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PubMed1997

Miniaturized graphite sensors doped with metal-bathophenanthroline complexes for the selective potentiometric determination of uric acid in biological fluids.

Miniaturized poly(vinyl chloride) matrix membrane sensors in an all-solid-state graphite support, responsive to urate anion, were developed. The membranes incorporate lipophilic ion-pair complexes of urate anion with ruthenium(III), iron(II), nickel(II) and copper(I) bathophenanthroline (4,7-diphenyl-1,10-phenanthroline) counter cations. The sensors demonstrate a near-Nernstian response to urate over the concentration range 1 x 10(-2)-1 x 10(-5) mol l-1 and have micromolar detection limits and good selectivity properties. The response is virtually unaffected by pH changes in the range 7-10 and the response times are 5-10 s in aqueous solutions and in human serum and urine samples. A flow injection detector incorporating an iron(II) bathophenanthroline-urate graphite sensor was used for continuous monitoring of uric acid. The minimum detectable concentration was approximately 8 micrograms ml-1 and the sample throughput was approximately 120 h-1. Direct potentiometric determination of uric acid in the static and hydrodynamic modes of operation over the range 15 micrograms ml-1-1.5 mg ml-1 showed average recoveries of 98.7 and 97.8% with RSDs of 0.6 and 0.7%, respectively. Application of the method to the determination of uric acid in human serum and urine gave results that compared favourably with those obtained by the standard spectrophotometric method.

Flow Injection Analysis↗
PubMed1976

The reliability of a mechanized procedure (Perkin-Elmer C4) for the Enzymatic determination of uric acid according to Kageyama.

The enzymatic determination of the uric acie concentration in urine and serum according to Kageyama ((1971), Clin. Chim. Acta 31, 421--426), which excludes the deproteinization of samples, was adapted to the C4 automatic analyzer (Perkin-Elmer). The reliability of this procedure and its correlation with an UV-method were investigated. The interaction from-sample-to-sample was considerable, but this could be reduced by the addition of Brij-35. The recovery of uric acid added to protein-containing samples (about 96%) was better than with the UV-method. Novaminsulfone was the only substance tested which interfered significantly.

Autoanalysis↗
PubMed1975

The influx of uric acid and other purines into everted jejunal sacs of the rat and hamster.

The in vitro transport of [2-14-C]uric acid, [8-14-C]hypoxanthine, and [8-14-C]xanthine, each dissolved in Krebs--Ringer bicarbonate buffer, was studied with everted jejunal sacs from rat and hamster. No evidence could be obtained for the development of a concentration gradient between the intracellular fluid and the incubation medium or between the sac contents and the incubation medium, for any of the three oxypurines. Inhibitiors of active transport, such as anaerobiosis for dinitrophenol, had no significant effect on the rate of transport. A large percentage of hypoxanthine and xanthine was oxidized to urine acid in the sac-wall homogenate, sac contents, and incubation medium during the course of the incubation. This oxidation could be prevented by addition of allopurinol (3 mM) to the incubation medium, but concentration gradients were still not obtained. No active transport mechanism could be demonstrated for uric acid, hypoxanthine, or xanthine in rat or hamster jejunum.

Allopurinol↗
PubMed1985

A high-performance liquid chromatographic method for the determination of pseudouridine and uric acid in native human urine and ultrafiltered serum.

A simple and reliable HPLC method for quantitative determination of pseudouridine and uric acid in human urine and serum using a cation-exchange resin is described. This method is straightforward (12 runs of urine samples per day since the sample is only diluted into buffer and then chromatographed), sensitive, and highly reproducible. The column is stable over long periods (approximately 3 months of uninterrupted use at a time; it is thereafter easily restored to the original state). Mean excretion values for pseudouridine (in mumol/mmol creatinine) are 26.4 +/- 3.1 (17 female adults), 23.8 +/- 2.5 (12 male adults), 164.7 +/- 32.2 (37 male preterm infants); mean values for uric acid (mumol/mmol creatinine) are, respectively, 310.3 +/- 90.5, 278.2 +/- 56.1, and 1108 +/- 314. Human serum is deproteinized by pressure ultrafiltration in microcollodion bags with a nominal exclusion molecular weight of 12,400 and then put directly onto the HPLC column. The complete procedure takes 4 h.

Adult↗
PubMed1965

Micromethod for the determination of uric acid in biological fluids.

