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PubMed1991

Plasma accumulation of hypoxanthine, uric acid and creatine kinase following exhausting runs of differing durations in man.

During exhausting exercise adenylate kinase in the muscle cells is activated and a degradation of adenosine 5'-diphosphate occurs. Consequently, degradation products of adenosine 5'-monophosphate including hypoxanthine and uric acid, accumulate in plasma. The aim of this study was to compare the concentration changes of hypoxanthine and uric acid in plasma following running of varying duration and intensity. In addition, plasma creatine kinase activity was measured to assess the possible relationship between metabolic stress and protein release. Four groups of competitive male runners ran 100 m (n = 7), 800 m (n = 11), 5000 m (n = 7) and 42,000 m (n = 7), respectively, at an exhausting pace. Subsequent to the 100 m event (mean running time 11 s) plasma concentrations of hypoxanthine and uric acid increased by 364% and 36% respectively (P less than 0.05), indicating a very high rate of adenine nucleotide degradation during the event. Following the 800-m event (mean running time 125 s), hypoxanthine and uric acid concentrations had increased by 1598% and 66%, respectively (P less than 0.05). Both the events of longer duration, 5000 m and 42,000 m, also caused a significant increase in plasma concentration of hypoxanthine (742% and 237% respectively, P less than 0.05) and plasma uric acid (54% and 34% respectively, P less than 0.05). Plasma activities of creatine kinase were significantly increased at 24 h only following the 5000 m and 42,000 m events (64% and 1186% respectively, P less than 0.05). Changes in plasma creatine kinase activity showed no correlation with changes in plasma concentration of either hypoxanthine or uric acid for the 5000 m and 42,000 m events (r = 0.00-0.45, P greater than 0.05).

Adenosine Triphosphate↗
PubMed1987

Stimulation of uric acid release from the perfused rat liver by platelet activating factor or potassium.

The stimulation of hepatic glycogenolysis by platelet activating factor (AGEPC) or increased perfusate potassium concentration ([K+]o), but not phenylephrine, causes a transient increase in uric acid release into the effluent perfusate of perfused rat livers. Uric acid was identified in chromatograms of perfusate samples using reversed-phase h.p.l.c., which show a peak which co-elutes with authentic uric acid, and by the fact that the A293 of perfusate samples decreases in the presence of uricase. Uric acid release is dose-dependent with respect to both AGEPC and [K+]o, and is blocked completely by prior exposure of the perfused liver to 5 mM-allopurinol, a specific inhibitor of xanthine oxidase (XOD). Allopurinol inhibits the increase in portal vein pressure induced by AGEPC, increased [K+]o or phenylephrine; the inhibitory effect increases with increasing concentrations of the agents. Also, allopurinol inhibits the second phase of O2 uptake and glucose release characteristic of concentrations of AGEPC or increased [K+]o equal to or greater than their reported half-maximal concentration for glucose release. The ratio of xanthine dehydrogenase (XDH) to XOD activity in extracts of freeze-clamped perfused livers is not affected by treatment of the livers with AGEPC or increased [K+]o. The results suggest that uric acid production may be an indicator of ischaemia within localized hepatic sinusoids, and that allopurinol partially protects the hepatocyte from the effects of AGEPC or increased [K+]o by inhibiting XOD-dependent superoxide production. We propose that the second phase of the glycogenolytic response to these agents results from ischaemia and subsequent reperfusion. Activation of XOD in vivo and hence O2-derived free radical production may be involved in the response of the liver to vasoactive agonists under a variety of pathophysiological conditions.

Allopurinol↗
PubMed2005

Effect of smoking on uric acid and other metabolic markers throughout normal pregnancy.

