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PubMed1999

Uric acid urolithiasis and crystallization inhibitors.

An in vitro study of the inhibitory effects that some substances occasionally present in urine can provoke on the crystallization of uric acid has been performed. The most remarkable crystallization inhibitory effects were produced by mucine at concentrations of >0.5 mg/l. Pentosan polysulfate and chondroitin sulfate also clearly increased the uric acid crystallization times at concentrations of >100 mg/l. Saponins, such as escin and glycyrrhizic acid, also produced a notable delay in uric acid crystallization times at concentrations of >10 mg/l. Similar effects were observed in the presence of a surfactant substance, lauryl sulfate. N-Acetyl-L-cysteine caused crystallization perturbations only when it was present at concentrations of >50 mg/l. Citric acid and phytic acid caused no effects on uric acid crystallization even at the highest concentrations assayed (1,000 and 5 mg/l, respectively). From the results obtained it can be deduced that mainly glycoproteins, glycosaminoglycans and surfactant substances can exert protective effects against uric acid crystallization.

Acetylcysteine↗
PubMed1978

Transfer and dynamics of uric acid in the pregnant rhesus monkey. II. A mathematical model.

The objective of the present study was to develop a mathematical model of the dynamics of uric acid between fetal and maternal compartments in the term pregnant rhesus monkey. In 3 different animals 14C-labeled uric acid was injected into the fetal circulation, the amniotic fluid and the maternal circulation, respectively. In one experiment no uric acid was administered and the fetus was deliberately killed at the beginning of the experiment. Samples of fetal and maternal blood, maternal urine and amniotic fluid were collected at regular intervals. Semilogarithmic time-activity curves were constructed and time constants were determined. An open four-compartment model (fetal-placental plasma, fetal-placental interstitial space, amniotic fluid and maternal plasma) was applied to describe the intercompartmental dynamics of uric acid. Transplacental clearance was approx. 1 ml X min-1 in both directions, maternal renal clearance was about 17 ml X min-1. These results and the calculated values of the other intercompartmental clearances support earlier results, obtained with the steady infusion method. Uric acid concentrations in amniotic fluid and fetal plasma appeared to increase significantly during the experiments. The rise in amniotic fluid levels can only be explained by accepting a yet undefined compartment in which uric acid is produced and cleared directly into the amniotic cavity. It is speculated that this additional compartment could be the fetal lung.

Amniotic Fluid↗
PubMed1994

Effect of theophylline on serum uric acid levels in children with asthma.

This study was undertaken to investigate the effect of theophylline on serum uric acid levels in children with asthma. Twenty-seven asthmatic children, including 21 patients who were treated with slow-release theophylline and 6 patients not receiving any type of theophylline preparation, were enrolled in this study. Serum uric acid levels were increased in the asthmatic children treated with theophylline compared to those not receiving this agent (6.28 +/- 0.29 mg/dl, mean +/- SEM, vs. 4.82 +/- 0.52 mg/dl, p < 0.05). A significant positive correlation between the serum levels of uric acid and theophylline was demonstrated in the patients of this study (rs = 0.596, p < 0.01). All the patients in whom theophylline administration was stopped showed significant decreases in serum uric acid levels (p < 0.05). From these results, we conclude that theophylline increases serum uric acid levels in children with asthma, just as it does in adult asthmatics.

Adolescent↗
PubMed2006

Uric acid crystals in the semen of a patient with symptoms of chronic prostatitis.

