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PubMed2005

Uric acid and oxidative stress.

Uric acid is the final product of purine metabolism in humans. The final two reactions of its production catalyzing the conversion of hypoxanthine to xanthine and the latter to uric acid are catalysed by the enzyme xanthine oxidoreductase, which may attain two inter-convertible forms, namely xanthine dehydrogenase or xanthine oxidase. The latter uses molecular oxygen as electron acceptor and generates superoxide anion and other reactive oxygen products. The role of uric acid in conditions associated with oxidative stress is not entirely clear. Evidence mainly based on epidemiological studies suggests that increased serum levels of uric acid are a risk factor for cardiovascular disease where oxidative stress plays an important pathophysiological role. Also, allopurinol, a xanthine oxidoreductase inhibitor that lowers serum levels of uric acid exerts protective effects in situations associated with oxidative stress (e.g. ischaemia-reperfusion injury, cardiovascular disease). However, there is increasing experimental and clinical evidence showing that uric acid has an important role in vivo as an antioxidant. This review presents the current evidence regarding the antioxidant role of uric acid and suggests that it has an important role as an oxidative stress marker and a potential therapeutic role as an antioxidant. Further well designed clinical studies are needed to clarify the potential use of uric acid (or uric acid precursors) in diseases associated with oxidative stress.

Animals↗
PubMed1978

[Diagnostic value of the CSF uric acid level (author's transl)].

Uric acid is the end-product of purine metabolism, and purines are the nitrogenous bases derived from the breakdown of nucleic acids. The CSF uric acid level is thought to be the index of the turnover of the nucleic acid and the degree of the cellular destruction in the brain. CSF uric acid levels were investigated in normal controls (30 cases) and in patients with brain tumor (20 cases), microcephalus (8 cases) and craniostenosis (4 cases). The mean values and standard deviations of CSF uric acid levels in normal controls were as follows; Newborn--9 yrs 0.34 +/- 0.09 mg/dl; 10 yrs--19 yrs 0.50 +/- 0.18 mg/dl; 20 yrs--29 yrs 0.46 +/- 0.05 mg/dl; 30 yrs--39 yrs 0.35 +/- 0.10 mg/dl; 40 yrs--49 yrs 0.35 +/- 0.23 mg/dl. Thereafter 0.72 +/- 0.21 mg/dl. The increased CSF uric acid levels after the age of 50 is thought to be due to the cellular destruction in the brain. CSF uric acid levels increased in patients with highly malignant brain tumor such as grade 3 or 4 astrocytoma and sarcomatous meningioma, but were normal in patients with grade 2 astrocytoma and meningiomas of meingothelial or fibroblastic type. CSF uric acid levels decreased in patients with microcephalus, but were almost normal in patients with craniostenosis. There is a significant correlation between CSF uric acid levels and the degree of brain atrophy in infants.

Adolescent↗
PubMed1999

When and why a water-soluble antioxidant becomes pro-oxidant during copper-induced low-density lipoprotein oxidation: a study using uric acid.

The inclusion of uric acid in the incubation medium during copper-induced low-density lipoprotein (LDL) oxidation exerted either an antioxidant or pro-oxidant effect. The pro-oxidant effect, as mirrored by an enhanced formation of conjugated dienes, lipid peroxides, thiobarbituric acid-reactive substances and increase in negative charge, occurred when uric acid was added late during the inhibitory or lag phase and during the subsequent extensive propagation phase of copper-stimulated LDL oxidation. The pro-oxidant effect of uric acid was specific for copper-induced LDL oxidation and required the presence of copper as either Cu(I) or Cu(II). In addition, it became much more evident when the copper to LDL molar ratio was below a threshold value of approx. 50. In native LDL, the shift between the antioxidant and the pro-oxidant activities was related to the availability of lipid hydroperoxides formed during the early phases of copper-promoted LDL oxidation. The artificial enrichment of isolated LDL with alpha-tocopherol delayed the onset of the pro-oxidant activity of uric acid and also decreased the rate of stimulated lipid peroxidation. However, previous depletion of alpha-tocopherol was not a prerequisite for unmasking the pro-oxidant activity of uric acid, since this became apparent even when alpha-tocopherol was still present in significant amounts (more than 50% of the original values) in LDL. These results suggest, irrespective of the levels of endogenous alpha-tocopherol, that uric acid may enhance LDL oxidation by reducing Cu(II) to Cu(I), thus making more Cu(I) available for subsequent radical decomposition of lipid peroxides and propagation reactions.

Amidines↗
PubMed2006

Uric acid--a uremic toxin?

Uric acid might often be regarded as a simple marker of renal disease. Although it is well known that hyperuricemia causes gout which is associated with renal insufficiency and cardiovascular disease, one might think that it could attribute to the intrarenal urate crystal, but not to uric acid per se. In order to clarify the role of uric acid in the kidney, we hypothesized that uric acid causes renal disease. To generate mild hyperuricemia without intrarenal crystal in rats, we used low doses of an uricase inhibitor (2% oxonic acid). Hyperuricemia induced systemic hypertension, glomerular hypertrophy/hypertension, afferent arteriolar sclerosis, and macrophage infiltration in normal rat kidney. In progressive renal disease, such as cyclosporine nephropathy and remnant kidney in rat, uric acid accelerated the progression of renal disease. Thus, we concluded that uric acid is not a simple marker, but a cause of renal disease.

Animals↗