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PubMed1999

Extraction of rutin from buckwheat (Fagopyrum esculentumMoench) seeds and determination by capillary electrophoresis.

The content of the flavonoid rutin was determined in different milling fractions of buckwheat seeds and in buckwheat stems, leaves, and flowers. The extraction was performed by using a solvent containing 60% of ethanol and 5% of ammonia in water. The extracts were analyzed by capillary electrophoresis (running buffer of 50 mM borate (pH 9.3), 100 mM sodium dodecyl sulfate; determination at 380 nm). In bran fractions the concentration of rutin was 131-476 ppm, and in flour fractions 19-168 ppm. On average, about 300, 1000, and 46000 ppm of rutin were found in leaves, stems, and flowers, respectively. The results indicate that buckwheat could be an important nutritional source of flavonoids, especially in countries with a low mean daily flavonoid intake.

Electrophoresis, Capillary↗
PubMed2002

Fast- and slow-release tablets for oral administration of flavonoids: rutin and quercetin.

Many derivatives of rutin (Rt) and its metabolite quercetin (Q) are employed in clinics for cardiovascular chronic pathology, and are also known for their antiulcer behavior in vivo and antiproliferative and antimutagenic activity in vitro. Unfortunately, the absorption of quercetin and rutin from the gastrointestinal tract is slow and irregular, probably due to their very slight solubility in water and slow dissolution rate. In this work the dissolution rate of the drugs from oral formulations has been improved using some enhancers such as cross-linked sodium carboxy, methylcellulose (CMC-XL), sodium carboxymethylstarch (E), and cross-linked polyvinylpyrrolidone (P). The drugs were loaded on the hydrophilic carriers by different techniques such as mixing or co-milling. The in vitro dissolution profiles of the mixed or co-milled drug/polymer systems, obtained in various media with different pH, were compared. The results show that the drug dissolution rate from the co-milled drug/carrier systems is faster than that from mixed systems, and CMC-XL and sodium carboxymethylstarch systems are able to enhance the dissolution rate. For this reason, these co-milled drug/carrier systems were used for the production of both fast- and slow-release tablets. The co-milled drug/CMC-XL system was used for the preparation of fast-release tablets containing rutin, while three different fast-release tablets were formulated and tested using respectively Q/CMC-XL, Q/E, and Q/P co-milled systems. The effect of the presence of sodium lauryl sulfate in the aqueous medium on the dissolution profile of flavonoids alone was also studied. The prolonged-release formulations have been developed using hydroxypropylmethylcellulose (HPMC) of different viscosity grades as retarding polymer. An extended release of the drugs for times ranging from 6 to 14 hr could be obtained, depending on the type and viscosity of the HPMC used.

Administration, Oral↗
PubMed2000

Chemoprevention studies of the flavonoids quercetin and rutin in normal and azoxymethane-treated mouse colon.

In this study we investigated the chemopreventive effects of quercetin and rutin when added to standard AIN-76A diet and fed to normal and azoxymethane (AOM)-treated mice. Early changes in colonic mucosa were analyzed, including colonic cell proliferation, apoptotic cell death, cyclin D(1) expression and focal areas of dysplasia (FAD). The findings show that the number of colonic epithelial cells per crypt column increased (P: < 0.01) in each normal mouse group fed the flavonoids; AOM administration increased colonic crypt cell proliferation and resulted in a marked rise of bromodeoxyuridine-labeled cells in the lower proliferative zone of the crypt. Both supplementary dietary quercetin and rutin increased the apoptotic index and caused a redistribution of apoptotic cells along the crypt axis in normal mice fed a standard AIN-76A diet. The number of apoptotic cells/column and apoptotic indices markedly increased (P: < 0.01) in the AOM-treated group compared with untreated animals; apoptotic cells expanded throughout the colonic crypts after flavonoid supplementation and AOM administration. Positive cyclin D(1) expression was detected in mice on diets supplemented either with quercetin (P: < 0.01) or rutin (P: < 0.05). AOM administration resulted in the formation of FAD. Both the number of mice exhibiting FAD and the total numer of FAD observed were significantly reduced (P: < 0.01) in AOM-treated animals fed flavonoids compared with mice maintained on the standard AIN-76A diet. Surprisingly, however, quercetin alone was able to induce FAD in 22% of normal mice fed the standard AIN-76A diet.

Animals↗
PubMed1982

Carcinogenicity test of quercetin and rutin in golden hamsters by oral administration.

