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PubMed1978

Immobilized-enzyme membrane sandwich reactor used in automated micro-scale assay of plasma uric acid.

We describe the automated microassay of plasma uric acid by use of an immobilized uricase-membrane sandwich reactor. Hydrogen peroxide, formed when uric acid is oxidized, oxidatively couples two molecules of p-hydroxyphenylacetic acid in the presence of peroxidase to produce a highly fluorescent compound. The specificity of the uricase reaction is coupled with a significantly lower cost of analysis.

Autoanalysis↗
PubMed1989

Increased uric acid in the developing brain and spinal cord following cytomegalovirus infection.

Tissue concentrations of uric acid were determined in the spinal cord, cerebellum, caudate-putamen, and cerebral cortex of developing mice following intraventricular inoculation with murine cytomegalovirus (MCMV) on postnatal day 10. Transient signs of neurological impairment were observed in MCMV-infected animals beginning on days 13-16 and continuing until days 19-21. At the onset of neurological impairment, uric acid concentrations in tissues from infected animals were 17-60-fold greater than in control animals. On postnatal day 70, 60 days after inoculation and 40 days after resolution of neurological signs, uric acid levels were still two- to threefold greater in infected animals. Histological examination revealed signs of focal ischemia in the cerebral and cerebellar cortices of MCMV-infected mice only at the onset of neurological impairment, with ischemic cell changes in some pyramidal neurons of the cerebral cortex. These results indicate that uric acid may be a sensitive marker of persistent vascular pathology resulting from cytomegalovirus infection of the developing nervous system.

Aging↗
PubMed1986

Cecal degradation of uric acid in Gambel quail.

In birds, urine enters the lower gastrointestinal tract from paired ureters and can be moved in a retrograde fashion into the colon and digestive ceca. As a major constituent of urine, uric acid is carried into these regions of the gastrointestinal tract. In these locations the chemical composition of the urine, including uric acid, could be altered. To examine this possibility the postrenal degradation of uric acid in the hindgut (ceca, colon, and ileum) of the Gambel quail (Callipepla gambelii) was investigated in vitro to determine the location of activity and the possible source of uricolytic enzymes. Significant breakdown of uric acid was observed in all cecal preparations; only minor amounts were degraded in the ileum and colon. The cecal degradation amounted to 15-49% of the uric acid estimated to be produced by the quail. Attempts to demonstrate uric acid decomposition by bacteria cultured from ceca gave inconclusive results.

Animals↗
PubMed2001

Systemic uric acid administration increases serum antioxidant capacity in healthy volunteers.

Oxidative stress plays an important role in the development of atherosclerosis and contributes to tissue damage that occurs as a consequence, particularly in myocardial infarction and acute stroke. Antioxidant properties of uric acid have long been recognized and, as a result of its comparatively high serum concentrations, it is the most abundant scavenger of free radicals in humans. Elevation of serum uric acid concentration occurs as a physiologic response to increased oxidative stress-for example, during acute exercise-thus providing a counter-regulatory increase in antioxidant defenses. In view of its antioxidant properties, uric acid may have potentially important and beneficial effects within the cardiovascular system. We wished to investigate whether administration of uric acid was feasible and if it could have an impact on antioxidant function in vivo. We have, therefore, performed a randomized, placebo-controlled double-blind study of the effects of systemic administration of uric acid, 1,000 mg, in healthy volunteers, compared with vitamin C, 1,000 mg. We observed a significant increase in serum free-radical scavenging capacity from baseline during uric acid and vitamin C infusion, using two methodologically distinct antioxidant assays. The effect of uric acid was substantially greater than that of vitamin C.

Adult↗
PubMed2002

Plasma lactate and uric acid responses to racing in pacing Standardbreds and relationships with performance.

