Regular ingestion of tea does not inhibit in vivo lipid peroxidation in humans.

Prospective studies suggest that tea may protect against cardiovascular disease. A potential mechanism for such an effect involves inhibition of lipid peroxidation by polyphenolic antioxidants derived from tea. Our objective was to determine whether regular ingestion of tea could inhibit in vivo lipid peroxidation. Two controlled intervention studies assessed the effects of regular ingestion of tea on lipid peroxidation determined by measurement of urinary F(2)-isoprostane excretion. Study 1: The effects of 1000 mL/d of green tea and black tea were compared with hot water containing caffeine in 13 subjects with elevated blood pressure using a randomized 3-period (7 d each) crossover design. Study 2: The effects of 1250 mL/d of black tea were compared with hot water in 22 subjects with mildly raised serum total cholesterol concentrations using a randomized 2-period (4 wk each) crossover design. F(2)-isoprostane excretion was not altered after regular ingestion of green tea (273 +/- 48 pmol/mmol creatinine) or black tea (274 +/- 39 pmol/mmol creatinine) in comparison with hot water (263 +/- 47 pmol/mmol creatinine; Study 1), or by regular ingestion of black tea (334 +/- 71 pmol/mmol creatinine) in comparison with hot water (355 +/- 75 pmol/mmol creatinine; Study 2). These results do not support the suggestion that polyphenolic antioxidants derived from tea inhibit in vivo lipid peroxidation.     

Effect of smoking cessation on serum apolipoprotein A-I and A-II concentrations.

This study investigated the effects of 6 weeks' smoking cessation on serum levels of total-cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C) and apolipoproteins A-I and A-II (apo A-I and apo A-II) in 64 subjects of both sexes. Smoking cessation was associated with an increase in levels of apo A-II. Concurrent changes in weight and alcohol consumption during attempted smoking cessation, together with change in thiocyanate level, were entered as predictor variables into a multiple regression analysis. The change in apo A-II was found to be best accounted for by change in plasma thiocyanate level, and, in women, change in HDL-C and apo A-I by change in weight. The changes induced by smoking cessation may be due, at least in part, to associated changes in alcohol consumption and/or dietary intake, but in the case of apo A-II there is evidence of a more direct effect.     

Ingestion of red wine significantly increases plasma phenolic acid concentrations but does not acutely affect ex vivo lipoprotein oxidizability

BACKGROUND: Reduced lipoprotein oxidizability by red wine phenols has been proposed as the basis for a relatively lower incidence of coronary heart disease in red wine drinkers. We showed previously that caffeic and protocatechuic acids isolated from red wine exhibit antioxidant activity in vitro. However, there is no information in the literature on the absorption of these compounds after red wine ingestion. OBJECTIVES: We sought to determine whether certain phenolic acids can be detected in the circulation after red wine consumption and if their presence has an acute effect on serum and LDL oxidation ex vivo. DESIGN: Twelve healthy male nonsmokers consumed red wine, phenol-stripped red wine, dealcoholized red wine, or water, each at a separate visit, in random order and 1 wk apart. Beverages were consumed over 30 min and blood was sampled just before beverage consumption and 1, 2, and 4 h after consumption. Plasma caffeic, protocatechuic, and 4-O-methylgallic acids were measured by gas chromatography-mass spectrometry. We also measured copper-induced serum and LDL oxidizability ex vivo and serum uric acid. RESULTS: Caffeic acid and 4-O-methylgallic acid concentrations increased significantly (P < 0.025) after consumption of red wine and dealcoholized red wine compared with water or phenol-stripped red wine. Uric acid increased significantly (P < 0.001) after ingestion of red wine, phenol-stripped red wine, and dealcoholized red wine. There was no effect on ex vivo serum or LDL oxidation after any of the beverages. CONCLUSION: Although red wine and dealcoholized red wine consumption acutely increase plasma phenolic acid and serum uric acid concentrations, the increase is insufficient to influence ex vivo lipoprotein oxidation.     