Quercetin and its glycoside, rutin were tested for carcinogenicity in non-inbred golden hamsters of both sexes. In Experiment I, 10% quercetin, 10% rutin, or control diet was given to animals for 735 days. In this experiment, tumors appeared mainly in the forestomach, but the incidence was not statistically different among the three groups. Quercetin and rutin were not carcinogenic under these conditions. In Experiment II, Group 1 was given 4% quercetin diet for 709 days. Group 2 was given 1% quercetin diet for 351 days and then the basal diet for 350 days. Group 3 was given 1% quercetin diet and then 1% croton oil diet and Group 4 was given the basal diet followed by 1% croton oil diet, for the same periods as Group 2. Group 5 was given the basal diet for 701 days. In Experiment II, papillomas of the forestomach appeared in Groups 1, 2, and 5, and papillomatosis in Group 3 and 4. There were no statistical differences among experimental groups and respective controls. Thus, quercetin was not carcinogenic when given at the concentrations of 4% and 1%; even with the administration of 1% croton oil after 1% quercetin, there was no increase in tumor incidence.

Administration, Oral↗
PubMed1990

Mutagenic activity in the wine-making process: correlations with rutin and quercetin levels.

Mutagenic activity was monitored during the time course of the vinification process of a Portuguese red wine using the Ames assay. Dependence upon faecalase treatment for detection of mutagenicity was evaluated concurrently with HPLC analysis of the flavonoids rutin and quercetin. Rutin (quercetin-o-3-rutinoside) is liberated from the grapes during the first 10 days of the process and is hydrolysed as the vinification process proceeds. This explains the levels of the free quercetin in the wine and mutagenicity in the absence of faecalase treatment. Mutagenicity in the presence of faecalase during the first 26 days of the process correlates with the levels of rutin, and in the absence of faecalase the highest mutagenic activity detected (160th day) coincides with the highest level of free quercetin. Our results do not rule out the possibility that other mutagens are present in wines, in particular oxidative-type mutagens.

Animals↗
PubMed2000

Protective effects of N-acetylcysteine and rutin on the lipid peroxidation of the lung epithelium during the adult respiratory distress syndrome.

This study investigates the effects of N-acetylcysteine (NAC) and rutin on the lung oxidative burden of patients with early adult respiratory distress syndrome (ARDS). The protection was evaluated by measuring expired ethane and malondialdehyde (MDA), and oxidized (GSSG) and reduced glutathione (GSH) in the epithelial lining fluid of 36 patients who developed ARDS less than 24 hours before enrollment in the study. The patients were randomly assigned to 3 groups, receiving 250 mL 5% dextrose in water (group 1), NAC 50 mg/kg body weight in 5% dextrose (group 2), and NAC 50 mg/kg + rutin 5 mg/kg in 5% dextrose (group 3). Ethane and MDA concentrations were significantly reduced in the treatment groups after day 6. GSH was 30% increased in the treatment groups. No significant variations were observed in the control group until day 9. The trial confirms that NAC and rutin are efficient in protecting the lungs of patients with ARDS.

APACHE↗
PubMed1995

Prevention by alpha-tocopherol and rutin of glutathione and ATP depletion induced by oxidized LDL in cultured endothelial cells.

1. Oxidized low density lipoproteins (LDL) are thought to play an important role in atherogenesis. Mildly oxidized LDL are cytotoxic to cultured endothelial cells. Toxic doses of oxidized LDL promote the peroxidation of cellular lipids (beginning at 6 h and being maximal after 12 h of pulse with oxidized LDL) and glutathione and ATP depletion (beginning after 15 h of pulse and evolving concurrently with the cytotoxicity). 2. Antioxidants from 3 different classes (rutin, ascorbic acid and alpha-tocopherol) were compared as to their ability to inhibit the cytotoxic effect of oxidized LDL to endothelial cells. 3. Effective concentrations of alpha-tocopherol inhibited cellular lipid peroxidation, glutathione and ATP depletion and the cytotoxic effect. 4. Ascorbic acid was less effective than alpha-tocopherol and rutin, and exhibited a dose-dependent biphasic effect in the presence of oxidized LDL. 5. Effective concentrations of rutin inhibited glutathione and ATP depletion as well as cytotoxicity, but did not block cellular lipid peroxidation. This suggests that the glutathione and ATP depletion is directly correlated to the cytotoxicity of oxidized LDL, whereas cellular lipid peroxidation is probably not directly the cause of cellular damage leading to cell death. 6. The association of antioxidants of 3 different classes allowed the suppression of the biphasic effect of ascorbic acid and increased the efficacy of the protective effect. The potential consequences for prevention of the pathogenic role of oxidized LDL in endothelial injury are discussed.