Relationships between racing performance and plasma lactate and uric acid concentrations after racing were investigated in pacing Standardbred racehorses. The study was undertaken in order to better understand factors that limit racing performance. Twenty horses were tested after races of 1760 m and 28 horses after races over 2160 m. Blood samples were taken 30-60 min before and 8 and 30 min after a race. There were no significant differences between the race distances for prerace and 8 min postrace plasma lactates. Significant low correlations were obtained for plasma lactate concentration 8 min postrace and the number of race wins (r = 0.29, P = 0.04), number of race placings (1st, 2nd or 3rd; r = 0.34, P = 0.02) and lifetime earnings (r = 0.29, P = 0.04). Net lactate was correlated with the number of race placings (r = 0.31, P = 0.03). There were no significant correlations between performance indices and plasma uric acid concentrations in races of 1760 m. For races over 2160 m, correlations were found between plasma uric acid concentration at 8 min postrace and the number of race wins (r = 0.37, P = 0.06, 95% confidence limits 0-0.65). As well, there was a significant correlation between uric acid concentration at 8 min postrace and lifetime earnings (r = 0.35, P = 0.07, 95% confidence limits 0.06-0.64). Only 10-15% of the variability in retrospective career performance in pacing Standardbreds can be explained by these metabolic markers of the muscle anaerobic response to racing. Plasma lactate and uric acid responses to maximal exercise are unlikely to be useful for evaluating racing performance in pacing Standardbreds in univariate analysis.

Animals↗
PubMed1994

Effect of probe size on the concentration of brain extracellular uric acid monitored with carbon paste electrodes.

We have investigated further the anomalously high concentration of brain extracellular uric acid detected with in vivo sampling probes reported recently. The contribution by uric acid and 5-hydroxyindoleacetic acid (5-HIAA) to peak 2 recorded in rat striatum with chronically implanted carbon paste electrodes (CPEs) of different sizes was estimated by comparing peak current densities and the effect of the monoamine oxidase inhibitor pargyline. The concentration of uric acid in the extracellular fluid was some 50 times greater for 320-microns-diameter CPEs than for 160-microns-diameter electrodes, where the urate level was estimated at approximately 1 microM. The concentration of 5-HIAA was similar for 320-, 260-, and 160-microns-diameter CPEs. These data provide an explanation for the previously observed differences in 5-HIAA/urate ratios recorded with 320-microns-diameter CPEs and smaller carbon fibre electrodes. The results also indicate that chronically implanted sampling probes of diameter > 160 microns perturb the surrounding tissue, which produces uric acid by a mechanism yet unknown, although preliminary histological data suggest that glial cells may be involved.

Animals↗
PubMed1978

[Comparative studies on the determination of uric acid with the continuous flow machine, the manual reduction method and the enzymatic color test].

The manual and automatised determination of uric acid by means of phosphotungstic acid as well as the enzymatic test are compared: 1. When the manual reduction method is performed in the deproteinisation losses of uric acid develop (too low pH-value, absorption). For the precipitation of protein the pH-value 3 must not be undercut. Use uranyl acetate (no trichloro-acetic acid). 2. By dialysing of serum the automatized method avoid errors in precipitation. On the other hand, the simultaneous determination of non-uric acid chromogens is valid as for the manual method. Therefore, the automatically established values are higher. 3. Normal regions for the automatized phosphotungstic acid method are: males 4.8--8.2, females 3.5--7.5 mg uric acid/100 ml serum. 4. Comparisons of the quality of the manual and automatized reduction method for the enzymatic colour test are performed: In the precision the methods tested achieve comparable results (VK 2.1--3.5). The investigations of the correctness by means of control sera achieved acceptable results. The enzymatic colour test gives, since scarcely influenced by pharmaca and nearly specifically, the most reliable results. When using reduction methods analytic and preanalytic sources of error (e.g. pharmaca) must vastly be excluded. The automatised reduction method gives the advantage that there do no more appear any losses of uric acid. There is another normal region for the methods tested.

Automation↗
PubMed1996

Influence of four diets on uric acid metabolism and endogenous acid production in healthy beagles.

OBJECTIVE: To evaluate the influence of 3 diets used to dissolve or prevent ammonium urate uroliths in dogs, and a diet formulated for growth, on 24-hour excretions of uric acid, ammonia, net acid, titratable acid, bicarbonate, and creatinine; 24-hour urine volumes; pH values of 24-hour urine samples; plasma uric acid concentration; serum creatinine concentration; and endogenous creatinine clearance values. DESIGN: Randomized block. ANIMALS: Six reproductively intact female Beagles, 3.9 to 4.2 years old, weighing 8.5 to 11.1 kg. PROCEDURES: Four diets were evaluated for their ability to dissolve magnesium ammonium phosphate hexahydrate (struvite) uroliths (diet S); to minimize uric acid excretion (diet U); to minimize clinical signs associated with renal failure (diet K); and to promote growth in pups (diet P). Each diet was fed for 14 days; then 24-hour urine samples were collected. An adult maintenance diet was fed during a 7-day washout period. RESULTS: Consumption of diet U was associated with lowest plasma uric acid concentration, lowest 24-hour urinary uric acid, ammonia, titratable acid, and net acid excretions, lowest endogenous creatinine clearance values, highest 24-hour urinary bicarbonate excretion and urine pH values, and highest 24-hour urine volumes. Consumption of diet P was associated with opposite results; results of consumption of diets S and K were intermediate between those for diets U and P. CONCLUSION: Consumption of diet U by healthy Beagles is associated with reduced magnitude of urinary excretion of uric acid and ammonia, with alkaluria, and with polyuria, which may be beneficial in the management of ammonium urate uroliths in dogs. CLINICAL RELEVANCE: Results support use of diet U for management of ammonium urate urolithiasis in dogs.

