Cardioprotective effect of red wine may be mediated by urate.


Considerable evidence suggests that red wine consumption results in increased serum antioxidant activity (1, 2), and that this is associated with reduced oxidation of low-density lipoprotein (3). This has been proposed to explain the low incidence of coronary heart disease in France-the “French paradox” (4). Red wine contains high concentrations of polyphenolic substances, including flavonoids (5), and these have been implicated as the source of the increased serum antioxidant capacity of red wine drinkers (6). Whitehead et al. (2) recently showed that red wine drinking results in an acute increase in serum total antioxidant capacity measured by an enhanced chemiluminescence method, and that the pattern of this response can be reproduced in vitro by a mixture of polyphenolics. However, it remains to be established whether red wine drinking results in an increase in serum polyphenolic concentrations sufficient to explain the observed increased antioxidant capacity. An antioxidant present at relatively high concentration in human serum, but which has hitherto received little attention, is urate. Urate has been estimated to contribute 3565% of the total plasma peroxyl radical scavenging capacity (7), and is important in the recycling of the ascorbyl radical. We report changes in serum urate concentrations after consumption of port wine (a blend of red wine and brandy), which suggests that polyphenolics may not be the only species that result in increased antioxidant activity after the consumption of alcoholic beverages. Six healthy men consumed 250 mL of port wine and, on a separate occasion, 250 mL of water containing an equivalent amount of ethanol (40 g). Blood samples were taken by venesection into plain glass bottles containing serum separator gel (Vacutainer Plus; Becton Dickinson, Meylan, France) at baseline and every 30 min for 2 h. The subjects remained sitting during this time and a tourniquet was applied only briefly during venesection. The study was approved by the United Bristol Healthcare NHS Trust Research Ethics Committee. The total antioxidant capacity of the port wine (Investiture Port, Averys, Bristol, UK), determined by the enhanced luminescence method of Whitehead et al. (8), was 7079 .tmoVL, and its pattern of luminescent recovery was similar to that reported for other red wines (2). Thirty minutes after the ingestion of port, there was a 23% increase in serum urate concentration measured by a uricase method (9) (Boehringer Mannheim, Lewes, UK)-mean increase 81 ± 27 mol/L (paired Wilcoxon test, P <0.05)-and a 24% increase in serum total antioxidant capacity measured by the enhanced chemiluminescence method (8)-mean increase 109 ± 43 jmoVL (P <0.05) (Fig. 1). Both measures declined slowly thereafter, with a half-life of -2.4 h. Ethanol ingestion alone resulted in no significant change in either marker. There was a significant correlation between the increase in serum total antioxidant capacity (y) and the increase in serum urate concentration (x): y = 1.38x 8.46 (r = 0.863, P <0.0001). Given that the enhanced chemiluminescence assay shows a 1:1 stoichiometnc relation between urate and Trolox calibrant (8), these data suggest that -73% of the acute increase in serum total antioxidant capacity after the ingestion of port wine may be attributable to an increase in serum urate concentration. The observed increase in serum urate concentration was not due to hemoconcentration alone because there was no change in serum total protein or urea concentrations. Port wine itself was found to exert a small negative interference with the urate method, but this would result in underestimation of the urate responses by 10% and would not alter the interpretation of the results. Urate is an end product of purine metabolism in humans; therefore, the observed acute effect of port ingestion must be due in some way either to stimulation of urate production by increasing the rate of purine breakdown, or to inhibition of urinary urate excretion. The latter effect would be unlikely to result in such an acute increase in serum urate production, and our own preliminary studies suggest that there is no reduction in urate clearance after port ingestion. Regular alcohol consumption results in hyperuricemia, through the inhibition of renal urate excretion (10), and an enhanced turnover of adenine nucleotides (11). However, the effect observed in the present study was not due to ethanol per se, given the lack of response after the acute ingestion of ethanol only. Further studies are required to elucidate the precise mechanism of this response, but the initial findings suggest that red wine polyphenolics may not be the only explanation for the French paradox.

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@article{Day1995CardioprotectiveEO, title={Cardioprotective effect of red wine may be mediated by urate.}, author={Andrew P Day and David Stansbie}, journal={Clinical chemistry}, year={1995}, volume={41 9}, pages={1319-20} }