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PubMedDate not supplied

[Pancreaticoduodenectomy--the rutin surgery?].

Pancreaticoduodenectomy with or without pylorus preserving remains the only possibility for cure for the patients with malignant tumors of duodenum, periampullary and cefalopancreatic region, and distal biliary tumors; Pancreaticoduodenectomy is proceeded also for benign tumors of the head of the pancreas (chronic pancreatitis, cysts) but today the standard became preserving duodenum pancreatectomy with good functional results comparing with standard Whipple resection. The last decade had shown a dramatically decrease of the postoperative death for this kind of operations, centers with high volume have been reported a postoperative mortality rate between 1-3%. Our study is a retrospective analysis witch compare the postoperative mortality between 1 January 1990-1 October 2002. The results have shown a decrease of the postoperative mortality from 30.4% (1990-1995) to 9.8% (1995-1999) and 3.6% in the last three years (2000-2002). Also the surgeon volume of operation is closely linked with the postoperative mortality, at the first operations the postoperative mortality rate is 20-33% and after 20 pancreaticoduodenectomy the rate decrease dramatically to 2.6-5.5%. We conclude that pancreatodudenectomy today is routine operation which mortality have decreased at 5% and should be performed in high volume hospitals by surgeons with sufficient experience to minimize the postoperative death.

Carcinoma↗
PubMed2004

Pelargonidin is absorbed and metabolized differently than cyanidin after marionberry consumption in pigs.

Weaning pigs (7.9 +/- 1.7 kg) were fed a freeze-dried powder of marionberry (MB) by stomach tube to study the absorption and metabolism of anthocyanins. Four major anthocyanins (ACNs) were found in MB: cyanidin-3-glucoside (Cy-3-glc, 78%), cyanidin-3-rutinoside (Cy-3-rutin, 20%), pelargonidin-3-glucoside (Pg-3-glc, 0.4%), and 1 unknown acylated cyanidin-based ACN (UACy, 1.5%). In the urine, the 4 original ACNs and 11 metabolites were identified and quantified. The main metabolites were glucuronidated and/or methylated forms of the original anthocyanins. Total recovery of the 4 original ACNs plus their related metabolites was 0.087 +/- 0.034% for Cy-3-glc, 0.084 +/- 0.026% for Cy-3-rutin, 0.583 +/- 0.229% for Pg-3-glc and 0.036 +/- 0.011% for UACy (mean +/- SD, n = 3), respectively. For the individual ACNs, the amount of metabolites recovered from Cy-3-rutin was lower than that of the original intact Cy-3-rutin, whereas the amounts of metabolites from Cy-3-glc and Pg-3-glc in the urine were much higher than their original forms. In pig plasma, the 2 original ACNs, Cy-3-glc and Cy-3-rutin, and a trace of 1 metabolite (cyanidin monoglucuronide) were detected. The plasma concentration:dose ratio of Cy-3-rutin was higher than that of Cy-3-glc. Different aglycones and/or sugar moieties may influence the absorption and metabolism of ACNs. Cy-3-glc and Cy-3-rutin had similar apparent excretion rates relative to dose, whereas Pg-3-glc had a much higher total urinary excretion than cyanidin-based anthocyanins. Most of Cy-3-glc and Pg-3-glc were excreted in the form of metabolites, whereas most of the Cy-3-rutin was excreted in its original unmetabolized form. Urinary recovery of the acylated anthocyanin was lower than that of nonacylated anthocyanins.

Animals↗
PubMed1997

Virucidal treatment of blood protein products with UVC radiation.