Adenosine Triphosphate↗
PubMed2000

Lack of effect of the flavonoids, myricetin, quercetin, and rutin, on repair of H2O2-induced DNA single-strand breaks in Caco-2, Hep G2, and V79 cells.

In the present study the effects of three flavonoids on the repair of H2O2-induced DNA strand breaks were investigated in Caco-2, Hep G2, and V79 cells. At the concentrations used, myricetin, quercetin, rutin, and H2O2 did not significantly affect cell viability in all the cell lines. Catalase activity was measured in V79 cells and was found to be considerably lower than activities previously measured in Caco-2 and Hep G2 cells. Cells were exposed to 50 microM H2O2 for 0.5 hour at 37 degrees C. After treatment, DNA strand break repair in H2O2-treated cells was monitored at various time points over a 48-hour period using the alkaline single-cell gel electrophoresis assay. Caco-2 cells repaired faster than Hep G2 cells, which repaired considerably faster than V79 cells. Preincubation with 50 microM quercetin for 24 hours significantly decreased the extent of H2O2-induced DNA single-strand breaks throughout repair time points in Caco-2 cells (p < 0.05), but not in Hep G2 cells. Myricetin (50 microM) and rutin (50 microM) had no effect on repair in Caco-2 and Hep G2 cells. Preincubation for 10 hours with quercetin and rutin, but not myricetin, significantly decreased the initial extent of DNA damage induced by H2O2 in V79 cells (p < 0.05). However, from the results of this study, none of the three flavonoids increased the rate of repair of strand breaks in any of the cell types.

Caco-2 Cells↗
PubMed2005

Capillary electrophoresis with chemiluminescence detection of rutin and chlorogenic acid based on its enhancing effect for the luminol-ferricyanide system.

A capillary electrophoresis with chemiluminescence method has been developed for the determination of rutin and chlorogenic acid based on its enhancing effect on the luminol-ferricyanide system. Under the optimum conditions, the analytes could be separated within 5 min, and the detection limits of the proposed method were 0.22 microg/ml for rutin and 0.50 microg/ml for chlorogenic acid, respectively. The method was successfully applied to the analysis of rutin and chlorogenic acid in real samples.

Chlorogenic Acid↗
PubMed1990

Prevention of diabetes-increased aging effect on rat collagen-linked fluorescence by aminoguanidine and rutin.

Products from the advanced Maillard reaction, which increase during aging and diabetes, may contribute to the development of the typical pathology of aging and diabetes. These compounds are detectable only by their characteristic fluorescence, and few data based on long-term studies are available. For this reason, we studied subcutaneous skin collagen fluorescence in 57 nondiabetic (10- to 110-wk-old) and 74 streptozocin-induced diabetic (10- to 22-wk-old) rats. An exponential increase (r = 0.969, P less than 0.001) of collagen-linked fluorescence (excitation at 370 nm, emission at 440 nm) was observed with aging; after a lag, diabetes induced an earlier dramatic elevation of the fluorescence, suggesting a more complicated phenomenon than simple accumulation. To prevent such increases, the effects of 1 g.kg-1.day-1 aminoguanidine, suggested to be an inhibitor of the advanced glycosylation reaction, and 1 g.kg-1.day-1 rutin, an aldose reductase inhibitor, in drinking water were tested. Both treatments had a significant lowering effect on collagen fluorescence in diabetic rats. The mechanisms by which aminoguanidine and rutin prevent the accumulation of fluorescence are unknown, but these observations raise the question of whether they could be identical. If fluorescence is a marker for age-related pathologies and diabetic sequelae, aminoguanidine and rutin could have therapeutic effects in their prevention.

Aging↗
PubMed2003

[Determination of adenosine, rutin and quercetin in Carthamus tinctorius by HPCE].

AIM: To develop a method for determination of adenosine, rutin and quercetin in Carthamus tinctorius L. by high performance capillary electrophoresis(HPCE). METHODS: A fused silica capillary (66.5 cm x 50 microns ID, an effective length of 58 cm) was used. The running buffer composed of 50 mmol.L-1 borax (pH 9.7) containing 18% methanol. The applied voltage was 24 kV and the capillary temperature was 20 degrees C. The detection wavelength was 210 nm. Rifampicin was used as internal standard. RESULTS: A good linearity between peak area ratio of the common peak to the internal standard and the concentration was found in the range of 10-160 mg.L-1 for adenosine, 100-2,000 mg.L-1 for rutin and 100-1,600 mg.L-1 for quercetin (r > 0.998). The average recoveries were 98.5%-100.5%, 96.9%-99.5% and 99.1%-99.5% for adenosine, rutin and quercetin, respectively. The relative standard deviation was less than 6.5% (n = 5). CONCLUSION: The method is simple, rapid and with satisfactory recoveries and good reproducibilities. It can be used to control the quality of Carthamus tinctorius.