OBJECTIVES: Smoking, pregnancy, and preeclampsia are all associated with changes in markers of the metabolic syndrome. Several markers are increased in all three conditions. However, smoking is negatively associated with preeclampsia, and therefore some markers would be expected to behave differently in smokers during pregnancy. We compared several metabolic markers of the metabolic syndrome in healthy primigravid smokers and nonsmokers over normal pregnancy to explore mechanisms for the reduced risk of preeclampsia in smokers. STUDY DESIGN: Plasma was obtained from 63 women throughout pregnancy who delivered at term. Smoking status was determined by urinary cotinine concentrations measured by HPLC. Uric acid, creatinine, free fatty acids, triglycerides, and total cholesterol were measured with diagnostic kits. Data were analyzed by repeated-measures ANOVA. RESULTS: The smoking groups were not different by delivery gestational age, maternal age, body mass index, or race. Uric acid, cholesterol, and triglyceride concentrations increased during pregnancy (significant for time, P < 0.0001). Mean uric acid and creatinine concentrations were different by smoking status (P < 0.001 and P = 0.046). Nonsmokers had the lowest concentrations of uric acid, and women who quit smoking had the highest concentrations. Uric acid concentrations remained significantly different controlling for serum creatinine CONCLUSIONS: Women have changes in markers of the metabolic syndrome during pregnancy, and uric acid is further influenced by smoking. The difference in uric acid concentrations by smoking status may be secondary to increased production through the xanthine oxidase pathway but is not simply a result of altered glomerular function because the association persists after controlling for creatinine.

Adult↗
PubMed2005

[Significance of the changes of urinary uric acid in OSAHS before and after UPPP].

OBJECTIVE: To assess the value of urinary uric acid excretion and urinary uric acid/creatinine ratio as the marker of obstructive sleep apnea-hypopnea syndrome (OSAHS) before and after Uvulopalatopharyngoplasty (UPPP). METHOD: Twenty three cases diagnosed as OSAHS by polysomnography (PSG) were treated as trial group, 12 cases excluded from OSAHS by PSG were taken as control group,and 15 patients of the trial group were treated by UPPP and were taken as before UPPP therapy group and after UPPP therapy group. The makers above were compared in these groups. RESULT: The overnight change in urinary uric acid/creatinine ratio in trial group is 0.46+/-0.25, and after UPPP therapy group (0.13+/-0.2) significantly lower than before UPPP therapy group (0.49 +/-0.32), P < 0.01. CONCLUSION: The urinary uric acid excretion and overnight change in urinary uric acid/creatinine are good markers to determine the effects of UPPP on OSAHS.

Adult↗
PubMed2004

Disposition of uric acid upon administration of ofloxacin alone and in combination with other anti-tuberculosis drugs.

Disposition of uric acid upon administration of ofloxacin (O) alone and in combination with other anti-tuberculosis drugs, rifampicin (R), isoniazid (H) and pyrazinamide (Z) was studied. Twelve male healthy volunteers were investigated on four different occasions with the four drugs alone or in combinations. A partially balanced incomplete block design was adopted and the subjects were randomly allocated to each group. Uric acid concentration in urine samples excreted over 0-8 hr, were determined after coding the samples. There was significant decrease in the group receiving Z when compared to other groups. Though there was a decrease in uric acid excretion in the group receiving O, it was not statistically significant. Rifampicin and H seem to increase the uric acid excretion. The incidence of arthralgia was mainly due to Z and not due to either O or other drugs in the treatment of pulmonary tuberculosis.

Adult↗
PubMed2004

[Does coffee drinking influence serum uric acid concentration?].

The drinking of coffee, a commonly used beverage, was a subject of many studies, mainly regarded to coffee influence on cardiovascular system. However, only one study indicates that coffee drinking in male adults may lead to decrease in serum uric acid level. Hyperuricaemia is a risk factor of many diseases. The aim of this study was to examine the influence of coffee drinking on serum uric acid concentration. 1955 working persons aged from 18 to 65 years were included into research. There were 571 women among them. We determined energy expenditure during professional work, blood pressure, body mass index, and measured serum levels of uric acid, glucose and creatinine. The amount of coffee and ethanol consumption was evaluated on the ground of an interview. It was showed that persons drinking coffee have lower serum uric acid concentration than non-drinkers, especially among women, who drank more coffee then men. Uricaemia was correlated negatively with number of cups of coffee consumed and positively with body mass index, ethanol consumption and diastolic blood pressure. The author conclude that: 1) among women drinking on an average 10 cups of coffee per week appeared a decrease in serum uric acid concentration and a lower risk of development of hyperuricaemia, 2) elevated serum uric acid concentration is accompanied by elevated blood pressure and increased body mass index.