OBJECTIVE: To report the finding of red and brownish precipitates with morphology and chemistry compatible with uric acid crystals in semen in a patient with symptoms of chronic prostatitis. DESIGN: Case report. SETTING: Academic clinical biochemistry and immunology laboratory. PATIENT(S): A 35-year-old man with clinical symptoms of prostatitis. INTERVENTION(S): Uric acid crystals were detected in the semen samples. Treatment with a low purine diet relieved the symptoms. MAIN OUTCOME MEASURE(S): Study of chemical and morphological characteristics of crystals found in the semen using standard semen analysis and transrectal ultrasound. Analysis of serum, urine, and seminal plasma uric acid levels. RESULT(S): Uric acid crystals were detected in semen. A transrectal ultrasound revealed the presence of microcalcifications in the prostate gland. After treatment with a low purine diet, the patient experienced considerable relief of the clinical symptoms. Determination of uric acid and creatinine levels in serum and seminal plasma were carried out before and after treatment. There were no abnormalities or presence of crystals in the post-treatment semen analysis. CONCLUSION(S): The presence of uric acid crystals in semen of a patient with symptoms of chronic prostatitis can be attributed to the pelvic pain.

Adult↗
PubMed2002

The inflammatory process in the mechanism of decreased serum uric acid concentrations during acute gouty arthritis.

OBJECTIVE: To clarify the mechanism of decreased serum uric acid (SUA) concentrations during acute gouty arthritis. METHODS: Data from patients with acute gouty arthritis during and after an attack were investigated retrospectively. Other investigations, including changes in urinary excretion and biochemical markers, were performed prospectively. RESULTS: SUA was significantly lower in the acute phase (7.5 +/- 1.4 mg/dl) than in the intercritical phase (8.5 +/- 0.9 mg/dl) (p < 0.0001). During the acute gout phase, a normal SUA level was found in 20 of 41 patients (49%). C-reactive protein (CRP) during acute attacks was significantly correlated with plasma interleukin 6 (IL-6) and cortisol (r = 0.645, p < 0.005; r = 0.460, p < 0.05). Percentage change in SUA at onset of attack correlated with CRP and IL-6 (r = 0.762, p < 0.0001; r = 0.630, p < 0.005), as well as with increased urinary excretion of uric acid, estimated by percentage change in fractional excretion of uric acid (FEua) during attack (r = 0.447, p < 0.05). Further, change in FEua was correlated with plasma cortisol levels during the acute attack (r = 0.534, p < 0.05). CONCLUSION: Decrease in SUA during acute gouty arthritis is associated with increased urinary excretion of uric acid; an inflammatory process may play a role in the mechanism.

Acute Disease↗
PubMed1993

Measurement of uric acid as a marker of oxygen tension in the lung.

Changes in O2 tension such as those associated with hypoxic ischemia or hyperoxia may potentially modulate purine nucleotide turnover and production of associated catabolites. We used an isolated perfused rat lung preparation to evaluate the effect of O2 tension on pulmonary uric acid production. Three O2 concentrations (21%, normoxia; 95%, hyperoxia; 0%, hypoxia) were utilized for both pulmonary ventilation and equilibration of recirculating perfusate. All gas mixtures contained 5% CO2 and were balanced with N2. We used Certified Virus Free Sprague-Dawley male rats weighting 250-300 g, four to five rats in each exposure regimen. After a 10-min equilibration period, we measured uric acid levels at 0 and 60 min in lung perfusate and at 60 min in lung tissue. After 60 min of ventilation/perfusion, we observed significant uric acid accumulation in both lung tissue (25-60%) and perfusate (8- to 10-fold) for all three O2 regimens. However, hypoxia produced substantially greater net uric acid concentrations (net = the difference between zero and 60 min) than either normoxia or hyperoxia (1.5-fold in lung tissue, and 2-fold in perfusate, respectively). The data suggest that pulmonary hypoxia results in greater purine catabolism leading to increased uric acid production. Vascular space uric acid, as measured in the recirculating perfusate, was proportional to lung weight changes (r = 0.99) with hypoxia exhibiting the greatest values, possibly reflecting a linkage between tissue perturbation and uric acid release. Thus, measurement of uric acid may serve as a useful marker of adenine nucleotide turnover and lung injury.

Animals↗
PubMed1979

High steady-state levels of uric acid produced in rats by dietary training and potassium oxonate.

