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PubMed1980

Limited value of uric acid to creatinine ratios in estimating uric acid excretion.

The value of the uric acid to creatinine ratio and the uric acid to creatinine clearance ratio in predicting 24-hour urinary uric acid excretion was assessed in 49 patients with normal enzyme activity and 22 patients with purine enzyme deficiencies. A 24-hour urinary uric acid to creatinine ratio greater than 0.75 was found in six of nine patients with a partial deficiency of hypoxanthine-guanine phosphoribosyltransferase and in all patients with Lesch-Nyhan syndrome. A ratio of less than 0.10 suggested xanthinuria or severe purine nucleoside phosphorylase deficiency. Neither ratio calculated from 2-hour timed collections of the 24-hour specimen showed a high correlation with 24-hour urine uric acid excretion in patients with normal enzyme activity, perhaps because of a diurnal variation in urinary uric acid excretion. The spot-urine uric acid to creatinine ratio does not accurately predict the 24-hour urine uric acid excretion in patients with normal enzyme activity.

Adolescent↗
PubMed1984

Purine metabolism in high and low uric acid lines of chickens: de novo uric acid synthesis in isolated hepatocytes and phosphoribosylpyrophosphate amidotransferase activities.

The de novo biosynthesis of uric acid was examined in isolated hepatocytes from the high and low uric acid lines of chickens. Rates of incorporation of radiolabeled glycine into uric acid by hepatocytes from the high uric acid (HUA) line were approximately 3.6-fold greater than found in low uric acid (LUA) control hepatocytes. Uric acid synthesis rates in these cells were positively correlated with plasma uric acid levels (r = +0.77; P less than 0.01). The activity of phosphoribosylpyrophosphate (PRPP) amidotransferase was measured in acetone powder preparations from liver and kidney tissues of the HUA and LUA lines. Activities in kidney tissues were about 21% lower than those found in livers. PRPP amidotransferase activities in liver and kidney tissues did not correlate significantly with plasma uric acid levels. The increased synthesis of uric acid in the HUA line may be the result of the increased PRPP synthetase activities and PRPP pool sizes previously reported for these tissues.

Amidophosphoribosyltransferase↗
PubMed1994

Uric acid nephrolithiasis.

Uric acid is the end-product of purine nucleotide metabolism in man. The renal handling of urate is a complicated process, resulting in a fractional clearance of 8.2-10.3%. The anhydrous form is thermodynamically the most stable uric acid crystal. Uric acid is a weak acid that ionizes with a Pka at pH 5.75. At the normal acidic region, uric acid solubility is strongly increased by urinary pH. The prevalence of uric acid stones varies between countries, reflecting climatic, dietary, and ethnical differences, ranging from 2.1% (in Texas) to 37.7% (in Iran). The risk for uric acid stone formation correlates with the degree of uric acid supersaturation in the urine, depending on uric acid concentration and urinary pH. Hyperuricosuria is the major risk factor, the most common cause being increased purine intake in the diet. Acquired and hereditary diseases accompanied by hyperuricosuria and stone disease include: gout, in strong correlation with the amount of uric acid excreted, myelo- and lymphoproliferative disorders, multiple myeloma, secondary polycythemia, pernicious anemia and hemolytic disorders, hemoglobinopathies and thalassemia, the complete or partial deficiency of HGPRT, superactivity of PRPP synthetase, and hereditary renal hypouricemia. A common denominator in patients with idiopathic and gouty stone formers is a low urinary pH. Uric acid nephrolithiasis is indicated in the presence of a radiolucent stone, a persistent undue urine acidity and uric acid crystals in fresh urine samples. A radiolucent stone in combination with normal or acidic pH should raise the possibility of urate stones.(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗
PubMed1992

Voltammetric monitoring of brain extracellular levels of serotonin, 5-hydroxyindoleacetic acid and uric acid as assessed by simultaneous microdialysis.

We have previously developed a microcomputer-assisted curve-fitting method for measuring the components of the mixed electrochemical signals recorded by differential normal pulse voltammetry in the living brain. It was initially used for resolution of the dopamine and dihydroxyphenylacetic acid components of the catechol signal (peak 2). This report shows how it can be applied to analysis of the indoleamine/uric acid (UA) components of the more complex peak 3. The voltammogram is modeled as a mixture of 3 normal curves of known parameters corresponding to the oxidation of UA, 5-hydroxyindoleacetic acid and serotonin, which is solved by non-linear iterative procedures. Performance was assessed by treatments with drugs having well-known effects on the substances monitored, pargyline and allopurinol, and by the chromatographic analysis of microdialysates collected simultaneously from the contralateral side.

Allopurinol↗
PubMed1984

Inhibition of oxidative degradation of hyaluronic acid by uric acid.