Adult↗
PubMed1983

Purine metabolism in high- and low-uric acid lines of chickens: hypoxanthine/guanine phosphoribosyltransferase activities.

The activity of hypoxanthine/guanine phosphoribosyltransferase (HGPRT) was examined in the livers and kidneys of two genetic lines of chickens selected for different plasma uric acid levels. Previous work demonstrated that the high-uric acid line (HUA) had significantly greater de novo uric acid synthesis rates in kidney tissue compared to the low-uric acid line (LUA). In addition, phosphoribosylpyrophosphate (PRPP) synthetase and xanthine dehydrogenase activities in livers and kidneys were significantly higher in the HUA compared to the LUA line. PRPP pool sizes were also significantly higher in both livers and kidneys of HUA birds. HGPRT activities in livers of HUA birds were significantly (P less than 0.05) greater than in LUA birds. The mean value of liver HGPRT was 7.36 +/- 0.25 pmole inosine-5'-monophosphate (IMP) and 6.05 +/- 0.27 pmole IMP produced/micrograms protein/hr, respectively, for the HUA and LUA lines. There were no significant differences (P greater than 0.05) in kidney HGPRT activities between the two groups. The mean value of kidney HGPRT was 52.87 +/- 1.62 pmole IMP and 50.72 +/- 1.62 pmole IMP produced/micrograms protein/hr, respectively, for the HUA and LUA line. Elevated liver HGPRT may serve to enhance the regeneration of PRPP in the HUA liver. Elevated liver PRPP synthetase and PRPP pool size suggest an increased flux through the de novo purine biosynthetic pathway in HUA birds. The resulting additional pyrophosphate from the glutamine PRPP amidotransferase reaction would stimulate recovery of PRPP and spare the system from a substantial loss of energy.

Animals↗
PubMed1979

Serum uric acid levels in untreated and PUVA-treated patients with psoriasis.

Elevated uric acid serum levels are a frequent finding in psoriasis and, despite some reports to the contrary, it is generally believed that an association does exist between hyperuricemia and psoriasis. It seems a convincing idea that the rapid epidermal turnover in psoriasis might lead to an increased purine breakdown and may thus influence the uric acid serum levels. Consequently, a relationship might well be expected between hyperuricemia and the extent of psoriatic skin involvement. The present study was undertaken in order to prove or disprove such an assumption and to investigate the influence of oral photochemotherapy on the serum uric acid levels in psoriatic subjects.

Furocoumarins↗
PubMed1997

Renal metabolism of uric acid in type I insulin-dependent diabetic patients: relation to metabolic compensation.

Patients with insulin-dependent diabetes mellitus and poor glycemic control show hypouricemia with hyperuricosuria. In the present study, we have evaluated whether a good glycemic control influences the renal handling of uric acid. Sixteen patients (8 male, mean age 22.4 +/- 7.2 years) were studied under two situations, poor glycemic control (glycemia > 11 mmol/L and HbA1 c > 10%) and good glycemic control (glycemia < 6 mmol/L and HbA1 c < 8.5%). A group of 16 normal subjects served as the control group (8 male, mean age 21.9 +/- 9.1 years). In the poor glycemic control phase, patients showed lower plasma uric acid levels (0.18 +/- 0.06 mmol/L) and higher fractional urinary excretion of uric acid (16.1 +/- 9.3%) than the controls (0.28 +/- 0.06 and 8.2 +/- 1.9%, respectively). When a good glycemic control was reached, plasma uric acid increased (0.22 +/- 0.05), but it was still lower than that of the controls and fractional excretion of UA was normalized. Plasma uric acid was inversely correlated to glycemia (r = -0.34, p < 0.05) and to HbA1 c (r = -0.56, p < 0.0008) and fractional excretion of uric acid was directly correlated to glycemia (r = 0.39, p < 0.03) and HbA1 c (r = 0.73, p < 0.00005). These results indicate that the hypouricemia and hyperuricosuria of insulin-dependent diabetes mellitus is corrected by an adequate glycemic control, suggesting that these alterations are of a functional origin and due to a defective metabolic control.