The virus safety of blood derivatives continues to be of concern, especially with respect to nonenveloped and/or heat-stable viruses. Previously, we demonstrated that treatment of whole plasma, AHF concentrate or fibrinogen with short wavelength ultraviolet light (UVC) results in the inactivation of > or = 10(6) infectious doses (ID) of encephalomyocarditis virus (EMCV), hepatitis A virus (HAV) and porcine parvovirus (PPV), each of which is nonenveloped. Protein recovery was enhanced greatly by inclusion of the flavonoid, rutin, added prior to UVC exposure to quench reactive oxygen species. We now report on the treatment of albumin and intravenous immune globulin (IVIG) isolated by a previously described, integrated chromatographic method. Albumin was treated with either 0.1 or 0.2 J/cm2 UVC in the presence of 0.8 or 1.6 mM rutin; IVIG was treated with either 0.05 or 0.1 J/cm2 UVC in the presence of 0.5 or 1.0 mM rutin. Our results show that > or = 10(6.9) ID of EMCV and PPV were inactivated under each of the conditions studied except the treatment of albumin with 0.1 J/cm2 UVC in the presence of 1.6 mM rutin where 10(4.3) ID of EMCV and > or = 10(6.9) ID of PPV were killed. It appears that the sensitivity of PPV to UVC exceeds that of EMCV and that virus kill with UVC is higher in IVIG than in albumin. In the absence of rutin, UVC increased the extent of aggregation of both albumin and IVIG by two- to three-fold. With rutin present, the increase in albumin aggregation was reduced, and it was virtually eliminated by subsequent processing on Sephacryl S-200, a step in the existing procedure designed to remove aggregates. The increase in aggregation of IVIG appeared to be eliminated on inclusion of either 0.5 mM or 1 mM rutin. We conclude that both albumin and IVIG can be treated with UVC to inactivate > or = 10(6) ID of nonenveloped viruses. The inclusion of rutin during treatment helps protect against protein aggregation.

Blood Proteins↗
PubMed1998

Antiradical and chelating effects in flavonoid protection against silica-induced cell injury.

Quercetin, dihydroquercetin, and rutin are capable of scavenging superoxide anion (rate constants of the reaction with superoxide at pH 10 were 1.7 x 10(5), 1.5 x 10(5), and 0.5 x 10(5) M-1 s-1, respectively). At the same time rutin and quercetin but not dihydroquercetin are iron ion chelators. These substances were used to elucidate the role of radical scavenging and iron chelating in flavonoid protection against asbestos-induced oxidative cellular injury. Exposure of rat peritoneal macrophages to chrysotile asbestos fibers resulted in "frustrated" phagocytosis, cell injury, and a LDH release. Quercetin, dihydroquercetin, and rutin were effective in protecting the phagocytic cells against injury caused by asbestos. Moreover, these flavonoids exhibited cellular protection in the same order of effectiveness as that observed for the quenching of superoxide: quercetin > dihydroquercetin > rutin. Exposure of human red blood cells to asbestos fibers also caused progressive cell injury and lysis. Quercetin and rutin protected the red cells (quercetin > rutin), whereas dihydroquercetin was ineffective in preventing asbestos-induced hemolysis. The protective ability of quercetin and rutin may be related to their iron-chelating activity. Due to this these flavonoids can be located on asbestos surface in sites of initiation of free radical reactions and their antiradical moieties can scavenge reactive oxygen species immediately after the appearance. Thus, both antiradical and chelating effects appear to be involved in the flavonoid protection against silica-induced cell injury.

Animals↗
PubMed2006

Flavonoids suppresses the enhancing effect of beta-carotene on DNA damage induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in A549 cells.