To reduce the inherent variability in serum uric acid levels of animals allowed ad libitum exposure to food containing potassium oxonate and uric acid, male Sprague-Dawley rats were trained to eat their daily food allotment in a 1.25-hr period each morning. After training the rats were fed a food mixture containing 5% potassium oxonate and 2% uric acid (w/w each). Serum blood levels of uric acid reached a steady state within 2 hr; these levels were maintained for an additional 4 hr. It is believed that the stomach emptying rate is a zero-order process under these experimental conditions.

Animals↗
PubMed1997

[Extracorporeal shock wave lithotripsy for uric acid stones in upper urinary tract].

Since 1987, 121 patients with uric acid stones in upper urinary tract have been treated by an EDAP LT-01 ultrasound-guided piezoelectric lithotriptor. One hundred and twenty-one patients had 167 renal stones 0.5-3.5 cm in diameter (mean 0.86 cm), 9 had ureteral stones 0.6-1.3 cm (mean 0.84 cm). Auxiliary treatment were given to 2 patients with upper ureteral stones, the others were treated by ESWL in situ. A success rate of 80.99% (98 patients) was achieved in one session, 12.40% (15) in two sessions, 4.96% (6) in three sessions, and 1.65% (2) in four sessions. No serious complications were encounterd. Therefore, ESWL with the ultrasound-guided piezoelectric lithotriptor is considered to be a satisfactory procedure for the treatment of uric acid stones. The ultrasound localization of uric acid stones, the shocking methods during ESWL and the application of alkaline medicine after ESWL were discussed.

Adult↗
PubMed1978

Uric acid metabolism in homozygous and heterozygous muscular dystrophic mice.

The homozygous muscular dystrophic mice (dydy) were found to have significantly higher plasma uric acid than their heterozygous littermate controls (Dydy), and the Swiss albino mice. Because the rate of uric acid excretion did not compensate for the elevated plasma levels, U/P (urine/plasma) urate was lower in dydy mice. With RNA supplement, plasma and urinary urate were increased in both dydy and Dydy mice; again U/P urate was lower in dydy mice. It appears that the dydy mice to a certain extent are comparable to some gouty subjects, whose hyperuricemia is not accompanied by a corresponding increase in urinary uric acid. There was no difference in converting uric acid to allantoin either on basal diet alone or with RNA supplement. Oxonic acid effectively, though transiently, blocked the uricase activity in both dydy and Dydy mice resulting in hyperuricemia and hyperuricosuria with decreased allantoin. Uric acid content was increased markedly in the kidney without histological evidence of urate deposition, apparently related to the unsustained effect of oxonic acid, which was rapidly excreted.

Allantoin↗
PubMed2004

Oxidation of uric acid in rheumatoid arthritis: is allantoin a marker of oxidative stress?

Free radicals are implicated in many diseases including atherosclerosis, cancer and also in rheumatoid arthritis. Reaction of uric acid with free radicals, such as hydroxyl radical and hypochlorous acid (HOCl) results in allantoin production. In this study, we measured the serum allantoin levels, oxidation products of uric acid, as a marker of free radical generation in rheumatoid arthritis. Fasting blood samples were obtained from 21 rheumatoid patients and 15 healthy controls. In this study, the serum allantoin and uric acid levels were measured by a gas chromatography-mass spectrometry method and the ratios were calculated. The mean allantoin and uric acid levels and ratios in the patient group were 22.1 +/- 11.3, 280.5 +/- 65.0 and 8.0 +/- 3.7 microM, while in the control group they were 13.6 +/- 6.3, 278.3 +/- 53.6 and 4.9 +/- 2.1 microM, respectively. The effects of gender, age, menopausal status, duration of disease and medications on serum allantoin and uric acid levels of the patient and control groups were studied. Our results suggest that uric acid acts as a free radical scavenger and thus is converted to allantoin. Increased allantoin levels suggest the possible involvement of free radicals in rheumatoid arthritis.

Age Factors↗
PubMed1976

Uric acid excretion by the chick as an indicator of dietary protein quality.