Adolescent↗
PubMed1998

[Determination of uric acid, creatinine and pseudouridine in human urine by high performance capillary zone electrophoresis].

A simultaneous determination of uric acid, creatinine and pseudouridine in human urine by high performance capillary zone electrophoresis(HPCZE) is described. The urine samples were refrigerated and filtered. Then the samples were directly introduced into the capillary and a phosphate buffer solution(pH 6.1) was employed. The capillary used was 36 cm x 50 microns i.d. and detection was carried out with a UV monitor at 210 nm. The calibration curve showed a good linearity for uric acid, creatinine, and pseudouridine in the concentration range of 2-80 mg/L and their correlation coefficients were 0.996, 0.996 and 0.999 respectively. Within day CV for assaying the urine samples of uric acid, creatinine and pseudouridine were 5.0%, 3.0%, and 4.4%, and the corresponding between day data were 6.5%, 5.9%, and 5.3%, respectively. The recoveries of uric acid, creatinine and pseudouridine were 99.0%, 102.%, 92.2%, respectively. The total time for separation and determination was within 10 min. This method is characterized by direct assay of urine samples without any pretreatment. The results show that HPCZE is a simple, rapid, sensitive and reliable assay method.

Creatinine↗
PubMed2002

Uric acid--a marker for systemic inflammatory response in patients with congestive heart failure?

Congestive heart failure is associated with hyperuricemia and elevations in the levels of circulating markers for inflammation. The purpose of this study was to assess the relationship between levels of serum uric acid, activity of the renin-angiotensin-aldosterone system and TNF-alpha in heart failure patients with respect to the extent of left ventricular dysfunction. Circulating uric acid, TNF-alpha, plasma renin activity and concentrations of aldosterone were measured in 30 patients with congestive heart failure, divided into subgroups according to their NYHA class (II-IV). We found a significant step-by-step increase in TNF-alpha among the subgroups. Significant differences among the subgroups were found for the values of uric acid and the values of plasma renin and aldosterone. Serum uric acid correlated significantly with TNF-alpha concentrations (r = 0.36, P < 0.05) leukocytes (r = 0.38, P = 0.03) and ejection fraction (r = 0.64, P < 0.01). No significant correlation was found between the activity of the renin-angiotensin-aldosterone system and uricemia (r = 0.34). In a multivariate model, uric acid concentration was predicted significantly by the ejection fraction and blood leukocytes, this relationship being independent of serum creatinine, treatment modality, age and gender. We conclude that serum uric acid may reflect the severity of systolic dysfunction and the activation of an inflammatory reaction in patients with congestive heart failure.

Aged↗
PubMed2002

[Clinical study of treatment on chronic uric acid nephropathy by integrating Western and traditional Chinese medicine].

OBJECTIVE: To investigate the ameliorative effect on chronic uric acid nephropathy (CUAN) by integrating western and traditional Chinese medicine (IWTCM). METHODS: The 136 CUAN patients were divided into two groups at random, the therapy group of 86 patients were treated by Chinese medicine and allopurinol, and the control group of 50 patients were treated only by allopurinol. The curative effect and the related index such as blood uric acid, renal function, urinary protein, microproteins, blood lipid and hyperviscosity were determined before and after being treated. RESULTS: After three months treatment, the total effective rate in the therapy group (90.7%) was significantly higher (P < 0.01) than that of the control group (56%). The therapy group is also superior to the control group in improving renal function, lipid metabolism and hyperviscosity, decreasing blood uric acid, urinary protein, microproteins in evidence (P < 0.05, P < 0.01). CONCLUSION: IWTCM can obviously improve the ameliorative effect on chronic uric acid nephropathy.

