Consumption of fruits and vegetables has been associated with reduced risk of chronic diseases such as cardiovascular disease and cancer. Phytochemicals, especially phenolics, in fruits and vegetables are suggested to be the major bioactive compounds for the health benefits. However, the phenolic contents and their antioxidant activities in fruits and vegetables were underestimated in the literature, because bound phenolics were not included. This study was designed to investigate the profiles of total phenolics, including both soluble free and bound forms in common fruits, by applying solvent extraction, base digestion, and solid-phase extraction methods. Cranberry had the highest total phenolic content, followed by apple, red grape, strawberry, pineapple, banana, peach, lemon, orange, pear, and grapefruit. Total antioxidant activity was measured using the TOSC assay. Cranberry had the highest total antioxidant activity (177.0 +/- 4.3 micromol of vitamin C equiv/g of fruit), followed by apple, red grape, strawberry, peach, lemon, pear, banana, orange, grapefruit, and pineapple. Antiproliferation activities were also studied in vitro using HepG(2) human liver-cancer cells, and cranberry showed the highest inhibitory effect with an EC(50) of 14.5 +/- 0.5 mg/mL, followed by lemon, apple, strawberry, red grape, banana, grapefruit, and peach. A bioactivity index (BI) for dietary cancer prevention is proposed to provide a new alternative biomarker for future epidemiological studies in dietary cancer prevention and health promotion.

Epidemiological studies have shown that consumption of fruits and vegetables is associated with reduced risk of chronic diseases. Increased consumption of fruits and vegetables containing high levels of phytochemicals has been recommended to prevent chronic diseases related to oxidative stress in the human body. In this study, 10 common vegetables were selected on the basis of consumption per capita data in the United States. A more complete profile of phenolic distributions, including both free and bound phenolics in these vegetables, is reported here using new and modified methods. Broccoli possessed the highest total phenolic content, followed by spinach, yellow onion, red pepper, carrot, cabbage, potato, lettuce, celery, and cucumber. Red pepper had the highest total antioxidant activity, followed by broccoli, carrot, spinach, cabbage, yellow onion, celery, potato, lettuce, and cucumber. The phenolics antioxidant index (PAI) was proposed to evaluate the quality/quantity of phenolic contents in these vegetables and was calculated from the corrected total antioxidant activities by eliminating vitamin C contributions. Antiproliferative activities were also studied in vitro using HepG(2) human liver cancer cells. Spinach showed the highest inhibitory effect, followed by cabbage, red pepper, onion, and broccoli. On the basis of these results, the bioactivity index (BI) for dietary cancer prevention is proposed to provide a simple reference for consumers to choose vegetables in accordance with their beneficial activities. The BI could be a new alternative biomarker for future epidemiological studies in dietary cancer prevention and health promotion.

Objectives The aim of this study was to determine whether oxidative stress is increased in calcified, stenotic aortic valves and to examine mechanisms that might contribute to increased oxidative stress. Background Oxidative stress is increased in atherosclerotic lesions and might play an important role in plaque progression and calcification. The role of oxidative stress in valve disease is not clear. Methods Superoxide (dihydroethidium fluorescence and lucigenin-enhanced chemiluminescence), hydrogen peroxide (H2O2) (dichlorofluorescein fluorescence), and expression and activity of pro- and anti-oxidant enzymes were measured in normal valves from hearts not suitable for transplantation and stenotic aortic valves that were removed during surgical replacement of the valve. Results In normal valves, superoxide levels were relatively low and distributed homogeneously throughout the valve. In stenotic valves, superoxide levels were increased 2-fold near the calcified regions of the valve (p < 0.05); noncalcified regions did not differ significantly from normal valves. Hydrogen peroxide levels were also markedly elevated in calcified regions of stenotic valves. Nicotinamide adenine dinucleotide phosphate oxidase activity was not increased in calcified regions of stenotic valves. Superoxide levels in stenotic valves were significantly reduced by inhibition of nitric oxide synthases (NOS), which suggests uncoupling of the enzyme. Antioxidant mechanisms were reduced in calcified regions of the aortic valve, because total superoxide dismutase (SOD) activity and expression of all 3 SOD isoforms was significantly decreased. Catalase expression also was reduced in pericalcific regions. Conclusions This study provides the first evidence that oxidative stress is increased in calcified regions of stenotic aortic valves from humans. Increased oxidative stress is due at least in part to reduction in expression and activity of antioxidant enzymes and perhaps to uncoupled NOS activity. Thus, mechanisms of oxidative stress differ greatly between stenotic aortic valves and atherosclerotic arteries.

