221-233) / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.