In humans an enzyme called uricase has mutated, resulting in higher uric acid levels. Hyperuricemia is connected to cardiovascular and kidney disease. This could be the result of reactive oxygen species (ROS) causing damage to the inner endothelial lining of blood vessels.
The effect of the enzyme xanthine oxidase is the production of uric acid and ROS. Hypertension and vascular disease, caused by hyperuricemia, can be reversed by supplementing with l-arginine, a building block for nitric oxide (NO). The authors propose that uric acid causes dysfunction to the endothelium by an inhibition of NO production.
Oxonic acid causes hyperuricemia. In this study rats were given oxonic acid and allopurinal to show that allopurinal, an inhibitor of xanthine oxidase enzyme, reversed oxonic acid induced hyperuricemia. Uric acid was also shown to reduce production of NO in cultured endothelial cells and resulted in the production of less nitrates and nitrites.
Uric acid was shown by the authors to reduce nitric oxide production, both baseline levels and that induced by vascular endothelial growth factor (VEGF) in cultured cells. VEGF is a chemical produced by endotelial cells to promote the growth of new tiny blood vessels, which are necessary for tumors to grow.
CONCLUSION: Uric acid in rats causes a reduction of nitric oxide that can be partly reversed by supplementing with l-arginine. Uric acid also caused a reduction of nitric oxide production in culture of vascular endothelial cells. The authors state that hyperuricemia causes endothelial dysfunction and, possibly, vascular disease and hypertension, by nitic oxide inhibition. More studies need to be done.
NOTE: Flavonoids, black tea, astragulus, cocoa polyphenols, and white mulberry twigs have been shown to have xanthine oxidase inhibitor activity.
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