Abstract-Oxidative stress may contribute to hypertension. The goals of this study were to determine whether extracellular superoxide dismutase (ECSOD) reduces arterial pressure in spontaneously hypertensive rats (SHR) and whether its heparin-binding domain (HBD), which is responsible for cellular binding, is necessary for the function of ECSOD. Three days after intravenous injection of an adenoviral vector expressing human ECSOD (AdECSOD), mean arterial pressure (MAP) decreased from 165Ϯ4 mm Hg (meanϮSE, nϭ7) to 124Ϯ3 mm Hg (nϭ7) in adult anesthetized SHR (PϽ0.01) but was not altered in normotensive Wistar-Kyoto rats. Cardiac output was not changed in SHR 3 days after AdECSOD. Gene transfer of ECSOD with deletion of the HBD (AdECSOD⌬HBD) had no effect on SHR MAP, even though plasma SOD activity was greater after AdECSOD⌬HBD than after AdECSOD. Immunohistochemistry revealed intense staining for ECSOD in blood vessels and kidneys after AdECSOD but not after AdECSOD⌬HBD. Impaired relaxation of the carotid artery to acetylcholine in SHR was significantly improved after AdECSOD. Cumulative sodium balance in SHR was reduced by AdECSOD compared with AdECSOD⌬HBD. Gene transfer of ECSOD also reduced MAP in conscious SHR, although the effect was not as profound as in anesthetized SHR. In summary, gene transfer of ECSOD, with a strict requirement for its HBD, reduces systemic vascular resistance and arterial pressure in a genetic model of hypertension. This reduction in arterial pressure may be mediated by vasomotor and/or renal mechanisms.

Abstract-Angiotensin II (Ang II) produces inflammation and endothelial dysfunction in blood vessels. We tested the hypothesis that interleukin 10 (IL-10), an antiinflammatory cytokine, protects against Ang II-induced vascular dysfunction. Responses of carotid arteries from wild-type and IL-10 -deficient mice (IL-10 Ϫ/Ϫ ) were examined in vitro after overnight incubation with vehicle or Ang II (1 nmol/L). In arteries from wild-type mice, acetylcholine (an endothelium-dependent agonist) produced relaxation that was not affected by Ang II. In contrast, relaxation to acetylcholine in arteries from IL-10 Ϫ/Ϫ mice was reduced by Ͼ50% by Ang II (PϽ0.05) and this effect was prevented by a scavenger of superoxide. Vascular superoxide increased Ϸ2-fold (PϽ0.05) after treatment with Ang II in IL-10

The inflammatory milieu of acute myocardial infarction (MI) is theoretically conducive to enhanced cytokine synthesis within the brain. We tested the hypothesis that synthesis of tumor necrosis factor-alpha (TNF-alpha), an indicator of proinflammatory cytokine activity, increases in brain after MI. MI was induced in rats by ligating the left anterior descending coronary artery and confirmed by echocardiography. Plasma and tissue levels of TNF-alpha were measured using ELISA; TNF-alpha mRNA was measured with real-time PCR. Heart, brain, and plasma samples were obtained 0.5, 1, 4, or 24 h or 4 wk after MI. TNF-alpha synthesis increased in the brain, heart, and plasma within minutes to hours after MI and was sustained over the interval tested. Among the brain tissues examined, TNF-alpha increased selectively in hypothalamus. Chronic treatment with pentoxifylline prevented the increases in TNF-alpha in brain, heart, and plasma measured 4 wk after MI. MI-induced cytokine synthesis in the hypothalamus and its prevention by pentoxifylline have important implications in the context of the development of heart failure after MI.

Oats are a good source of soluble dietary fiber, especially β-glucan, which has outstanding functional and nutritional properties. β-Glucan is considered to be the major active component of oats because of its cholesterol-lowering and antidiabetic effects. However, the nutritional benefits of oats appear to go beyond fiber to bioactive phytochemicals with strong antioxidant and anti-inflammatory effects. In this review, we summarize current knowledge on the chemistry, stability, bioavailability, and health effects of two unique phytochemicals in oats, avenanthramides, and avenacosides A and B. We conclude that studies on the beneficial effects of avenanthramides and avenacosides A and B are still in their infancy, and additional health benefits of these unique oat components may yet be identified.

Oxidative stress and matrix metalloproteinases (MMPs) contribute to hemorrhagic transformation after ischemic stroke and brain injury after intracerebral hemorrhage (ICH). The goal of this study was to develop a new model of spontaneous ICH, based on the hypothesis that acute, superimposed on chronic, hypertension produces ICH. We hypothesized that increases in angiotensin II (AngII)-mediated oxidative stress and activation of MMPs are associated with, and may precede, spontaneous ICH during hypertension. In C57BL/6 mice, chronic hypertension was produced with AngII infusion and an inhibitor of nitric oxide synthase. During chronic hypertension, mice with acute hypertension from injections of AngII developed ICH. Oxidative stress and MMP levels increased in the brain even before developing ICH. Active MMPs colocalized with a marker of oxidative stress, especially on cerebral vessels that appeared to lead toward regions with ICH. Incidence of ICH and levels of oxidative stress and MMP-9 were greater in mice with acute hypertension produced by AngII than by norepinephrine. In summary, we have developed an experimental model of ICH during hypertension that may facilitate studies in genetically altered mice. We speculate that acute hypertension, especially when induced by AngII, may be critical in spontaneous ICH during chronic hypertension, possibly through oxidative stress and MMP-9.