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Red Wine Consumption (red + wine_consumption)
Selected AbstractsAlcohol consumption and risk of prostate cancer in middle-aged menINTERNATIONAL JOURNAL OF CANCER, Issue 1 2005W. Marieke Schoonen Abstract Alcohol consumption is a modifiable lifestyle factor that may affect prostate cancer risk. Alcohol alters the hormonal milieu and contains chemical substances such as flavonoids (red wine), which may alter tumor cell growth. Data from a population-based case-control study in King County, WA, were utilized to evaluate the association of alcohol consumption with prostate cancer in middle-aged men. A total of 753 newly diagnosed prostate cancer cases, 40,64 years of age, participated in the study. Seven hundred three control subjects, frequency matched to cases by age, were selected through random digit dialing. All participants completed an in-person interview on lifetime alcohol consumption and other risk factors for prostate cancer. Logistic regression models were used to estimate odds ratios (OR) and assess significance (95% confidence intervals [CI]). All tests of statistical significance were two-sided. No clear association with prostate cancer risk was seen for overall alcohol consumption. Each additional glass of red wine consumed per week showed a statistically significant 6% decrease in relative risk (OR = 0.94; 95% CI = 0.90,0.98), and there was evidence for a decline in risk estimates across increasing categories of red wine intake (trend p = 0.02). No clear associations were seen for consumption of beer or liquor. Our present study suggests that consumption of beer or liquor is not associated with prostate cancer. There may be, however, a reduced relative risk associated with increasing level of red wine consumption. Further research is needed to evaluate the potential negative association between red wine intake and prostate cancer risk. [source] Polyphenolics Increase t-PA and u-PA Gene Transcription in Cultured Human Endothelial CellsALCOHOLISM, Issue 2 2001Laila H. Abou-Agag Background: Moderate red wine consumption has been associated with a reduced risk for coronary heart disease, and this cardioprotection may be mediated, in part, by promoting fibrinolysis. This protection may be attributed to the combined or perhaps synergistic effects of alcohol and other red wine components (i.e., polyphenolics). These studies were carried out to determine whether individual phenolics (i.e., catechin, epicatechin, quercetin, and resveratrol) affect fibrinolytic protein (tissue-type plasminogen activator [t-PA] and urokinase-type PA [u-PA]) e-pression and surface-localized fibrinolytic activity in cultured human umbilical vein endothelial cells (HUVECs). Methods: Cultured HUVECs were preincubated (1 hr, 37°C) in the absence or presence of varying concentrations of catechin, epicatechin, quercetin, and resveratrol (0.001,10 ,M) and then were washed and incubated for various times in the absence of phenolics. Secreted t-PA/u-PA antigen (24 hr, enzyme-linked immunoadsorbent assay) and mRNA [0,16 hr, reverse transcription-polymerase chain reaction(RT-PCR)] levels and fibrinolytic activity (direct activation of HUVEC-bound 125I-labeled glutamyl-plasminogen, quantitation of 125I-labeled M r 20 kDa plasmin light-chain) were measured. Transient transfections of cultured HUVECs were carried out with the pt-PA222/luc and pu-PA236/luc promoter constructs, by using lipofectamine. Results: Each of the phenolics similarly increased t-PA and u-PA antigen (2- to 3-fold) and mRNA (3- to 4-fold) levels, concomitant with an increase (2- to 3-fold) in sustained (24 hr), surface-localized fibrinolytic activity. Transcription inhibitor actinomycin D abolished the induction of t-PA and u-PA mRNA e-pression by these phenolics. Transfections with the pt-PA222/luc and pu-PA236/luc promoter constructs showed 2- to 3-fold and 2- to 4-fold increases in luciferase activity for t-PA and u-PA, respectively. Conclusions: These results demonstrate that each of these phenolics up-regulates both t-PA and u-PA gene transcription, which results in the sustained increased e-pression of surface-localized fibrinolytic activity in cultured HUVECs. Wine phenolics increase fibrinolytic activity, independent of ethanol, and it is likely that the overall cardioprotective benefits associated with moderate red wine consumption are attributable to the combined, additive, or perhaps synergistic effects of alcohol and other wine components. [source] Ethanol and red wine polyphenols induce the short-term downregulation of PAI-1 gene expression in vivo in rat aortic endotheliumJOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 9 2007Hernan E Grenett Abstract Moderate alcohol or red wine consumption reduces the risk of cardiovascular mortality. This cardiovascular protection is likely due to the additive, combined and/or synergistic effects of alcohol itself or other components of wine, in particular polyphenols. Experiments were carried out to determine whether ethanol/polyphenols also decrease plasminogen activator inhibitor type 1 (PAI-1) mRNA expression in vivo, using the rat as an animal model. Male Sprague,Dawley rats were gavaged with ethanol, the individual polyphenols catechin and quercetin or saline vehicle. The in vivo effect of ethanol or individual polyphenols on PAI-1 mRNA was then assessed by in situ hybridisation and quantitative reverse transcriptase (RT) polymerase chain reaction (RT-PCR). PAI-1 mRNA expression was significantly reduced in the endothelial and smooth muscle cells of the thoracic aorta of all experimental rats. RT-PCR analysis of PAI-1 mRNA levels in vascular tissue showed a ,55% reduction in PAI-1 mRNA consistent with the decrease in aortic endothelium PAI-1 mRNA observed with in situ hybridisation. This decrease may enhance endothelial cell (EC)-mediated fibrinolytic activity in vivo. The cardioprotection afforded by moderate red wine consumption can therefore be attributed in part to the combined effects of ethanol and individual polyphenols on EC fibrinolysis. Copyright © 2007 Society of Chemical Industry [source] A central role of eNOS in the protective effect of wine against metabolic syndromeCELL BIOCHEMISTRY AND FUNCTION, Issue 4 2006Federico Leighton Abstract The positive health effects derived from moderate wine consumption are pleiotropic. They appear as improvements in cardiovascular risk factors such as plasma lipids, haemostatic mechanisms, endothelial function and antioxidant defences. The active principles would be ethanol and mainly polyphenols. Results from our and other laboratories support the unifying hypothesis that the improvements in risk factors after red wine consumption are mediated by endothelial nitric oxide synthase (eNOS). Many genes are involved, but the participation of eNOS would be a constant feature. The metabolic syndrome is a cluster of metabolic risk factors associated with high risk of cardiovascular disease (CVD). The National Cholesterol Education Programmmes Adult Treatment Panel III (NCEPATP III) clinical definition of the metabolic syndrome requires the presence of at least three risk factors, from among abdominal obesity, high plasma triacylglycerols, low plasma HDL, high blood pressure and high fasting plasma glucose. The molecular mechanisms responsible for the metabolic syndrome are not known. Since metabolic syndrome apparently affects 10,30% of the population in the world, research on its pathogenesis and control is needed. The recent finding that eNOS knockout mice present a cluster of cardiovascular risk factors comparable to those of the metabolic syndrome suggests that defects in eNOS function may cause human metabolic syndrome. These mice are hypertensive, insulin resistant and dyslipidemic. Further support for a pathogenic role of eNOS comes from the finding in humans that eNOS polymorphisms associate with insulin resistance and diabetes, with hypertension, with inflammatory and oxidative stress markers and with albuminuria. So, the data sustain the hypothesis that eNOS enhancement should reduce metabolic syndrome incidence and its consequences. Therefore red wine, since it enhances eNOS function, should be considered as a potential tool for the control of metabolic syndrome. This hypothesis is supported by epidemiological observations and needs experimental validation in human intervention studies. Copyright © 2005 John Wiley & Sons, Ltd. [source] | ||||||||||