Archive for the ‘quercetin’ Category

AHFS Drug Information (2010)[40] identifies quercetin as an inhibitor of CYP2C8, and specifically names it as a drug with potential to have harmful interactions with taxol/paclitaxel

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Posted 19 Jun 2011 — by James Street
Category Chemotherapy, docetaxel, Drug Interactions, Drugs, quercetin, quercetin

Drug interactions

Quercetin is contraindicated with some antibiotics; it may interact with fluoroquinolones (an antibiotic), as quercetin competitively binds to bacterial DNA gyrase. Whether this inhibits or enhances the effect of fluoroquinolones is not certain.[39]

AHFS Drug Information (2010)[40] identifies quercetin as an inhibitor of CYP2C8, and specifically names it as a drug with potential to have harmful interactions with taxol/paclitaxel. As paclitaxel is metabolized primarily by CYP2C8, its bioavailability may be increased unpredictably, potentially leading to harmful side effects.[41][42]

Quercetin is described as an inhibitor of CYP2C9.[43] Quercetin is an inhibitor[44] and inducer[45] of CYP3A4 (in other words, it reduces the enzyme’s activity in the short term, but the body responds by producing more of it). CYP2C9 and CPY3A4 are members of the cytochrome P450 mixed-function oxidase system, and as such are enzymes involved in the metabolism of xenobiotics in the body. In either case, quercetin may alter serum levels, and potentially, effects of drugs metabolized by these enzymes.

The impact of quercetin on cisplatin-induced clastogenesis and apoptosis in murine marrow cells

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Posted 09 Jun 2011 — by James Street
Category Chemotherapy, Cisplatin, quercetin, quercetin
  1. Sabry M. Attia*

+ Author Affiliations


  1. Department of Pharmacology, College of Pharmacy, King Saud University, PO 2457, Riyadh 11451, Saudi Arabia
  1. *To whom correspondence should be addressed. Tel:             +966 542927708 begin_of_the_skype_highlighting +966 542927708 end_of_the_skype_highlighting ; Fax: +966 14677200; Email: attiasm@yahoo.com
  • Received December 5, 2009.
  • Revision received January 10, 2010.
  • Accepted January 14, 2010.

Abstract

  1. » Abstract
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The aim of the present investigation is to determine whether the quercetin in combination with cisplatin can ameliorate cisplatin-induced clastogenesis and apoptosis in the bone marrow cells of mice. The scoring of chromosomal aberrations, micronuclei and mitotic activity were undertaken in the current study as markers of clastogenicity. Apoptosis was analysed by the Annexin V–propidium iodide assay and the occurrence of a hypodiploid DNA peak. Oxidative stress markers such as bone marrow lipid peroxidation and reduced glutathione were assessed as a possible mechanism underlying this amelioration. Quercetin was neither clastogenic nor apoptogenic in mice at doses equivalent to 50 or 100 mg/kg for 2 days. Pre-treatment of mice with quercetin significantly reduced cisplatin-induced clastogenesis and apoptosis in the bone marrow cells and these effects were dose and time dependent. Prior administration of quercetin ahead of cisplatin challenge ameliorated oxidative stress markers. Overall, this study provides for the first time that quercetin has a protective role in the abatement of cisplatin-induced clastogenesis and apoptosis in the bone marrow cells of mice that resides, at least in part, in its antioxidant effects. Therefore, quercetin can be a good candidate to decrease the deleterious effects of cisplatin in the bone marrow cells of cancer patients treated with this drug.

