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Quercetin and quercetin glycosides from food or dietary supplements appear in body tissues almost exclusively as glucuronated, sulfated, and methylated quercetin conjugates, suggesting that the in vivo bioactivity of quercetin may be due to its metabolites. In this study, pre- and postabsorptive metabolism of orally ingested quercetin was examined by comparing the metabolite pattern in gastrointestinal (GI) tissues, contents, and internal tissues. F344 rats (n = 6) were fed for 6 wk a diet containing 0.45% quercetin and the metabolite patterns were determined in the tissues and contents of stomach, small intestine, cecum, and colon and in liver, kidney, and plasma using LC- MS/MS. GI contents contained predominantly unmetabolized quercetin at 94-100%, whereas quercetin in GI tissues was present as 11 different sulfated, glucuronated, and methylated metabolites at 32% in stomach, 88% in small intestine, 27% in cecum, and 46% in colon. Quercetin was further metabolized postabsorption and found in liver, kidney, and plasma almost exclusively as sulfated methyl-quercetin glucuronide. The unique pattern of quercetin metabolites in each GI tissue indicates extensive biotransformation before absorption and distribution in rats. [ABSTRACT FROM AUTHOR]

Aims: (1) Determination of whether isoflavones, as antioxidants and estrogen-like substances, reduce the atherosclerotic process. (2) Assessment of isoflavone anti-atherosclerotic effectiveness by means of measuring plasma markers of atherosclerosis: homocysteine (Hcy), antioxidant status, and lipid peroxidation. (3) Testing of isoflavone antioxidant effectiveness in the presence and absence of oxidative stress induced by exercise. Methods: Thirty subjects paired by aerobic fitness level were randomly assigned to either a placebo or high-genistein isoflavone extract (HGI, 150 mg/day) treatment. Blood samples were collected before and within 5 min, after 30 min at 80% peak oxygen consumption (VO2pk) exercise, and before and after 4-week supplementation. Results: Plasma genistein and daidzein were significantly increased by 4-week HGI supplementation before and after exercise (p < 0.05). HGI decreased pre-exercise (pre-ex) plasma malondialdehyde (MDA) (p < 0.05) and Hcy (p = 0.01), and increased pre-ex blood total glutathione (TGSH) (p = 0.01), but did not diminish the increase of MDA and the decrease of TGSH due to the exercise. Furthermore, HGI supplementation enhanced pre-ex total antioxidant capacity (p < 0.05), but did not influence plasma vitamin C and E and uric acid concentrations. Conclusion: Isoflavones reduce plasma Hcy and have antioxidant activity in healthy young men. However, the effect of isoflavones on antioxidant systems may not be potent enough to diminish an abrupt surge of oxidative stress due to acute exercise. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Our aim was to determine the speed of onset of total parenteral nutrition (TPN)-induced mucosal atrophy, and whether this is associated with changes in intestinal blood flow and tissue metabolism in neonatal piglets. Piglets were implanted with jugular venous and duodenal catheters and either a portal venous or superior mesenteric artery (SMA) blood flow probe. At 3 wk of age, piglets were randomly assigned to receive continuous enteral formula feeding (n = 8) or TPN (n = 17) for 24 or 48 h. Blood flow was recorded continuously and piglets were given an i.v. bolus of bromodeoxyuridine and 13C-phenylalanine to measure crypt cell proliferation and protein synthesis, respectively. After 8 h of TPN, portal and SMA blood flow decreased 30% compared with enteral feeding (P < 0.01), and remained near levels of food-deprived piglets for the remaining 48 h of TPN. After 24 h, TPN reduced jejunal inducible nitric oxide synthase (iNOS) activity and protein abundance (P < 0.05), small intestinal weight, and villous height (P < 0.01) compared with enterally fed piglets. Cell proliferation and DNA mass were decreased (P < 0.05) and apoptosis increased (P < 0.05) after 48 h of TPN. Protein synthesis was lower (P < 0.05) after 24 h of TPN, and protein mass was lower (P < 0.05) after 48 h of TPN, compared with enteral feeding. These data indicate that the transition from enteral to parenteral nutrition induced a rapid (<8 h) decrease in intestinal blood flow, and this likely precedes villous atrophy and the suppression of protein synthesis at 24 h, and of cell proliferation and survival at 48 h. [ABSTRACT FROM AUTHOR]

The article presents an exploratory study which aims to identify what kinds of food and nutrition information consumers are accessing from Web recipes. The authors have investigated the number and kinds of recipe Web sites accessed by college students, the forms of nutrition information associated with these sites, and the credentials of those providing the information. The researchers selected an area of the Dietary Guidelines and chose antioxidant vegetables as a recipe focus in assessing how college students select recipe Web sites. Results reveal that selection of recipes from the Internet lacks adequate nutrition information for consumers to make informed decisions. The findings suggest that nutrition guidance principles need to be developed for professionals publishing on the Web.

