Free radicals and reactive oxygen species (ROS) have been implicated in contributing to the processes of aging and disease. Humans protect themselves from these damaging compounds, in part, by absorbing antioxidants from high-antioxidant foods. This report describes the effects of consuming 1.5 g/kg body weight of corn syrup or buckwheat honey on the antioxidant and reducing capacities of plasma in healthy human adults. The corn syrup treatment contained 0.21 +/- 0.06 mg of phenolic antioxidants per gram, and the two buckwheat honey treatments contained 0.79 +/- 0.02 and 1.71 +/- 0.21 mg of phenolic antioxidants per gram. Following consumption of the two honey treatments, plasma total-phenolic content increased (P < 0.05) as did plasma antioxidant and reducing capacities (P < 0.05). These data support the concept that phenolic antioxidants from processed honey are bioavailable, and that they increase antioxidant activity of plasma. It can be speculated that these compounds may augment defenses against oxidative stress and that they might be able to protect humans from oxidative stress. Given that the average sweetener intake by humans is estimated to be in excess of 70 kg per year, the substitution of honey in some foods for traditional sweeteners could result in an enhanced antioxidant defense system in healthy adults.

The aim of this study was to examine the effects of procyanidins derived from cocoa on vascular smooth muscle. Two hypotheses were tested: 1) extracts of cocoa, which are rich in procyanidins, cause endothelium-dependent relaxation (EDR), and 2) extracts of cocoa activate endothelial nitric oxide synthase (NOS). The experiments were carried out on aortic rings obtained from New Zealand White rabbits. The polymeric procyanidins (tetramer through decamer of catechin) caused an EDR. In addition, the Ca(2+)-dependent NOS activity, measured by the L-arginine to L-citrulline conversion assay, was significantly increased in aortic endothelial cells exposed to polymeric procyanidins, whereas monomeric compounds had no such effect. These findings demonstrate that polymeric procyanidins cause an EDR that is mediated by activation of NOS.

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1. Published data on the effects of red wine, ethanol and flavonoids on endothelium-dependent relaxation are equivocal. The present study was undertaken to determine the effects of red wine, ethanol and selected flavonoids present in red wine on endothelium-dependent relaxation. 2. Aortic rings from New Zealand White rabbits were set up in organ baths (20 ml) and contracted with noradrenaline (10(-6) mol/l). An attempt was made to elicit dose-dependent relaxant responses to red wine (15, 30, 40, 80 or 120 microliters), ethanol (5.4, 10.8 and 16.2 microliters) and the flavonoids catechin, epicatechin, quercetin and polymeric phenols (10(-7) to 10(-4) mol/l). In some experiments, endothelium-dependent relaxation to cumulative doses of acetylcholine (10(-9) to 10(-6) mol/l) was determined before and after incubating the rings for 15 min with red wine (120 microliters), ethanol (16.2 microliters), quercetin (10(-5) mol/l), catechin (10(-5) mol/l), epicatechin (10(-5) mol/l) and PPs (10(-5) mol/l) respectively. cGMP was also measured in some rings in the control state and after addition of 120 microliters of red wine, sodium nitroprusside (10(-4) mol/l) and polymeric phenols (10(-5) mol/l). 3. Red wine evoked a dose-dependent relaxation in aortic rings. The highest volumes of wine (120 microliters) relaxed the vessels by 71.35 +/- 7.89% of the maximal contraction (8.95 +/- 0.97 g). Polymeric phenols also relaxed the precontracted rings. These responses were abolished by NG-L-arginine methyl ester (L-NAME) and by removal of endothelium. Addition of red wine, polymeric phenols and sodium nitroprusside increased the cGMP content of the rings. In tissues previously incubated with red wine and polymeric phenols, endothelium-dependent relaxation in response to acetylcholine was attenuated. Ethanol had no such effect. 4. Acute exposure of aortic rings to red wine and polymeric phenols evokes an endothelium-dependent relaxation which is mediated by nitric oxide. However, prior exposure to both red wine and polymeric phenols has a second effect in that it attenuates the endothelium-dependent relaxation evoked by acetylcholine. Since this effect is restored by arginine, it is likely to be due to depletion of substrate for nitric oxide synthase.