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Urate as a physiological substrate for myeloperoxidase: implications for hyperuricemia and inflammation
Flavia C Meotti1, Guy N L Jameson, Rufus Turner
1Free Radical Research Group, Department of Pathology, University of Otago, P. O. Box 4345, 8140 Christchurch, New Zealand.
The Journal of Biological Chemistry
|January 27, 2011
Summary
Urate is a physiological substrate for myeloperoxidase (MPO), forming reactive intermediates that may worsen cardiovascular disease inflammation. This study reveals urate
Area of Science:
- Biochemistry
- Cardiovascular Research
- Inflammation Studies
Background:
- Elevated urate and myeloperoxidase (MPO) levels are linked to poor cardiovascular outcomes.
- The precise interaction between urate and MPO in cardiovascular disease pathogenesis remains unclear.
Purpose of the Study:
- To investigate if urate serves as a physiological substrate for MPO.
- To determine if their interaction products exacerbate inflammation.
Main Methods:
- Enzymatic assays measuring urate oxidation by MPO and hydrogen peroxide.
- Kinetic analysis of MPO redox intermediates with urate.
- Assessment of urate's effect on glutathione and nitric oxide consumption.
- Analysis of allantoin production in human plasma with stimulated neutrophils.
Main Results:
- Urate is readily oxidized by MPO to 5-hydroxyisourate, decaying to allantoin.
- Urate acts as a substrate for MPO, competing with chloride, especially at hyperuricemic levels.
- Urate oxidation generates a free radical intermediate, promoting glutathione consumption and MPO-dependent nitric oxide breakdown.
- Stimulated neutrophils produce allantoin via NADPH oxidase, MPO, and superoxide.
Conclusions:
- Urate is a physiological substrate for MPO, generating a urate radical.
- The urate radical's reactions with superoxide and nitric oxide offer a potential mechanism linking urate and MPO in cardiovascular disease.
- This interaction may contribute to inflammation in cardiovascular conditions.
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