This study investigated the individual and combined effects of beta-carotene with a common flavonoid (naringin, quercetin or rutin) on DNA damage induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a potent tobacco-related carcinogen in human. A human lung cancer cell line, A549, was pre-incubated with beta-carotene, a flavonoid, or both for 1h followed by incubation with NNK for 4 h. Then, we determined DNA strand breaks and the level of 7-methylguanine (7-mGua), a product of NNK metabolism by cytochrome P450 (CYP). We showed that beta-carotene at 20 microM significantly enhanced NNK-induced DNA strand breaks and 7-mGua levels by 90% (p < 0.05) and 70% (p < 0.05), respectively, and that the effect of beta-carotene was associated with an increased metabolism of NNK by CYP because the concomitant addition of 1-aminobenzotriazole, a CYP inhibitor, with beta-carotene to cells strongly inhibited NNK-induced DNA strand breaks. In contrast to beta-carotene, incubation of cells with naringin, quercetin or rutin added at 23 microM led to significant inhibition of NNK-induced DNA strand breaks, and the effect was in the order of quercetin > naringin > rutin. However, these flavonoids did not significantly affect the level of 7-mGua induced by NNK. Co-incubation of beta-carotene with any of these flavonoids significantly inhibited the enhancing effect of beta-carotene on NNK-induced DNA strand breaks; the effects of flavonoids were dose-dependent and were also in the order of quercetin > naringin > rutin. Co-incubation of beta-carotene with any of these flavonoids also significantly inhibited the loss of beta-carotene incorporated into the cells, and the effects of the flavonoids were also in the order of quercetin > naringin > rutin. The protective effects of these flavonoids may be attributed to their antioxidant activities because they significantly decreased intracellular ROS, and the effects were also in the order of quercetin > naringin > rutin. These in vitro results suggest that a combination of beta-carotene with naringin, rutin, or quercetin may increase the safety of beta-carotene.

DNA Damage↗
PubMedDate not supplied

t-BOOH-induced oxidative damage in sickle red blood cells and the role of flavonoids.

Sickle cell anemia is a genetic disease characterized byan increase in generation of reactive oxygen species, abnormal iron release and low antioxidant activity which can lead to cell injury. Several therapies have been used to decrease the oxidative damage in these patients. In this study, we investigated the effect of flavonoids (quercetin and rutin) on the oxidation of red blood cells (RBC) from sickle cell anemia patients following exposure of the cells to tert-butyl hydroperoxide (t-BOOH). Quercetin provided greater protection against Hb oxidation, the binding of Hb to membrane and lipid peroxidation than did rutin. Quercetin (150 microM) reduced Hb oxidation by 30% and increased the level of oxyHb from 17.5 to 29 microM. Rutin prevented Hb oxidation only at concentrations higher than 200 microM and did not prevent the binding of Hb to RBC membrane. These distinct effects of the flavonoids probably reflect their structural characteristics. Thus, quercetin, which possesses a suitable structure for free-radical scavenging and ion quelation, was a more effective antioxidant than rutin. The presence of rutinose at position C(3) in rutin may impair its antioxidant effect. The presence of ascorbic acid enhanced the protective effect of quercetin and rutin against oxidative stress in sickle Hb and lipid peroxidation. This synergistic action helped to maintain a constant supply of flavonoids and thus, rescue the cells from the injury caused by free radicals and iron ions.

Anemia, Sickle Cell↗
PubMed1987

On the mechanism of antithrombotic action of flavonoids.

Flavonols (quercetin and rutin) and flavanes (cyanidol and meciadonol) were studied for their effect on non-enzymatic lipid peroxidation, lipoxygenase and cyclo-oxygenase activities, binding to albumin and platelet membranes. These biochemical properties of four flavonoids were compared with respect to their antithrombotic action in vivo and their efficacy at influencing the platelet-endothelium interaction in vitro. All four flavonoids inhibited the ascorbate-stimulated formation of malondialdehyde by boiled rat liver microsomes (quercetin greater than rutin approximately cyanidol approximately meciadonol) and inhibited platelet lipoxygenase activity (quercetin greater than cyanidol greater than meciadonol greater than rutin) whereas only flavonols, but not flavanes, stimulated cyclo-oxygenase and were bound to platelet membranes. The same two flavonols dispersed platelet thrombi which were adhering to the rabbit aortic endothelium in vitro (EC50 for quercetin was 80 nM and for rutin 500 nM) and prevented platelets from aggregation over blood-superfused collagen strip in vivo (ED50 for quercetin was 5 nmol/kg and for rutin 33 nmol/kg i.v.). Cyanidol and meciadonol were not effective as anti-thrombotic agents. It is concluded that activated platelets adhering to vascular endothelium generate lipid peroxides and oxygen-free radicals which inhibit endothelial biosynthesis of prostacyclin and destroy endothelium-derived relaxing factor (EDRF). Flavonols are anti-thrombotic because they are selectively bound to mural platelet thrombi and owing to their free radical scavenging properties resuscitate biosynthesis and action of endothelial prostacyclin and EDRF. Thus, flavonols release the thrombolytic and vasoprotective endothelial mediators only in these vascular segments which are covered by a carpet of aggregating platelets.