Ammonia↗
PubMed1998

[The effect of uric acid, creatine phosphate and carnitine on lipid peroxidation in cerebral cortex and myocardium homogenates].

BACKGROUND: Uric acid as the product of purine nucleotide degradation is an integrate component of blood plasma. This metabolite is considered to be one of the important naturally occurring antioxidants building up the antioxidation system of the organism. Creatine phosphate and carnitine are important substances participating in energy metabolism of the cells. Energy production is closely related to the level of reduction systems and thus also to the antiradical ability of the cell. By this mechanism could creatine phosphate and carnitine improve the antioxidative capacity of the cell. METHODS: In homogenates of rat brain cortex and myocardium was the production of oxygen radicals stimulated by mixture of Fe2+ ions and ascorbate. Oxygen radicals may induce lipid peroxidation by the means of the reaction with lipid structures. We tried to inhibit the process of lipid peroxidation by addition of uric acid, creatine phosphate and carnitine into the incubation medium. Intensity of lipoperoxidation was measured by detection of substances giving positive reaction with thiobarbituric acid (TBA) in homogenates of brain cortex and myocardium. RESULTS: Uric acid in concentrations of 1 and 0.5 mmol.l-1 markedly inhibits the production of compounds reacting with TBA. This effect was not found in 0.05 mmol.l-1 concentration. Creatine phosphate and carnitine in 1 mmol.l-1 concentrations also decreased the value of lipid peroxides in homogenates of brain cortex, but their effect was lower than the effect of uric acid. This effect was not seen in myocardium homogenates.

Animals↗
PubMed2004

Effect of icodextrin on transperitoneal uric acid and albumin transport in vitro.

In the present study, we compared the influence of icodextrin (2 g/dL) on uric acid (20 mg/dL) and albumin (1 g/dL) transfer through isolated rabbit parietal peritoneum. In separate series of experiments, we used a mathematical model to calculate the transport rate of solutes from the interstitial to the mesothelial side of peritoneal membrane (I --> M) and in the opposite direction (M --> I) before and after introduction of glucose polymer. In control conditions, the rates of uric acid and albumin passage across the rabbit peritoneum remained constant. Mean values [x +/- standard error of the mean (SEM)] of the diffusive permeability coefficient P were 1.936 +/- 0.324 (I --> M) and 2.078 +/- 0.186 (M --> I) for uric acid and 0.341 +/- 0.066 (I --> M) and 0.389 +/- 0.084 (M --> I) for albumin (all x10(-4) cm/s), respectively. The introduction of glucose polymer into the experimental system did not alter the I --> M transport of either solute; but, in the opposite direction, it caused a 17% decline in the P for uric acid (p < 0.05), and an increase of 77% in the same parameter for albumin (p < 0.03). Hence, I --> M transfer dominated M --> I transfer of uric acid (p < 0.04). In contrast, in albumin transport, M --> I was higher than I --> M (p < 0.02). We conclude that, in vitro, icodextrin modifies the diffusive permeability of the peritoneum and induces transport asymmetry for some small and large solutes.

Albumins↗
PubMed2001

Chemiluminescence assay for uric acid in human serum and urine using flow-injection with immobilized reagents technology.

A novel chemiluminescence (CL) flow sensor for the determination of uric acid in human urine and serum has been developed by using controlled-reagent-release technology. The reagents involved in the chemiluminescence (CL) reaction, luminol and periodate, are immobilized on anion-exchange resin packed in a column. After injection of water, chemiluminescence generated by released luminol and periodate in alkaline media is inhibited in presence of uric acid. By measuring the decreased chemiluminescence (CL) intensity the uric acid is sensed. The decreased response is linear in the 5.0-500.0 ng mL(-1) range, with a detection limit of 1.8 ng mL(-1). The flow sensor showed remarkable operational stability and could be easily reused for over 80 h with sampling frequency of 100 h(-1). The proposed sensor was applied to the determination of uric acid in human urine and serum, and monitoring metabolic uric acid in human urine with RSD less than 3.0%.