It has been postulated that glycosaminoglycans in the trabeculum have an influence on aqueous humor drainage. Ascorbate reduces the viscosity of hyaluronic acid, and also increases outflow facility. Our recent observation of high urate concentrations in some glaucomatous eyes led us to study the influence of urate on oxidative degradation of hyaluronic acid by ascorbate. The viscosity of rooster comb hyaluronic acid was reduced slowly by ascorbate. Cupric sulfate accelerated ascorbate oxidation and also enhanced hyaluronic acid degradation. Urate inhibited ascorbate oxidation and prevented the copper catalyzed oxidative degradation of rooster comb hyaluronic acid. The range of urate concentrations used in this study was within the range of urate concentrations observed in glaucomatous eyes. The partially purified umbilical cord hyaluronic acid had lower viscosity than rooster comb hyaluronic acid, and rapidly degraded in the presence of ascorbate. The ascorbate effect on umbilical cord hyaluronic acid was partially prevented by urate.

Animals↗
PubMed1987

Voltammetric evidence in vivo of cholinergic modulation of extracellular ascorbic acid and uric acid in rat striatum.

The cholinergic agonist pilocarpine (2 and 4 mg/kg) produced a dose-related increase in striatal AA levels as measured by linear sweep voltammetry. The cholinergic antagonist scopolamine (0.5 and 0.6 mg/kg) blocked the pilocarpine-induced increase in AA levels, but methscopolamine (which does not cross the blood-brain barrier) reduced the pilocarpine effect only by about 20%. Pilocarpine alone had little effect on UA levels. Scopolamine (0.6 mg/kg) produced a dramatic increase in UA levels that was reduced by pilocarpine. Methscopolamine had little effect (less than 10%) on extracellular UA levels. Thus cholinergic drugs modulate striatal extracellular AA levels by predominantly central rather than peripheral effects.

Animals↗
PubMed1978

Serotonin, folic acid, and uric acid metabolism in the diagnosis of neuropsychiatric disorders.

Metabolic compensation appears possible within the serotonergic, folate, purine system and it seems possible that clinical illness may result when the system can no longer compensate. For example, elevated serotonin, induced by stress accumulation of tryptophan, could be compensated by a lowered folate ratio, normalizing the beta-carboline index and preventing hallucinations. Conversely, deficient serotonin, induced by a psychological loss or transport deficit, could be compensated by raising the folate ratio, which would normalize the beta-carboline index and prevent further depression. Increased purine turnover would seemingly lower the folate ratio, compensating perhaps for hallucinatory activity or mania. Several genetic defects of enzymes or transport proteins could seemingly preclude normal compensations within the system.

Adolescent↗
PubMed1980

Purine metabolism studies in the high and low uric acid containing lines of chickens: de novo uric acid synthesis and xanthine dehydrogenase activities.

De novo purine synthesis has been examined in two genetic lines of chickens selected for their plasma uric acid levels. Synthesis rates were determined using aqueous extracts of tissue acetone powders. The high uric acid line (HUA) had significantly greater kidney synthesis rates compared to the low uric acid (LUA) birds (P less than .05). The mean value of kidney de novo uric acid synthesis rates was 5.65 +/- .65 micrograms and 3.6 +/- .24 micrograms uric acid synthesized/mg acetone powder/hour, respectively, for the HUA and LUA birds. Kidney uric acid synthesis rates were significantly correlated to plasma uric acid levels (P = .07). No correlation was seen between liver de novo uric acid synthesis rates and plasma uric acid levels. Plasma uric acid levels were monitored in both lines from hatching through 42 weeks of age. In the HUA line peaks of uric acid level were noted during the 2nd, 4th, and 8th week followed by a fairly abrupt rise in levels after the 20th week, whereas in the LUA males a broad peak in the early weeks was followed by a gradual rise in levels after the 20th week. The LUA females had slightly elevated levels during the first weeks; however, no significant changes occurred after the 20th week. Xanthine dehydrogenase (XDH) activities in kidney acetone powders from the HUA line were significantly higher compared to those from the LUA line (P less than .05). The mean value of kidney XDH activity was 85.41 +/- 13.81 and 46.35 +/- 6.71 mmoles NAD reduced per milligram acetone powder per hour, respectively, for the HUA and LUA lines. There was no significant correlation between liver XDH activities and plasma uric acid levels; however, the activity was significantly higher in the HUA than in the LUA line.

Animals↗
PubMed2002

Renal underexcretion of uric acid is present in patients with apparent high urinary uric acid output.