Angiogenesis is an early event in the development of chemically induced skin tumors

In this study we have analyzed the vascular response induced in the two- stage carcinogenesis model in SENCAR mice. The role of angiogenesis has not been explored in this model, which is the paradigm of multistage carcinogenesis and a model for neoplastic lesions derived from exophytic premalignant lesions (e.g. colon carcinoma, bladder papilloma). We investigated if angiogenesis is involved in the formation of papillomas and in the progression from papilloma to carcinoma. To this end we analyzed the vasculature of normal and hyperplastic skin, focal epidermal hyperplasias that are precursors of papillomas, papillomas at different stages and squamous cell carcinomas. We also analyzed the vascularization of papillomas induced in two strains of mice that differ in their susceptibility to malignant progression. We show here that angiogenesis is turned on in the earliest stages of papilloma formation. In late stages, regardless of state of progression, the predominant response is an increase in the size of blood vessels. Thus, in the SENCAR mouse model, representative of exophytic tumors, the angiogenesis switch is a very early event, probably mechanistically related to the development of the primarily exophytic lesions. Therefore, the density of blood vessels cannot be used as a predictor of malignant progression in this model.      

Effects of alcohol and caloric restrictions on blood pressure and serum lipids in overweight men.

We have examined the independent and combined effects on blood pressure and blood lipids of alcohol restriction and weight loss in overweight male drinkers with a view to assessing overall effects on cardiovascular risk of two widely promoted nonpharmacological approaches for hypertension. Eighty-six men with a mean age of 44.3 years, a mean regular alcohol intake of 440 ml/wk (five or six standard drinks per day), a mean blood pressure of 137.4 mm Hg systolic and 84.8 mm Hg diastolic, and a mean body mass of 92.5 kg entered a controlled two-way factorial study. The subjects were randomly assigned to four groups for an 18-week intervention in which members of two groups drank only low-alcohol beer, thereby reducing their alcohol intake by 374 ml/wk, while those of the other two groups continued their normal alcohol intake. Within the low and normal alcohol intake groups subjects either continued their usual diet or reduced their caloric intake by 4,200-6,300 kJ/day (1,000-1,500 kcal/day) (with protein, fat, and carbohydrate provided as 15%, 30%, and 55% of total calories, respectively). Calorie reduction and alcohol restriction caused weight losses of 7.5 (p less than 0.001) and 2.1 (p less than 0.01) kg, respectively. Calorie reduction and alcohol restriction were associated with decreases in systolic blood pressure of 5.4 (p less than 0.001) and 4.8 (p less than 0.01) mm Hg, respectively, and in diastolic blood pressure of 4.2 (p less than 0.001) and 3.3 (p less than 0.01) mm Hg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic significance of urokinase plasminogen activator receptor and its cleaved forms in blood from patients with non‐small cell lung cancer

Urokinase plasminogen activator (uPA) cleaves its three‐domain cell surface receptor, uPAR, liberating domain I [uPAR(I)] and leaving the cleaved uPAR(II‐III) on the cell surface. Both intact and cleaved uPAR can be shed from the cell surface. uPAR(I) was previously shown to be a prognostic factor in lung tumour extracts. Here we analyse uPAR forms in blood from patients with non‐small cell lung cancer (NSCLC). Preoperatively sampled plasma/serum from 32 patients with NSCLC was analysed. Three time‐resolved fluoroimmunoassays (TR‐FIAs) measuring intact uPAR(I‐III) (TR‐FIA 1), uPAR(I‐III) + uPAR(II‐III) (TR‐FIA 2) and uPAR(I) (TR‐FIA 3) were applied. The Spearman rank correlations between plasma and serum levels of uPAR(I‐III), uPAR(I‐III) + uPAR(II‐III), and uPAR(I) were 0.89, 0.94 and 0.68 respectively. Survival analysis demonstrated that high levels of all uPAR forms were associated with shorter survival. Adjusted for histological subtype high plasma uPAR(I‐III) and uPAR(I) levels as well as serum uPAR(I) levels were significantly associated with shorter OS (hazards ratios = 4.3, 2.8 and 3.8 respectively). High blood levels of intact uPAR and its cleaved forms are associated with poor prognosis in NSCLC.