Animals↗
PubMed1997

Are high uric acid levels in patients with early pre-eclampsia an indication for delivery?

OBJECTIVE: To compare the perinatal mortality rates of pre-eclamptic patients with high, normal and low uric acid levels. DESIGN: Prospective analytic study. SETTING: Tertiary hospital to which many patients with severe pre-eclampsia are referred. SUBJECTS: Two hundred and twenty-nine patients with severe pre-eclampsia. INTERVENTION: Delivery for maternal or fetal reasons, not taking uric acid levels into account. MAIN OUTCOME MEASURE: Perinatal mortality rate. RESULTS: The mean uric acid level prior to delivery at a mean gestational age of 30.9 weeks was 0.4 mmol (SD 0.11). Twenty patients had uric acid levels of 0.28 mmol/l or lower and 25 patients values of 0.52 mmol/l or higher. The mean gestational age at admission and the admission-delivery interval for the high, normal and low uric acid groups were 29.2 weeks, 11.8 days; 29.2 weeks, 13.3 days and 27.1 weeks, 13 days respectively. For babies who weighed 1000 g or more at delivery, the perinatal mortality rates were 40, 11 and 50 respectively. CONCLUSION: There is no evidence from this study to support the association between perinatal deaths and higher uric acid levels in patients with severe pre-eclampsia.

Adult↗
PubMed1997

Effect of seed crystals of uric acid and monosodium urate on the crystallization of calcium oxalate in undiluted human urine in vitro.

1. The aim of this study was to determine whether seed crystals of uric acid or monosodium urate promote the epitaxial deposition of calcium oxalate in undiluted human urine. The effects of seed crystals of uric acid, monosodium urate or calcium oxalate on calcium oxalate crystallization induced in pooled 24-h urine samples collected from six healthy men were determined by [14C]oxalate deposition and Coulter counter particle analysis. The precipitated crystals were examined by scanning electron microscopy. 2. Seed crystals of uric acid, monosodium urate and calcium oxalate increased the precipitated particle volume in comparison with the control containing no seeds by 13.6%, 56.8% and 206.5% respectively, whereas the deposition of [14C]oxalate in these samples relative to the control was 1.4% (P < 0.05), 5.2% (P < 0.01) and 54% (P < 0.001) respectively. The crystalline particles deposited in the presence of monosodium urate seeds were smaller than those in the control samples. Scanning electron microscopy showed that large aggregates of calcium oxalate were formed in the presence of calcium oxalate seeds, which themselves were not visible. In contrast, monosodium urate and, to a lesser extent, uric acid seeds were scattered free on the membrane surfaces and attached like barnacles upon the surface of the calcium oxalate crystals. 3. It was concluded that seed crystals of monosodium urate and uric acid do not promote calcium oxalate deposition to a physiologically significant degree in urine. However, binding of monosodium urate and uric acid crystals and their subsequent enclosure within actively growing calcium oxalate crystals might occur in vivo, thereby explaining the occurrence of mixed urate/oxalate stones.

Calcium Oxalate↗
PubMed1994

Effect of uric acid on sodium oxalate-induced urolithiasis in rats--biochemical and histological evidences.

Effect of uric acid on sodium oxalate-induced biochemical and histological changes were studied in rats. Rats injected with sodium oxalate (0.7 mg/100 g body wt, ip) show calcium deposits in the lumen of kidney tubules. Uric acid administration was found to potentiate calcium oxalate calculi formation. Lipid peroxide formation was increased up to 100% in kidney and 28% in liver by sodium, oxalate treatment. Uric acid administration was found to reduce lipid peroxide level up to 12% in liver and 20% in kidney. From this study it is concluded that lipid peroxidation may not be the cause of sodium oxalate-induced urolithiasis and the results are discussed with reference to the epitaxic nature of uric acid on kidney stone formation.

Animals↗
PubMed1982

Effects of azaserine treatment on plasma glutamine concentration and uric acid production in chickens fed low and high protein diets.