Albumins↗
PubMed1985

Effect of bile acids on formation of the mutagen, quercetin, from two flavonol glycoside precursors by human gut bacterial preparations.

Human fecal cultures, induced with either of the flavonols, quercitrin or rutin, were grown in the presence of various concentrations of chenodeoxycholic acid, deoxycholic acid or cholic acid. Cell-free preparations (fecal preparations) from these cultures were then incubated with rutin or quercitrin. The formation of the aglycone, quercetin, was monitored by the Ames assay using tester strain TA98. The presence of chenodeoxycholic or deoxycholic acids in the quercitrin-induced culture resulted in a fecal preparation which enhanced the mutagenesis of quercitrin approximately two-fold at optimal concentrations of 0.6 mM and 0.8 mM respectively. Higher concentrations of these bile acids decreased the activity of the fecal preparations. Cholic acid gave similar results except a much higher concentration (3.0 mM) was required to achieve this effect. Analogous results with rutin-induced cultures were less clear cut: considerable variation in bile acid effect was noted among volunteers. The authors propose that bile acid in the medium may enhance the ability of rutin- and quercitrin-glycosidase elaborating organisms to successfully compete with other microbial populations. Additionally, the greater variation in results using rutin as inducer may reflect more heterogeneous populations of organisms active against this substrate. The possible role of bile acids and flavonols in bowel cancer is discussed.

Adult↗
PubMed2005

Evaluation of phenolics and sugars as inducers of quercetinase activity in Penicillium olsonii.

Quercetinase is produced by various filamentous fungi when grown on rutin as sole carbon and energy source. We investigated on the effect of 10 phenolics and two sugars, structurally related to substrates and products of the rutin catabolic pathway, on the induction of a quercetinase activity in Penicillium olsonii. Neither the sugars (glucose and rhamnose, two constituents of rutin), nor phenolics such as protocatechuic acid, salicylic acid, 4-hydroxy-benzoic acid and phloroglucinol were inducers. Rutin (maximum activity 150 nmol/min/mL after 5 days), quercetin (70 nmol/min/mL, 3 days), phloroglucinol carboxylic acid (60 nmol/min/mL, 3 days), 2-protocatechuoylphloroglucinolcarboxylic acid (50 nmol/min/mL, 5 days), 2,6-dihydroxy-carboxylic acid (90 nmol/min/mL, 7 days) and 2,4-dihydroxy-carboxylic acid (30 nmol/min/mL, 7 days) were demonstrated to be quercetinase inducers. We propose that rutin, quercetin and 2-protocatechuoyl-phloroglucinol carboxylic acid, the product of the reaction catalysed by quercetinase, act as inducers after their catabolic transformation in phloroglucinol carboxylic acid.

Carbohydrates↗
PubMed2007

Enzyme-catalyzed change of antioxidants content and antioxidant activity of asparagus juice.