A micro procedure for estimating uric acid in body fluids, based on the carbonate method, is described. Interferences are elucidated. The stoichiometry of the reaction is carefully worked out. Reliability of the method is established by comparison with two other methods, by recovery experiments, and by replicate analyses.

Body Fluids↗
PubMed1977

[Comparative study of uric acid concentration in serum and saliva of healthy or hyperuricemic subjects].

In normal or hyperuricemic subjects, the average values of serum and salivary uric acid concentration are very similar in each group of subjects. After absorption of a uricosuric drug, benzbromarone, a study of the variations of uric acid concentrations in the serum and saliva shows that they are parallel, which shows the stricts dependence salivary excretion on plasma concentration.

Benzbromarone↗
PubMed1986

Plasma fructose, uric acid, and inorganic phosphorus responses of hyperinsulinemic men fed fructose.

We fed 12 men with abnormally high insulin responses to a sucrose load and 12 controls normal diets containing 0, 7.5, or 15% of the calories as pure fructose for 5 weeks each in a crossover design. Purified wheat starch replaced the fructose in the 0 and 7.5% diets. The two groups were matched for age, height, and weight. At the beginning of the study and at the end of each of the three 5-week periods, plasma responses to a sucrose load (2 gm/kg body weight) were measured. Initially there were no significant differences in the plasma fructose, uric acid, or inorganic phosphorus responses of the two groups. Plasma fructose responses to a sucrose load were significantly higher after the men consumed the 7.5 and 15% fructose diets than after the 0% diet. Uric acid responses tended to be greater in the hyperinsulinemic men than in controls and increased as the levels of fructose in the diet increased. The inorganic phosphorus levels after a sucrose load were higher in the hyperinsulinemic men than in controls when they consumed the 7.5 and 15% fructose diets. These results indicate that moderate levels of dietary fructose can affect plasma fructose, uric acid, and inorganic phosphorus levels, especially in hyperinsulinemic men.

Adult↗
PubMed1991

Plasma uric acid in patients receiving anticonvulsant monotherapy.

In newly diagnosed adult patients with epilepsy followed prospectively on monotherapy, carbamazepine and phenytoin were associated with a fall in plasma uric acid, but sodium valproate and phenobarbitone were associated with a rise in plasma uric acid. The mechanisms and significance of these findings are discussed.

Adolescent↗
PubMed1969

Uric acid and plasma lipids in cerebrovascular disease. I. Prevalence of hyperuricaemia.

Serum uric acid levels measured by the phosphotungstic sodium cyanide method have been estimated in 60 patients suffering from a cerebrovascular incident. Patients with diseases known to predispose to hyperuricaemia were excluded. Twenty-five per cent. of patients with acute strokes had hyperuricaemia, and this did not appear to be a transitory phenomenon. These findings suggest that hyperuricaemia may be one of the factors in the pathogenesis of atheroma.

Adult↗
PubMed1993

[Relation between uric acid and lipid metabolism disorders].

We investigated values of uric acid and lipids in serum of 168 men, workers at a printing-house. The average uricemia found is significant higher in testees who have values of triglycerides more than 2.00 mmol/l, than in those ones who had lower values of triglycerides, P < 0.05. We could not find a notable difference of uricemia in testees who had higher values of cholesterol, but normal values of triglycerides related to those testees who had normal values of cholesterol in serum, P > 0.05.

Adult↗
PubMed1990

Precursors of essential hypertension: pulmonary function, heart rate, uric acid, serum cholesterol, and other serum chemistries.

Exploratory analyses were conducted in a nested case-control study of 1,031 incident cases of essential hypertension and 1,031 persistently normotensive controls from the Kaiser Permanente Multiphasic Health Checkup cohort in Northern California. Previous analyses have confirmed hypotheses that baseline weight, subsequent weight gain, alcohol consumption, parental history of hypertension, excessive use of salt, and centralized body fat distribution are predictive of developing hypertension. In the present study, pulmonary function tests, several serum chemistries, and heart rate were strongly predictive in univariate analyses. Adjusting for the risk factors mentioned above, forced vital capacity (p less than 0.001), serum uric acid (p = 0.003), serum cholesterol (p = 0.012), and heart rate (p = 0.014) remained independently predictive. Further adjustment for baseline blood pressure completely explained the association of heart rate with hypertension, and reduced the association with serum cholesterol to borderline significance. Forced vital capacity remained a strong, inverse predictor (odds ratio, fifth vs. first quintile = 0.22, 95% confidence interval (Cl) 0.11-0.46). Uric acid remained positively related to risk (odds ratio, fifth vs. first quintile = 2.19, 95% Cl 1.20-3.98). Although neither association is presently understood, both forced vital capacity and serum uric acid are closely linked to development of hypertension and may be markers of susceptibility or intermediate steps in pathways leading to hypertension.