Azaserine injected intravenously decreased uric acid in the blood and urine 1.6 and 2 times, respectively. It also resulted in 3 times larger increase in plasma glutamine concentration in chickens fed a 20% protein diet than in those fed a 5% protein diet, but it had no effect on liver glutamine synthetase activity in either dietary group. Thus the resultant concentration of plasma glutamine in the chickens fed the high protein diet was higher than in those fed the low protein diet, the reverse of the relationship observed before the injection. The infusion of ammonium acetate caused less of a rise in plasma glutamine concentration, but increased uric acid in the urine and blood, more with the high protein feeding than the low protein feeding. Pretreatment with azaserine further augmented the increase in plasma glutamine concentration caused by the infusion of ammonium acetate in the chickens fed the high protein diet but not in those fed the low protein diet, and concurrently removed the stimulatory effect of ammonia on uric acid in the blood and urine of both dietary groups. These data indicate that both glutamine in intact chickens and the increased glutamine in the ammonia-infused chickens are converted to uric acid more by high protein feeding than by low protein feeding, and this is a major reason for the low concentration of plasma glutamine in the chickens fed a high protein diet.

Acetates↗
PubMed2004

Uric acid and the state of the intrarenal renin-angiotensin system in humans.

BACKGROUND: Experimental hyperuricemia is marked by an activated intrarenal renin-angiotensin system (RAS). The renal vascular response to exogenous angiotensin II (Ang II) provides an indirect measure of intrarenal RAS activity. We tested the hypothesis that the serum uric acid concentration predicts the renal vascular response to Ang II. METHODS: A total of 249 subjects in high sodium balance had the renal plasma flow (RPF) response to Ang II measured. Para-aminohippuric acid (PAH) clearance was used to estimate RPF. Multivariable regression analysis determined if the serum uric acid concentration independently predicts the RPF response to Ang II. Variables considered included age, gender, race, body mass index (BMI), hypertension status, blood pressure, basal RPF, creatinine clearance, serum insulin, serum glucose, serum high-density lipoprotein (HDL), serum triglycerides, and plasma renin activity (PRA). RESULTS: Uric acid concentration negatively correlated with the RPF response to Ang II (r=-0.37, P < 0.001). In univariate analysis, age, BMI, hypertension, triglycerides, and blood pressure were negatively associated, and basal RPF, HDL, and female gender were positively associated with the RPF response to Ang II. In multivariable analysis, serum uric acid concentration independently predicted the RPF response to Ang II (beta=-5.3, P < 0.001). CONCLUSION: Serum uric acid independently predicted blunted renal vascular responsiveness to Ang II, consistent with results from experimental hyperuricemia showing an activated intrarenal RAS. This could be due to a direct effect of uric acid or reflect a more fundamental renal process. These data may have relevance to the association of uric acid with risk for hypertension and nephropathy.

Adult↗
PubMed1983

Uric acid effects on in vitro models of rheumatoid inflammatory and autoimmune processes.

A neutrophil monolayer system was used to study the effects of uric acid on neutrophil-aggregate interactions important in rheumatoid inflammation. No effect on immunoglobulin G aggregate phagocytosis was seen, but hyperuricaemic levels of uric acid were associated with an enhancement of phagocytosis-induced release of the azurophilic granular enzyme beta-glucuronidase. A trinitrophenyl-coupled mononuclear leucocyte rheumatoid factor plaque-forming assay was utilised to study uric acid effects on polyclonal activation of immunocompetent cells. Low levels of uric acid enhanced and high levels suppressed this system. Hyperuricaemia may enhance some aspects of rheumatoid inflammation, while uric acid may modulate an important component of rheumatoid autoimmunity.

Arthritis, Rheumatoid↗
PubMed1975

[Influence of parenteral fructose or glucose administration on uric acid formation and phosphate uptake of the human liver].

15 min. after intravenous administration of fructose (10 g/5 min, 0,5 g/kg/h) the hepatic uric acid production in healthy volunteers increased from 0,07 mg/100 g X min to 0,52 mg/100 g X min. After one hour the enhanced uric acid production was 0,3 mg 100 g X min. The enhanced uric acid production was accompanied by an increased hepatic phosphate uptake. The highest value was 13 mumol/100 g X min. During the control period the liver released small amounts of phosphate into the hepatic vein. The increased hepatic uric acid output correlated with an enhanced renal clearance, therefore the peripheral venous uric acid concentrations remained unchanged.

Fructose↗