The objective of this investigation was to determine whether uric acid excretion could serve as an indicator of dietary protein quality. In the first study, 15% protein diets were formulated using either whole egg protein, soybean meal, safflower meal or casein, or the latter 3 proteins supplemented with their most limiting amino acid (methionine, lysine and arginine, respectively). Chicks fed diets supplemented with the limiting amino acid grew more rapidly and efficiently and excreted less uric acid. Good agreement was noted between uric acid excretion and protein efficiency ratio (PER) as indicators of protein quality. Two studies were conducted with chicks fed diets containing raw soybean flakes or flakes autoclaved for varying periods of time and fed with or without methionine and lysine supplementation. Similar chick performance, uric acid excretion and PER were noted with chicks fed the soybean flakes which had been autoclaved for 20, 40 or 120 min. Poorer chick performance and PER were noted with chicks fed soybean flakes or flakes autoclaved for 10 min. When the diets were supplemented with methionine and lysine, the negative effects of inadequate heating were partially alleviated. The results indicated that adequate heating and amino acid supplementation of soybean flakes were both essential for maximal chick performance, that the two factors influence the utlization of the protein in different ways and that the two effects were additive.

Animal Feed↗
PubMed1975

Uric acid excretion by the rat kidney.

The renal excretion of uric acid was studied in nondiuretic (ND) male Wistar rats and in the same animals subsequently made diuretic (D) by the infusion of hypertonic saline. Clearances of endogenous urate and of inulin, determined chemically, were compared with the simultaneous clearance of 14C infused as [6(-14)C]urate or [2(-14)C]urate. In rats infused with [6(-14)C]urate the isotope/inulin clearance ratios were 0.29 +/- 0.09 (ND) and 0.31 +/- 0.11 (D) ml/min; the simultaneous urate (chemical)/inulin ratios were 0.21 +/- 0.07 (ND) and 0.24 +/- 0.08 (D) ml/min. In rats infused with [2(-14)C]urate the isotope/inulin clearance ratios were 1.02 +/- 0.5 (ND) and 1.13 +/- 0.9 ml/min (D); the simultaneous urate (chemical)/inulin clearance ratios were much lower-0.19 +/- 0.09 (ND) and 0.32 +/- 0.19 (D) ml/min. Thin-layer chromatography of urine after [6(-14)C]urate inl uric acid. In contrast, a similar analysis of urinary radioactivity after [2(-14)C]urate infusion revealed that more than 70% of the 14C was excreted as allantoin and not as uric acid.

Allantoin↗
PubMed1990

Uric acid levels and dopamine transmission in rat striatum: diurnal changes and effects of drugs.

Carbon paste disc electrodes were used to detect voltammetrically changes in the extracellular concentration of the purine metabolite, uric acid, and the dopamine metabolite, homovanillic acid (HVA), in the striatum of unanaesthetized, unrestrained rats under a variety of conditions. The motor activity level for each rat was recorded between the electrochemical scans. In totally unperturbed animals, there was a significant correlation between the levels of the two metabolites during the bright, relatively inactive, period of the diurnal cycle. During much of the dark (active) phase of the cycle, however, the uric acid signal showed no significant change compared with the light-on period, in contrast to the HVA signal which showed a marked increase. Significant variations in the concentration of striatal uric acid were observed during the switch-over from light to dark and dark to light conditions. The unilateral infusion of gamma-aminobutyric acid, taurine and haloperidol into the substantia nigra caused increases in the height of both the uric acid and HVA peak in the ipsilateral striatum; the size of these changes showed a significant correlation. Variable changes occurred on the contralateral side where no correlation was observed. Intraperitoneal administration of the mixed dopamine-receptor agonist, apomorphine, and the mixed antagonist, haloperidol, did not affect striatal uric acid levels significantly. These results suggest that, although there are conditions where parallel changes in dopamine release/receptor-activation and uric acid levels do occur in the striatum, neither the release of dopamine nor activation of dopamine receptors need necessarily lead to changes in the extracellular concentration of uric acid.