Adult↗
PubMedDate not supplied

[Serum uric acid levels in disorders of the rheumatic type].

Serum uric acid levels were investigated in a series of 1715 subjects. Of these 596 were patients suffering from inflammatory rheumatic disorders, 162 patients with gout, 236 with osteoarthrosis and 79 with systemic lupus erythematosus or diffuse scleroderma. 642 healthy subjects completed the series. On analyzing the results, very high uricemia values were found in patients with gout. Increased average uricemia values were observed in patients with psoriatic arthritis and diffuse connective tissue disorders (systemic lupus erythematosus and diffuse scleroderma). Hyperuricemia was found in psoriatic arthritis, rheumatoid arthritis, and in nosologic units classified under diffuse connective tissue disorders in 5.6 to 10.1% of patients. In the healthy subjects examined, hyperuricemia was recorded in 3.8% of cases.

Adolescent↗
PubMed2005

Negative cooperativity of uric acid binding to the transcriptional regulator HucR from Deinococcus radiodurans.

Members of the MarR family of winged helix transcriptional regulators have been shown to regulate multidrug and oxidative stress response, pathogenesis, and catabolism of aromatic compounds. Many respond to anionic lipophilic compounds in their capacity to bind DNA, and the co-crystal structure of MarR bound to salicylate revealed two ligand-binding pockets, SAL-A and SAL-B. The MarR homolog, HucR, from Deinococcus radiodurans has been shown to repress expression of a predicted uricase, and DNA-binding by HucR is antagonized by uric acid, the substrate of uricase. We provide a biochemical investigation of DNA-binding and uric acid-binding by HucR. Equilibrium analytical ultracentrifugation indicates that HucR exists as a dimer. Intrinsic fluorescence spectra suggest that the association of the HucR dimer with its cognate DNA involves conformational flexibility in the globular interior and/or dimerization domain of the protein, and near-UV circular dichroism spectra indicate a concomitant change in the helical twist of the DNA duplex. DNA-binding affinity, measured by electrophoretic mobility-shift assays, for HucR mutants bearing single amino acid substitutions suggests the importance of the beta-hairpin "wing" in DNA binding. Analysis of intrinsic fluorescence spectra demonstrates that uric acid induces conformational changes in HucR and binds with an apparent K(d)=11.6(+/-3.7)muM and a Hill coefficient of 0.7+/-0.1, indicating negative cooperativity. Fluorescence and DNA-binding properties of the HucR variants indicate that SAL-A is a low-affinity, uric acid-binding site and that negative cooperativity exists between homologous, high-affinity sites. The conservation of residues comprising site SAL-A suggests that it is a low-affinity, ligand-binding site in MarR homologs. Mechanistic considerations suggest that HucR is regulated by uric acid to maintain optimal cellular levels of this scavenger of free radicals in response to oxidative stress and DNA damage.

Bacterial Proteins↗
PubMed2006

Diabetes associated with a low serum uric acid level in a general Chinese population.

OBJECTIVE: Serum uric acid (UA) is reported as an important marker of hypertension, coronary heart disease, and diabetes; diabetic subjects have low UA levels. The relationship between UA and fasting plasma glucose (FPG) and 2-h plasma glucose concentrations in non-diabetic subjects as well as in diabetic subjects in general population is not well known. This was investigated in a general Chinese population. METHODS: A stratified, random cluster sampling method was performed to select a representative sample of general population aged 20-74 years in Qingdao in 2002. A total of 1288 men and 2344 women participated in the survey. The mean UA concentration was calculated for small glucose intervals and the trend was tested using general linear model. RESULTS: The mean concentrations of UA were 381, 393, 371, and 345 micromol/l in men with FPG of <6.1, 6.1-6.9, > or =7.0 mmol/l (newly diagnosed diabetes), and in those with prior history of diabetes. They were 308, 322, 301, and 293 micromol/l, respectively, in women. The UA levels declined with increasing FPG levels in individuals with newly diagnosed diabetes, with standardized coefficient of -0.26 in men and -0.20 in women, after multivariate adjustment for age, body mass index, triglycerides, and cardiovascular disease history. The relationship between 2-h glucose and UA was not as clear as that for FPG. CONCLUSION: Serum UA levels tended to increase with increasing FPG levels in non-diabetic individuals, but decrease in diabetic individuals.

