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Volume 148, Issue 1, Pages 131-139 (January 2000)


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Uric acid and serum antioxidant capacity: a reaction to atherosclerosis?

F.Javier NietoaCorresponding Author Informationemail address, Carlos Iribarrenb, Myron D. Grossc, George W. Comstocka, Richard G. Cutlerd

Received 2 November 1998; received in revised form 21 May 1999; accepted 2 June 1999. published online 16 August 2004.

Abstract 

Background: the evidence of a potential beneficial role of antioxidants in preventing atherosclerotic disease is not entirely consistent. Objective: to assess the longitudinal association of serum total antioxidant capacity and serum antioxidants with the presence of subclinical carotid atherosclerosis. Methods: Prospective case-control study nested within an historical cohort. Cases were 150 individuals with elevated carotid intimal-medial thickness measured by B-mode ultrasound at the first two examinations of the Atherosclerosis Risk in Communities Study (1987–92). Controls were 150 age–gender-matched individuals with low carotid intimal-medial thickness. Serum antioxidant vitamins, uric acid, and serum total antioxidant capacity were measured in frozen serum samples collected from the same individuals in 1974 (13–15 years prior to the determination of case-control status). Results: Compared to controls, atherosclerosis cases had significantly higher levels of serum total antioxidant capacity in 1974 than controls. This difference was almost entirely explained by increased serum concentration of uric acid in cases. In contrast with cross-sectional results, uric acid serum concentration in 1974, was significantly higher in cases than in controls, even after adjusting for the main cardiovascular risk factors. Cases had significantly lower levels of α-carotene in the 1974 sera than controls, but no other differences in serum antioxidant vitamin concentrations were observed. Conclusions: The higher serum uric acid concentration seemed associated with elevated total serum antioxidant capacity among individuals with atherosclerosis. This finding is consistent with experimental evidence suggesting that hyperuricemia may be a compensatory mechanism to counteract oxidative damage related to atherosclerosis and aging in humans.

a Department of Epidemiology, The Johns Hopkins University, School of Hygiene and Public Health, 615 North Wolfe Street, room W6009, Baltimore, MD 21205, USA

b Kaiser Permanente Division of Research, Oakland, CA 94611, USA

c Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, MN, 55454 USA

d Genox Corporation, Baltimore, MD 21230, USA

Corresponding Author InformationCorresponding author. Tel.: +1-410-9554380; fax: +1-410-9558086

PII: S0021-9150(99)00214-2


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