Daily Quercetin Supplementation Dose-Dependently Increases Plasma Quercetin Concentrations in Healthy Humans 1,2

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Posted 09 Jun 2011 — by James Street
Category quercetin
Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Sarah Egert3, Siegfried Wolffram4, Anja Bosy-Westphal3, Christine Boesch-Saadatmandi3, Anika Eva Wagner3, Jan Frank3, Gerald Rimbach3 and Manfred James Mueller3,*3 Institute of Human Nutrition and Food Science and 4 Institute of Animal Nutrition, Physiology and Metabolism, Christian-Albrechts-University Kiel, 24105 Kiel, Germany

Our aim was to investigate the effects of an oral supplementation of quercetin at 3 different doses on plasma concentrations of quercetin, parameters of oxidant/antioxidant status, inflammation, and metabolism. To this end, 35 healthy volunteers were randomly assigned to take 50, 100, or 150 mg/d (group Q50–Q150) quercetin for 2 wk. Fasting blood samples were collected at the beginning and end of the supplementation period. Compared with baseline, quercetin supplementation significantly increased plasma concentrations of quercetin by 178% (Q50), 359% (Q100), and 570% (Q150; P < 0.01 for all). High interindividual variation was found for plasma quercetin concentrations (36–57%). Quercetin did not affect concentrations of serum uric acid or plasma α- and γ-tocopherols, oxidized LDL, and tumor necrosis factor-α, or plasma antioxidative capacity as assessed by the ferric-reducing antioxidant potential and oxygen radical absorbance capacity assays. In addition, serum lipids and lipoproteins, body composition, and resting energy expenditure did not significantly change during quercetin supplementation. Pharmacokinetics of quercetin were investigated in a subgroup of 15 volunteers. The areas under the plasma concentration-time curves ranged from 76.1 µmol·min·L–1 to 305.8 µmol·min·L–1 (50- and 150-mg dosages, respectively). Median maximum plasma concentrations of quercetin (431 nmol/L) were observed 360 min after intake of 150 mg quercetin. In conclusion, daily supplementation of healthy humans with graded concentrations of quercetin for 2 wk dose-dependently increased plasma quercetin concentrations but did not affect antioxidant status, oxidized LDL, inflammation, or metabolism.

* To whom correspondence should be addressed. E-mail: mmueller@nutrfoodsc.uni-kiel.de.

Manuscript received 23 April 2008. Initial review completed 12 May 2008. Revision accepted 12 June 2008.

The impact of quercetin on cisplatin-induced clastogenesis and apoptosis in murine marrow cells

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Posted 02 Jun 2011 — by James Street
Category Antioxidants, antioxidents, Cisplatin, quercetin
  1. Sabry M. Attia*

+ Author Affiliations


  1. Department of Pharmacology, College of Pharmacy, King Saud University, PO 2457, Riyadh 11451, Saudi Arabia
  1. *To whom correspondence should be addressed. Tel:             +966 542927708 begin_of_the_skype_highlighting +966 542927708 end_of_the_skype_highlighting ; Fax: +966 14677200; Email: attiasm@yahoo.com
  • Received December 5, 2009.
  • Revision received January 10, 2010.
  • Accepted January 14, 2010.

Abstract

The aim of the present investigation is to determine whether the quercetin in combination with cisplatin can ameliorate cisplatin-induced clastogenesis and apoptosis in the bone marrow cells of mice. The scoring of chromosomal aberrations, micronuclei and mitotic activity were undertaken in the current study as markers of clastogenicity. Apoptosis was analysed by the Annexin V–propidium iodide assay and the occurrence of a hypodiploid DNA peak. Oxidative stress markers such as bone marrow lipid peroxidation and reduced glutathione were assessed as a possible mechanism underlying this amelioration. Quercetin was neither clastogenic nor apoptogenic in mice at doses equivalent to 50 or 100 mg/kg for 2 days. Pre-treatment of mice with quercetin significantly reduced cisplatin-induced clastogenesis and apoptosis in the bone marrow cells and these effects were dose and time dependent. Prior administration of quercetin ahead of cisplatin challenge ameliorated oxidative stress markers. Overall, this study provides for the first time that quercetin has a protective role in the abatement of cisplatin-induced clastogenesis and apoptosis in the bone marrow cells of mice that resides, at least in part, in its antioxidant effects. Therefore, quercetin can be a good candidate to decrease the deleterious effects of cisplatin in the bone marrow cells of cancer patients treated with this drug.

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