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may also modify lipid metabolism, but the data are, again, con- tradictory. Grape seed polyphenols have a hypocholesterolemic effect on rats fed a high-cholesterol diet.77 The comsumption of flavanones by normolipemic or hyperlipemic rats during 2–6 wk reduced total plasma cholesterol, LDL-cholesterol, and triglycerides.78−80 In contrast, in rabbits, dietary supplementa- tion with cocoa polyphenols for 10 d had no effect upon the plasma lipid profile.60,68 In apoE-deficient mice, catechins de- rived from tea did not affect plasma lipid concentrations, but induced a decrease in cholesterol and triglyceride levels in the aorta.60 In man, acute consumption of one cup of black tea or consumption of 6 cups of green or black tea over a 4-wk pe- riod had no effect on plasma concentrations of cholesterol and triglycerides.72,81 Several other clinical trials also failed to show any effects of isoflavones on plasma lipids.82−84 Polyphenols may exert antithrombotic effects. They inhibit platelet aggregation in vitro.85,86 They were also shown to inhibit platelet aggregation in several animal models: the con- sumption of red wine (rich in polyphenols), rather than white wine or alcohol, in the rat prevented the platelet rebound effect (measured by ex-vivo thrombin-induced platelet aggregation), otherwise observed in the hours following alcohol withdrawal.87 The consumption of red wine or non-alcoholic red wine reduces bleeding time and platelet aggregation induced by collagen in the rat.88 Thrombosis induced by stenosis of the coronary artery in the dog is inhibited when red wine or grape juice, but not white wine, is administered by gastric intubation.89 Platelet ag- gregation induced ex vivo by collagen is inhibited in the monkey by consumption for 7 d of grape juice, but not by orange juice or grapefruit juice.90 Evidence in humans is more limited. The consumption of a procyanidin-rich cocoa beverage by human subjects inhibited the activation of platelets when stimulated ex- vivo by epinephrine or ADP in the 2–6 h following ingestion.91 However, no effects were observed with other flavonoid-rich foods, such as onion, parsley, soy, citrus juices, or tea.81,92−95 Polyphenols can improve endothelial dysfunction, an early event in atherogenesis. Endothelial dysfunction is associated with different risk factors for atherosclerosis before the plaque is formed; its use as a prognostic tool for coronary heart disease has been proposed.96,97 The endothelial-dependent vasorelaxing ac- tivity of isolated polyphenols, such as wine anthocyanins,98 soy isoflavones,99 resveratrol, quercetin,100 and cocoa proanthocya- nidins,101 has been observed on isolated rat or rabbit aorta and in female macaques. These effects could be mediated by the pro- tection of the vasorelaxant factor nitric oxide against oxidation. In human subjects, endothelial dysfunction can be assessed by measuring the brachial artery flow-mediated dilation. The con- sumption of black tea (450 mL) increased artery dilation 2 h after intake by coronary patients.102 A similar improvement of endothelial function was observed when the same patients con- sumed 900 mL of tea/d during 4 wk. The consumption of 240 mL red wine during 30 d also counteracted the endothelial disfunc- tion induced by a high-fat diet.103 Associations between polyphenol intake or the consumption of polyphenol-rich foods were examined in several epidemio- logical studies. Both the consumption of tea and a moderate consumption of wine have been regularly associated to a lower risk of myocardial infarction in both case-control and cohort studies.104,105 However, an increased risk was observed in two studies carried out in the UK, where the consumption of tea is particularly high.106,107 This could be explained by an insuf- ficient adjustment for lifestyle factors. An inverse association between flavonol and flavone intake and the risk of coronary death or non-fatal myocardial infarction has been observed in several cohort studies.108−111 Catechin intake has also been as- sociated to a lower risk of coronary death but not to stroke.112,113 These results of molecular epidemiology are still fragmentory, as flavonols, flavone, and catechins do not account for more than one tenth of the total polyphenol intake.1 Reliable food com- position data are needed to estimate the consumption of other polyphenols and to study its association with disease risk. POLYPHENOLS AND CANCER Anticarcinogenic effects of polyphenols are well documented in animals. Polyphenols, when given to rats or mice before and/or after the administration of a carcinogenic agent or the implantation of a human cancer cell line, are most often pro- tective and induce a reduction of the number of tumors or of their growth.114 These effects have been observed at various sites, including mouth, stomach, duodenum, colon, liver, lung, mammary, or skin. Many polyphenols, such as quercetin, cat- echins, isoflavones, lignans, flavanones, ellagic acid, red wine polyphenols, resveratrol, or curcumin, were tested; all of them showed protective effects in some models. Different mecha- nisms have been suggested to explain their anticarcinogenic effects.115 First, polyphenols may act as blocking agents at the initiation stage. They influence the metabolism of procarcino- gens by modulating the expression of cytochrome P450 enzymes involved in their activation to carcinogens. They may also fa- cilitate their excretion by increasing the expression of phase II conjugating enzymes.116 This induction of phase II enzymes may have its origin in the toxicity of polyphenols. Polyphenols can form potentially toxic quinones in the body that are, them- selves, substrates of these enzymes.17 The intake of polyphenols could then activate these enzymes for their own detoxication and, thus, induce a general boosting of our defenses against toxic xenobiotics.117 Polyphenols may also limit the formation of initiated cells by stimulating DNA repair.118,119 Secondly, polyphenols can act as suppressing agents, and inhibit the formation and growth of tumors from initiated cells; they inhibit cell proliferation in vitro.120,121 It was also shown that some polyphenols can affect growth-related signal transduction pathways through inhibition of protein kinase C and AP-1-dependent transcriptional activity.122,123 They inhibit oncogene expression124 and the activity of ornithine decarboxy- lase, a key enzyme in the synthesis of polyamines associated to cell proliferation.125,126 They may also inhibit cell prolifera- tion through their effect on the metabolism of arachidonic acid. 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