Adenosine↗
PubMedDate not supplied

Effect of rutin on total antioxidant status of rats exposed to cigarette smoke.

Exposure to tobacco smoke impairs the antioxidant defense mechanisms. In female Wistar rats fed on regular rodent chow and supplemented with a flavonoids rutin, Trolox Equivalent Antioxidant Capacity (TEAC) was measured as an ABTS-radical cation reduction power in plasma, lungs, liver, brain and kidneys. Exposure to smoke reduced the TEAC values in the liver, brain and kidneys and enhanced antioxidant potential in lungs in comparison to control animals. In plasma no change of TEAC value was observed. Supplementation with rutin increased antioxidant status of plasma, but TEAC was reduced in kidneys, brain and liver of smoke-exposed animals when compared to the matched controls. In lung no change in TEAC was found. The results suggest a complex pattern of influence of tobacco smoke on blood and tissue antioxidant mechanisms. The enrichment of diet with non-nutrient antioxidant rutin did not result in direct improvement of tissue TEAC with the exception of blood plasma.

Animals↗
PubMed1985

Comparative study of antiproliferative effects of chlorpromazine, 7,8-dioxochlorpromazine, amantadine-N-mustard, rutin-N-mustard and alpha, beta and gamma interferon on K-562 cells in vitro.

The effects of rutin-N-mustard, amantadine-N-mustard, chlorpromazine and human interferon types alpha, beta and gamma (IFN-alpha, -beta and -gamma) were studied on the DNA, RNA and protein synthesis of K-562 cells. Monocyte-mediated cytotoxicity and immune spleen cell activity were examined in the presence of the same compounds (except for IFN-beta). The natural killer (NK) cell activity was tested in the presence of the two chlorpromazine compounds and the two N-mustard derivatives. Only 7,8-dioxochlorpromazine exerted an inhibitory effect on DNA synthesis. The protein synthesis of the cells was inhibited in the presence of IFN-alpha, -beta and -gamma. 7,8-Dioxochlorpromazine exerted some inhibition on both NK and immune spleen cell activity, while monocyte-mediated cytolysis was not altered. IFN-alpha, -beta and -gamma activated the cytolytic activity of monocytes and the NK activity in control experiments. Chlorpromazine, rutin-N-mustard and amantadine-N-mustard were ineffective in both tests in vitro. Rutin-N-mustard, 7,8-dioxochlorpromazine and the interferons may be assumed to have quite different antiproliferative mechanisms of actions.

Amantadine↗
PubMed2004

Characterization of non-covalent complexes of rutin with cyclodextrins by electrospray ionization tandem mass spectrometry.

Electrospray ionization tandem mass spectrometry (ESI-MS(n)) and the phase solubility method were used to characterize the gas-phase and solution-phase non-covalent complexes between rutin (R) and alpha-, beta- and gamma-cyclodextrins (CDs). The direct correlation between mass spectrometric results and solution-phase behavior is thus revealed. The order of the 1 : 1 association constants (K(c)) of the complexes between R and the three CDs in solution calculated from solubility diagrams is in good agreement with the order of their relative peak intensities and relative collision-induced dissociation (CID) energies of the complexes under the same ESI-MS(n) condition in both the positive and negative ion modes. Not only the binding stoichiometry but also the relative stabilities and even binding sites of the CD-R complexes can be elucidated by ESI-MS(n). The diagnostic fragmentation of CD-R complexes, with a significant contribution of covalent fragmentation of rutin leaving the quercetin (Q) moiety attached to the CDs, provides convincing evidence for the formation of inclusion complexes between R and CDs. The diagnostic fragment ions can be partly confirmed by the complexes between Q and CDs. The gas-phase stability order of the deprotonated CD-R complexes is beta-CD-R > alpha-CD-R > gamma-CD/R; beta-CD seems to bind R more strongly than the other CDs.

Cyclodextrins↗
PubMedDate not supplied

alpha-Tocopherol, ascorbic acid, and rutin inhibit synergistically the copper-promoted LDL oxidation and the cytotoxicity of oxidized LDL to cultured endothelial cells.