Animals↗
PubMed2001

[Relationship between mass of the left ventricular myocardium and uric acid metabolic imbalance in patients with arterial hypertension].

AIM: To analyse relationships between left ventricular myocardium mass (LVMM) and imbalance of uric acid metabolism in patients with arterial hypertension (AH). MATERIAL AND METHODS: Body mass index, waist/hip circumference index, levels of uric acid in the blood and urine, urinary excretion of albumin, LVMM were estimated in 106 patients with mild and moderate AH (70 males and 36 females, mean age 51 +/- 8.5 years). RESULTS: Hypertensive patients with and without metabolic imbalance of uric acid differ significantly by LVMM index. The latter was higher in metabolic imbalance of uric acid, being the highest if this imbalance combined with microalbuminuria. CONCLUSION: Imbalance of uric acid metabolism in AH patients may indicate affection of both the kidneys and the heart.

Adult↗
PubMed2000

D-tagatose, a stereoisomer of D-fructose, increases blood uric acid concentration.

D-Fructose has been found to increase uric acid production by accelerating the degradation of purine nucleotides, probably due to hepatocellular depletion of inorganic phosphate (Pi) by an accumulation of ketohexose-1-phosphate. The hyperuricemic effect of D-tagatose, a stereoisomer of D-fructose, may be greater than that of D-fructose, as the subsequent degradation of D-tagatose-1-phosphate is slower than the degradation of D-fructose-1-phosphate. We tested the effect of 30 g oral D-tagatose versus D-fructose on plasma uric acid and other metabolic parameters in 8 male subjects by a double-blind crossover design. Both the peak concentration and 4-hour area under the curve (AUC) of serum uric acid were significantly higher after D-tagatose compared with either 30 g D-fructose or plain water. The decline in serum Pi concentration was greater at 50 minutes after D-tagatose versus D-fructose. The thermogenic and lactacidemic responses to D-tagatose were blunted compared with D-fructose. D-Tagatose attenuated the glycemic and insulinemic responses to a meal that was consumed 255 minutes after its administration. Moreover, both fructose and D-tagatose increased plasma concentrations of cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1). The metabolic effects of D-tagatose occurred despite its putative poor absorption.

Administration, Oral↗
PubMed1975

Uric acid and divergent thinking: a possible relationship.

An exploratory investigation of the relationship between serum uric acid levels in male university students and their scores on tests of convergent and divergent thinking was carried out. The data suggested that uric acid levels are lower in highly divergent thinkers than in less divergent. This led to the speculation that uric acid may be an important biochemical precursor of intellectual functioning. If it does affect intellectual functioning, this may result from the action of uric acid as an endogenous cortical stimulant, or possibly from its action as a facilitator of learning.

Adult↗
PubMed1964

EFFECT OF URIC ACID ON RIBOFLAVINE PRODUCTION BY INTESTINAL COLIFORM BACTERIA.

Lau, H. S. (University of Kentucky, Lexington), and R. F. Wiseman. Effect of uric acid on riboflavine production by intestinal coliform bacteria. J. Bacteriol. 87:337-340. 1964.-Cultures of Escherichia coli, Aerobacter aerogenes, and Paracolobactrum species, isolated from human feces and from intestinal contents of rats, were tested for riboflavine synthesis in a chemically defined medium. Riboflavine was assayed by a fluorometric method and by microbiological assay. When uric acid was added to the synthetic medium at levels ranging from 10 to 750 mug/ml, it inhibited the production of riboflavine, but did not affect the growth of the bacteria. As the amount of uric acid in the medium was increased from 10 to 750 mug, there was a corresponding decrease in the amount of riboflavine produced. Some disappearance of uric acid was observed in the cultures. These results suggest that uric acid, or its degradation products, may have acted as an antimetabolite or an enzyme inactivator in the biosynthesis of riboflavine.

Antimetabolites↗