Adult↗
PubMed1993

Hypoxanthine, xanthine, and uric acid in newborn pigs during hypoxemia followed by resuscitation with room air or 100% oxygen.

OBJECTIVE: To determine if resuscitation with room air is as effective as resuscitation with an FIO2 of 1.0. DESIGN: Prospective, randomized laboratory study. SETTING: Experimental laboratory (neonatal or delivery ward). SUBJECTS: Twenty piglets, 1 to 2 wks of age. INTERVENTIONS: Piglets were randomized into two groups. Both groups underwent hypoxemia for 2 hrs and then underwent reoxygenation for 1 hr (group 1 with an FIO2 of 1.0 and group 2 with an FIO2 of 0.21). MEASUREMENTS AND MAIN RESULTS: Hypoxanthine, xanthine, uric acid, PaO2, oxygen saturation, pH, base excess or deficit, and arterial pressure. During hypoxemia (PaO2 26 to 49 torr [3.5 to 6.5 kPa]), the mean hypoxanthine concentrations increased (p < .02) from 26.1 to 115.4 mumol/L in plasma, from 20.9 to 81.7 mumol/L in cerebrospinal fluid, and from 12.9 to 21.5 mumol/L in vitreous humor. Xanthine concentrations changed in a similar way, whereas uric acid concentrations increased only in plasma. During reoxygenation, hypoxanthine concentrations increased both in cerebrospinal fluid and in the vitreous humor. Final concentrations in these two fluid areas were 81.8 and 39.4 mumol/L, respectively (p < .02). Xanthine concentrations increased similarly. In plasma, hypoxanthine and xanthine concentrations decreased during reoxygenation. The final mean concentration of hypoxanthine was 76.8 mumol/L (p < .02). No change in plasma or cerebrospinal fluid uric acid concentrations were found during reoxygenation. The other measurements varied throughout the experiment, but no differences were found between the groups. CONCLUSIONS: There were no significant differences between the two treatment groups at any stage in the experiments. In this porcine model of hypoxemia, resuscitation with room air was as effective as was resuscitation with an FIO2 of 1.0, when circulating concentrations of oxypurines were used as an end-point.

Air↗
PubMed1976

Creatine kinase activity in serum and uric acid solution.

Skeletal muscle creatine kinases from man and rabbit, activated to measured specific activities by thiol agents, were inactivated in human serum and in uric acid solution, and the extent of their subsequent reactivation by dithiothreitol was determined. Both enzymes were completely reactivated from uric acid solution but were only 60-70% reactivated from serum. No inactivation occurred within 14 days if serum samples contained dithiothreitol (0.01 M) and were stored at -17 degrees C.

Animals↗
PubMed1986

Binding of glycosaminoglycans to sodium urate and uric acid crystals.

The binding of heparin, chondroitin sulphate and the low molecular weight heparin analogue pentosan polysulphate to sodium urate and uric acid crystals was studied by the use of radioactively labelled glycosaminoglycans were used in the binding step, and varying amounts of unlabelled glycosaminoglycans for the competition experiments. The experiments were carried out in 140 mmol/l NaCl at pH 6, with or without 5 mmol/l CaCl2 in the solution. A reversible and almost complete binding of heparin and chondroitin sulphate to sodium urate crystals did occur in the presence of calcium, whereas pentosan polysulphate bound incompletely. The binding was much less pronounced in the calcium-free conditions. Uric acid crystals did not bind any of the three inhibitors, not even with calcium present. The clinical relevance depends on whether sodium urate microcrystals are present in the urine of calcium stone patients, to cause a binding and thereby a masking or inactivation of these inhibitors in the urine, which seems to be possible in the presence of calcium. However, the potential of pentosan polysulphate for the treatment of calcium stone patients does not seem to be at risk from this effect.

Binding, Competitive↗