The antioxidant and detoxification activity of almond skin polyphenols (ASP) may contribute to the inverse association observed between nut consumption and the incidence of cardiovascular disease. ASP can interact synergistically with vitamin C (VC) to enhance LDL resistance against oxidation. Thus, we tested the antioxidant capacity of ASP alone and in combination with VC to inhibit by 50% (EC50) DPPH, HOCl, ONOO-, and O2- radicals in vitro. ASP were obtained from methanolic (M) and gastrointestinal mimic (GI) extractions. The EC50 for ASP-M was 43.2, 21.3, 6.1, and 57.5 and for ASP-GI was >100, 4.4, 4.2, and >100 µmol/L gallic acid equivalents, respectivcly. ASP-GI + VC quenching of DPPH and HOCl was 22.9 and 61.3% more potent (P ≤0.001) than their calculated additive EC50. In contrast, ASP-M + VC against HOCl and O2- was 45.6 and 25.9% less potent (P ≤0.001) than their calculated additive effect. The capacity of ASP for detoxification was assessed by its effect on quinione reductase (QR) activity in Hepa1c1c7 cells. ASP-M (100 µmol/L) increased by 21.6% and ASP-GI (0.1 µmol/L) decreased by 16.2% QR activity. VC did not alter but ASP-GI + VC synergistically increased QR by 17.4%. These results suggest ASP possess antioxidant activity against free radicals and can enhance phase II enzyme activity. However, these actions are dependent upon the ASP dose, antioxidant combinations, and radical species. [ABSTRACT FROM AUTHOR]

The in vivo antioxidant efficacy of polyphenols such as flavonoids has not been unequivocally established. Similarly, the impact of these compounds on other actions such as enzyme induction and signal transduction have only been suggested by in vitro studies. We examined the temporal responses of plasma oxidative stress and redox status relative to the kinetics of flavonoids in a randomized cross-over study of 7 healthy adults aged 51-74 y fed an acute dose of 400 mg almond skin polyphenols or placebo. Plasma flavonoids, F2α-isoprostanes, glutathione peroxidase (GSHPx), reduced (GSH) and oxidized (GSSG) glutathione, and LDL oxidizability were measured over a10 h post feeding period. Almond polyphenols were bioavailable and increased the resistance of LDL to oxidation. Despite marked individual variability in responses, flavonoid intake patterns reflected their sequential absorption from the stomach, small intestine, and the action of gut flora on glycoside forms. Catechin had a bimodal pattern of bioavailability with maximal concentrations at 45 and 120 min. Naringenin reached its Tmax at 180 min. GSH followed a trimodal pattern corresponding with flavonoid bioavailability to plasma. GSHPx activity was associated with the bimodal catechin absorption pattern. Isoprostane patterns were affected by polyphenol-induced changes in GSH metabolism. [ABSTRACT FROM AUTHOR]

Oxidative stress induced by cigarette smoking is associated with the risk of cancer. Dietary antioxidants may reduce some oxidative damage related to carcinogenesis. Almonds are an excellent source of vitamin E (7 mg/30 g) and contain flavonoids (53 mg/30 g). Thus, we tested the effect of almonds (84 g/d) added to the diet for 4-wk on nucleic acid damage (urinary 8-OHdG; peripheral lymphocyte DNA strand breaks), lipid peroxidation (urinary MDA), and plasma antioxidant enzymes in 60 male (18-25 y) smokers (5-20 cigarettes/d) in a randomized, placebo-controlled (100 g pork providing calories equal to the almond intake), cross-over clinical trial. Pre-treatment values of 8-OHdG, MDA, and DNA strand breaks were significantly greater by 111, 50, and 300% in smokers than in 30 nonsmoking men. Superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase were significantly lower by 17, 7, and 10%, respectively, in smokers than nonsmokers. After almond consumption, plasma α-tocopherol, SOD, and GPX were significantly increased by 10, 20, and 16%, respectively; 8-OHdG, DNA strand breaks, and MDA were significantly decreased by 23, 31, and 38%. Post-treatment values of DNA damage and lipid peroxidation in smokers were not different from those of nonsmokers. These results indicate that daily consumption of almonds can enhance antioxidant defenses and diminish smoking-related oxidative damage. [ABSTRACT FROM AUTHOR]