Low-density lipoproteins (LDL) mildly oxidized by copper ions or UV radiations exhibit a cytotoxic effect to cultured endothelial cells. Rutin, a polyphenolic flavonoid, ascorbic acid, and alpha-tocopherol were able to inhibit the peroxidation of LDL and their subsequent cytotoxicity. The mixture of the three compounds (rutin/ascorbic acid/alpha-tocopherol, 4/4/1) exhibited a supra-additive antioxidant effect. The inhibition of the cytotoxic effect was well correlated with that of TBARS formation. Another important conclusion is that these antioxidants were able to prevent directly at the cellular level the cytotoxic effect of oxidized LDL, since cells preincubated with them were protected against the cytotoxic effect of previously oxidized LDL. The protective effect of antioxidants was limited because of their own toxicity. The antioxidant mixture permitted a maximal cytoprotective effect with relatively lower concentrations to be obtained and the cytotoxicity of high concentrations to be avoided. In conclusion, rutin, ascorbic acid, and alpha-tocopherol constitute two lines of defense in protecting cells against injury owing to oxidation of LDL (1) at the LDL level, by inhibiting the LDL oxidation and the subsequent cytotoxicity, and (2) at the cellular level, by protecting the cells directly, i.e., by increasing their resistance against the cytotoxic effect of oxidized LDL.

Animals↗
PubMed1989

Mutagenicity of rutin and the glycosidic activity of cultured cell-free microbial preparations of human faeces and saliva.

Genotoxic testing of flavonol glycosides, which account for most of the human intake of flavonoids, is dependent on the use of enzymatic extracts that exhibit beta-glycosidic activity. This study was aimed at characterizing further the beta-glycosidic activity of cultured cell-free microbial extracts from human faeces (faecalase) and saliva (salivase). Using o-nitrophenyl-beta-D-galactoside as substrate, the optimum pH and apparent Km and energy of activation were shown to be 7.6, 3.5 x 10(-4) M and 8.65 kcal/mol, respectively, for faecalase, and 7.4, 8.7 x 10(-5) M and 3.8 kcal/mol, respectively, for salivase. Rutin (quercetin-3-O-rutinoside) was shown to be a competitive inhibitor for faecalase, whereas no inhibitory activity could be found for salivase. Enzymatic hydrolysis of rutin gave the mutagenic product quercetin that was detected in the Ames assay and using high-performance liquid chromatography.

Cell-Free System↗
PubMed1984

Protective effect of quercetin and rutin on photosensitized lysis of human erythrocytes in the presence of hematoporphyrin.

Photosensitized hemolysis of human erythrocytes by hematoporphyrin was suppressed by flavonols such as quercetin and rutin at submillimolar concentrations. The suppression of photohemolysis was accompanied by inhibition of lipid peroxidation by the reagents. Quercetin and rutin were photooxidized in the presence of hematoporphyrin and the photooxidation was partially suppressed by 1 mM NaN3, a quencher of singlet molecular oxygen. Flavonols were also oxidized by radicals formed during degradation of lauroyl peroxide. These results indicate that flavonols can function as antioxidants in biological systems by terminating radical chain reactions and removing singlet molecular oxygen. A pharmacological function of flavonols, decrease of the increased permeability and fragility of capillary, was discussed in relation to their antioxidative functions.

Erythrocytes↗
PubMed2005

Separation and simultaneous determination of rutin, puerarin, daidzein, esculin and esculetin in medicinal preparations by non-aqueous capillary.

A simple method for the simultaneous determination of five bioactive components (rutin, puerarin, daidzein esculin and esculetin) in traditional medicinal preparations by non-aqueous capillary electrophoresis with UV detection has been developed for the first time. A running buffer composed of 15% acetonitrile, 2.5% acetic acid and 90 mM sodium cholate in methanol was found to be the most suitable for this separation. The limits of detection for five analytes were over the range of 0.050-1.216 microg ml(-1). The relative standard deviations (R.S.Ds.) of the migration times and the peak areas of the analytes were in the range of 1.3-2.9% and 2.2-2.7% (intraday), 1.7-1.9% and 2.8-3.6% (interday), respectively. In the tested concentration range, linear relationships (correlation coefficients: 0.9974 for rutin, 0.9976 for puerarin, 0.9981 for daidzein, 0.9972 for esculin and 0.9929 for esculetin) between peak areas and concentrations of the analytes were obtained. This method has been successfully applied to simultaneous determination of the five bioactive components with recoveries over the range of 89.4-107.4%.

Electrophoresis, Capillary↗