Chopra, M, Fitzsimons, PE, Strain, JJ, Thurnham, DI & Howard, AN. Nonalcoholic red wine extract and quercetin inhibit LDL oxidation without affecting plasma antioxidant vitamin and carotenoid concentrations. Clin. Chem., 46, 1162-1170

Northern Ireland Center for Diet and Health (NICHE), University of Ulster, Coleraine BT52 1SA, Northern Ireland.
Clinical Chemistry (Impact Factor: 7.91). 08/2000; 46(8 Pt 1):1162-70.
Source: PubMed


Antioxidant enrichment of LDL can increase its resistance to oxidation and hence reduce its atherogenicity. The objective of the present study was to investigate whether in vivo supplementation with nonalcoholic red wine extract and quercetin can increase the oxidative resistance of LDL, and also whether the supplementation has any effect on other antioxidative micronutrients present in the blood.
Twenty-one male subjects were supplemented with a placebo drink for 2 weeks and randomized into two groups. One group (n = 11) received the red wine extract (1 g/day, equivalent to 375 mL of red wine) and the other group (n = 10) quercetin (30 mg/day) for 2 weeks, followed by a 5-week washout period.
In the red wine extract-supplemented group, ex vivo copper-initiated oxidation of LDL (lag phase, mean +/- SD) was 40 +/- 11 min at the baseline, and increased significantly to 47 +/- 6 min [P <0.05 compared with placebo (38 +/- 4 min) and the washout values (40 +/- 5 min)]. In the quercetin-supplemented group, the lag phase was 44 +/- 11 and 40 +/- 5 min for the baseline and placebo, respectively, and increased significantly to 51 +/- 7 min [P <0.05 compared with placebo and washout (41 +/- 9 min)] after supplementation. Plasma lipids (triglycerides, total cholesterol, LDL- and HDL-cholesterol) did not change during the study period. Supplementation with red wine extract or quercetin had no effect on plasma vitamin C and E, retinol, and carotenoid concentrations.
Alcohol-free red wine extract and one of its components, quercetin, can inhibit LDL oxidation after in vivo supplementation; such "inhibition" is unrelated to changes in antioxidant vitamin and carotenoid concentrations.

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    • "This factor, along with blood cholesterol could be indicative of future risk of cardiovascular disease.[1415] Quercetin has also shown some effects on protecting the cell wall and low density lipoprotein (LDL) against oxidation.[1617] It also has shown beneficial effects on blood pressure in animals and human.[1819] "
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    ABSTRACT: Considering the increased production of free radicals and inflammatory factors in rheumatoid arthritis (RA) and the effects of bioflavonoid quercetin on reducing oxidative stress, inflammation and blood pressure, the present study examined the effects of bioflavonoid quercetin on total antioxidant capacity (TAC) of plasma, lipid peroxidation and blood pressure in women with RA. The current study was a randomized double-blind clinical trial in which 51 women with RA aged 19-70 years, were participated. Patients were assigned into quercetin (500 mg/day) or placebo groups for 8 weeks. Dietary intake was recorded using 24-h dietary recall questionnaire and the physical activity was assessed through an international short questionnaire of physical activity at the beginning and end of the study. Plasma TAC and malondialdehyde (MDA) using colorimetric method, oxidized low density lipoprotein (ox-LDL) and high sensitivity C-reactive protein (hs-CRP) using enzyme-linked immunosorbent assay method and also blood pressure were measured at the beginning and end of intervention. After 8 weeks there were no significant differences in TAC of plasma, ox-LDL, MDA, hs-CRP, systolic and diastolic blood pressure between quercetin and placebo groups and in each group comparing before and after. In this study, quercetin had no effect on oxidative and inflammatory status of plasma and blood pressure in patients with RA. Further studies are needed to ensure the effect of quercetin on oxidative stress and inflammation in human.
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    • "Except for anti-oxidative and anti-inflammatory effects of quercetin, which are repeatedly described in the literature (Boots et al., 2008; Gonzalez-Segovia et al., 2008; Hamalainen et al., 2007), published data on the effects of quercetin on lipid metabolism are rather inconsistent. Thus dietary quercetin supplementation either had no effect on fasted plasma lipids in rats (Yugarani et al., 1992) and humans (Chopra et al., 2000), or decreased fasted plasma lipids in rats (Kaku et al., 1999) and pigs (Gabler et al., 2005), or even increased fasted plasma lipids in rats (Vessal et al., 2003); quercetin and its glycoside have been shown to reduce plasma cholesterol in pigs (Gabler et al., 2005), guinea pigs (Zern et al., 2003), hamsters (Auger et al., 2005), rabbits (Kamada et al., 2005) and obese Zucker rats (Rivera et al., 2008) but increased plasma cholesterol in streptozotocin (STZ)induced diabetic rats (Vessal et al., 2003). Antidiabetic effects of quercetin have been assessed using different models with variable results. "
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    ABSTRACT: To study possible insulin sensitizing, anti-inflammatory and anti-oxidative effects of the flavonol quercetin, rats were fed a high-fat diet (19%, w/w) with (HFQ) or without (HF) 0.03% quercetin or a flavonoid-poor low-fat (5%, w/w) maintenance diet (LF) over 4 weeks. Body weight was measured weekly, and plasma concentrations of adiponectin, leptin, insulin, glucose, triacylglycerols, total cholesterol, as well as of markers of inflammation and oxidative stress were measured (12h fasted) at the end of the feeding period. Adiponectin and peroxisome-proliferator-activated-receptor (PPAR)-gamma mRNA were measured in adipose tissue (WAT) by real-time RT-PCR. PPAR-gamma transactivation was investigated by means of a reporter gene assay. HF feeding resulted in elevated fasted plasma glucose concentrations, while HFQ did not differ from LF feeding. In the HFQ group plasma concentrations and WAT mRNA levels of adiponectin were elevated compared with the HF group, however, PPAR-gamma mRNA concentration in WAT was decreased (HFQ vs. HF). Compared to both other groups quercetin feeding significantly reduced oxidative stress, measured by plasma 8-iso-PGF(2alpha), while body weight gain, body composition and plasma leptin levels were not affected. Neither quercetin nor its metabolites induced PPAR-gamma-mediated transactivation in vitro. Adiponectin stimulating effects of quercetin are PPAR-gamma-independent and prevent impairment of insulin sensitivity without affecting body weight and composition.
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    • "Oxidized LDL plays an important role in the formation of atherosclerotic plaques. Animal studies [5] [6] and some human intervention studies [7] [8] have reported that flavonoids delay the lag time of LDL to oxidation. "
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