OBJECTIVE: To compare renal handling of uric acid in patients with primary gout with that of a control group. METHODS: A case-control study of 100 patients with primary gout and 72 healthy controls was undertaken. Creatinine clearance, uric acid clearance, 24-hour uric acid urinary excretion, fractional excretion of uric acid, excretion of uric acid per volume of glomerular filtration, urinary uric acid to creatinine ratio, and glomerular uric acid filtered load were calculated using 24-hour urine samples. After treatment with allopurinol to achieve similar glomerular filtered load of uric acid, patients were again compared with controls. RESULTS: Patients with gout showed lower uric acid clearance, fractional excretion of uric acid, excretion of uric acid per volume of glomerular filtration, and urinary uric acid to creatinine ratio than controls at baseline, when patients showed hyperuricemia. Although the glomerular uric acid filtered load was much higher in patients with gout than controls, 24-hour uric acid excretion was not statistically different. After treatment with allopurinol, and achieving similar uric acid filtered loads, patients still showed lower figures than controls. When patients with 24-hour urinary uric acids levels >700 mg/day were compared with controls, they had lower uric acid clearance and fractional excretion of uric acid than controls, both at baseline and after achieving similar filtered loads with allopurinol therapy. CONCLUSIONS: Renal underexcretion is the main mechanism for the development of primary hyperuricemia in gout, but even patients showing apparent high 24-hour uric acid output show lower uric acid clearance than controls, indicating that relative, low-grade underexcretion of uric acid is at work.

Adult↗
PubMed1996

DNA breakage by uric acid and Cu(II): binding of uric acid to DNA and biological activity of the reaction.

Uric acid is present in human plasma in relatively high concentrations and is considered to be a natural physiological antioxidant. We have earlier shown that in the presence of Cu(II) and molecular oxygen, uric acid causes strand breakage in DNA. In this article, we show that uric acid fluorescence is quenched by addition of DNA, indicating the formation of uric acid-DNA complex. Uric acid-Cu(II)-mediated DNA strand scission is capable of bacteriophage inactivation and such inactivation is mediated through reduction of Cu(II) to Cu(I) and the generation of oxygen-derived radicals. It is indicated that the DNA breakage is repaired in E. coli and involves the repair of DNA polymerase.

Bacteriophage lambda↗
PubMed1991

[Uric acid and arterial hypertension. II. Evaluation of uric acid transport in the nephrons in primary arterial hypertension].

In forty patients with mild to moderate essential hypertension correlation between serum uric acid as well as renal excretion of urate and the transport of uric acid in nephron was evaluated. Quantity of the separate phases of uric acid transport in nephron was calculated based upon pharmacological tests with pyrazinamide and benzbromarone. The results obtained in twenty normotensive subjects were assumed to be a normal values. Positive correlation between serum uric acid and presecretory reabsorption of urate was found in hypertensive patients. However presecretory reabsorption of urate did not significantly differ between hypertensive patients with concomitant hyperuricemia and normotensive subjects. Tubular secretion of uric acid was significantly lower in hypertensive patients in comparison with normotensive subjects. Plasma uric acid correlated inversely++ with tubular secretion of urate in patients with essential hypertension. There was no difference in postsecretory reabsorption of uric acid between the groups. Plasma uric acid did not correlate with postsecretory reabsorption of urate in hypertensive patients. These findings suggest that decreased uric acid clearance in hypertension with concomitant hyperuricemia is connected with impaired tubular secretion of urate.

Adult↗
PubMed1986

[Biochemical studies of the cerebral ischemia in the rat--changes in cerebral free amino acids, catecholamines and uric acid].

Changes in cerebral free amino acids, catecholamines and uric acid levels were explored for up to 7 days after cerebral ischemia in the rat. Fifty male Sprague-Dawley rats were subjected to occlusion of the middle cerebral artery on the olfactory tract, under halothane anesthesia. The animals were decapitated at 2, 4, 6, 12, 24 hours and 2, 3, 5, 7 days after the surgery, respectively. The brains were rapidly removed. The cerebral hemispheres were divided into right and left halves, and homogenized in sulfosalicylic acid solution. Free amino acids were analyzed by colormetric method. Cathecholamines and uric acid were analyzed by high-performance liquid chromatography. Each parameters were measured both on the ischemic and contralateral hemispheres. The time course of changes in each parameters were observed by means of the ratio, which is the value of ischemic side divided by that of contralateral side. Free amino acids Dicarboxylic group; Decreases in glutamate and increases in glutamine suggest one aspect of detoxication of ammonia within the ischemia tissue. Monocarboxylic group; GABA, glycine, alanine were increased in early ischemic state, and gradually lowered to the normal values. These suggest the impairment of tricarboxylic acid (TCA) cycle in the ischemic tissues, since these amino acids are closely related to TCA cycle. Essential amino acids, except for tryptophan, were increased until the end of study. These increases suggest the utilization of essential amino acids for protein synthesis might be disturbed in the ischemic tissues. Catecholamines and precursors; Norepinephrine and dopamine were lowered gradually. On the other hand, phenylalanine and tyrosine were increased during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