A pectolytic enzyme preparation from Aspergillus niger (pectinase AN) decreased most rutin content and antioxidant activity of asparagus juice. To investigate the mechanism of such loss, we analyzed several possible related enzyme activities in pectinase AN. We found that the activity of pectinase AN to oxidize guaiacol had no significant difference with or without the presence of H2O2; thus it was laccase activity, not peroxidase (PO) activity, that pectinase AN contained. We did not find any polyphenol oxidase (PPO) activity in pectinase AN. Laccase in pectinase AN could be the major cause of loss of rutin and antioxidant activity of asparagus juice. When most laccase activity of pectinase AN was inactivated after heating at 70 degrees C for 1.5 min and incubated with asparagus juice, the loss rate of rutin was only 9% of that treated with unheated pectinase AN, and the antioxidant activity was even increased. Rhamnosidase activity was detected in pectinase AN and can change rutin in asparagus juice to quercetin-3-glucoside, which has higher antioxidant activity than rutin. This may explain the increase of antioxidant activity of asparagus juice treated with heated pectinase AN that still contained some rhamnosidase activity. The discovery of our research is helpful to produce juice with high antioxidant activity and high health benefits in the juice industry.

Antioxidants↗
PubMed2002

Polyphenols in red wine inhibit the proliferation and induce apoptosis of LNCaP cells.

OBJECTIVE: To assess the effect of five polyphenol constituents of red wine (quercetin, morin, rutin, gallic acid and tannic acid) on the proliferation of LNCaP cells, and to quantify the extent of apoptosis with each polyphenol. MATERIALS AND METHODS: LNCaP cells (500) were cultured in microtitre plates and treated with gallic acid, tannic acid, quercetin (1, 5 and 10 micromol/L), rutin and morin (25, 50 and 75 micromol/L). A colorimetric immunoassay was then used to determine the extent of proliferation at 24, 48, 72 and 96 h, and a cell-death detection assay to assess apoptosis at 24, 48 and 72 h. RESULTS: Gallic and tannic acid (5 and 10 micromol/L), morin (50 and 75 micromol/L), quercetin (5 and 10 micromol/L) and rutin (50 and 75 micromol/L) all significantly inhibited (P<0.05) cell proliferation compared with the control. Apoptotic indexes were significantly greater (P<0.01) in the presence of gallic (5 and 10 micromol/L) and tannic acid (5 and 10 micromol/L), and rutin (75 micromol/L, P<0.05) than in the control. The apoptotic effect of morin (75 micromol/L), although significant (P<0.01), only appeared at 72 h. Conversely, while significant (P<0.05) quercetin (5 and 10 micromol/L) had a transient (first 48 h) apoptotic effect compared with the control. CONCLUSION: Quercetin, rutin, morin, gallic acid and tannic acid inhibited the growth of LNCaP cells at different concentrations, and induced apoptosis. The results provide a strong rationale for studying the in vivo effects of these compounds.

Apoptosis↗
PubMed2006

In vitro degradation of the flavonol quercetin and of quercetin glycosides in the porcine hindgut.

The present study investigated the microbial degradation of the plant flavonol quercetin and its naturally occurring glycosides isoquercitrin and rutin in the porcine hindgut. The experiments were carried out with the semicontinuous colon-simulation technique. The fluid and particle phase of pig hindgut contents from freshly slaughtered animals were used for the in vitro incubations. Following a five-day equilibration period, quercetin, isoquercitrin or rutin were administered to fermentation vessels and their turnover rate was determined. None of the flavonols affected parameters of microbial fermentation like pH, redox potential or VFA production. The turnover rate for isoquercitrin was seven times higher than the turnover for the fermentation fluid. The turnover rates for quercetin and rutin were four and twofold higher than fluid turnover, respectively. After administration of isoquercitrin or rutin, their aglycone quercetin was detected as an intermediary metabolite. Under sterile conditions using autoclaved incubation fluids and hindgut contents, turnover rates for quercetin and rutin were still higher than the fluid turnover in the fermentation vessels. This indicates a certain chemical instability of the flavonols and/or adsorption to ingesta particles. Thus, flavonols are subjected to microbial metabolism in the porcine hindgut. The glycosidic structure strongly influences the rate of metabolism.

Adsorption↗