Adult↗
PubMed1985

Yeast species utilizing uric acid, adenine, n-alkylamines or diamines as sole source of carbon and energy.

Yeast strains utilizing uric acid, adenine, monoamines or diamines as sole source of carbon and energy were isolated from several soil samples by the enrichment culture method. The most common species was Trichosporon cutaneum. Strains of Candida catenulata, C. famata, C. parapsilosis, C. rugosa, Cryptococcus laurentii, Stephanoascus ciferrii and Tr. adeninovorans were also isolated. All strains utilizing uric acid as sole carbon source utilized some primary n-alkyl-l-amines, hydroxyamines or diamines as well. The ascomycetous yeast strains showing these characteristics all belonged to species known to assimilate hydrocarbons. Type strains of hydrocarbon-positive yeast species which were not found in the enrichment cultures generally assimilated putrescine, some type strains also butylamine or pentylamine, but none assimilated uric acid. Methanol-positive species were not isolated. Type strains of methanol-positive and of hydrocarbon-negative species did not assimilate uric acid, butylamine or putrescine. Assimilation of putrescine as sole source of carbon and energy may be a valuable diagnostic criterion in yeast taxonomy.

Adenine↗
PubMed2006

Effect of losartan versus candesartan on uric acid, renal function, and fibrinogen in patients with hypertension and hyperuricemia associated with diuretics.

BACKGROUND: Hyperuricemia may counter benefits of blood pressure (BP) reduction, although this is controversial. METHODS: We examined the effects of candesartan and losartan on uric acid, creatinine, and fibrinogen. Patients with hypertension and serum uric acid > or = 0.42 mmol/L (7 mg/dL) associated with diuretics were randomized to receive losartan 50 to 100 mg or candesartan 8 to 16 mg for 24 weeks. At randomization and after 24 weeks, systolic and diastolic BP, serum uric acid, creatinine, and fibrinogen were measured. RESULTS: A total of 59 patients were entered into the study (30 in the losartan and 29 in the candesartan group). Mean systolic and diastolic BP were reduced in the candesartan group, from 156 mm Hg at baseline to 132 mm Hg at 24 weeks, and from 90.9 to 80.8 mm Hg respectively, P < .0001), and in the losartan group from 150.3 to 132 mm Hg and from 89.6 to 77.6 respectively, P < 0001). Overall mean values of fibrinogen levels were again reduced from 4.39 g/L at baseline to 4.01 g/L at 24 weeks (P < .02). Mean values of serum uric acid in the losartan and candesartan groups were similar at baseline (0.44 and 0.46 mmol/L, respectively), but they were lower in the losartan group after 24 weeks (0.39 and 0.48 mmol/L, P = .01). Twelve patients (44%) in the candesartan group had a 10% increase in serum creatinine compared with four patients (14.2%) in the losartan group (P < .02). CONCLUSIONS: Candesartan and losartan lowered BP, but only losartan reduced uric acid. The lowering of fibrinogen in both groups may explain the reduction in stroke with angiotensin receptor blockers. The effect of persistent hyperuricemia on renal function requires further study.

Antihypertensive Agents↗
PubMed1979

Uric acid transport in brush border membrane vesicles isolated from rabbit kidney.

The transport of uric acid was studied in brush border membrane vesicles isolated from rabbit kidney. The uptake of uric acid by the vesicles was osmotically sensitive and occurred in the absence of significant uric acid degradation. Under the conditions used to evaluate transport, urate binding to the membranes represented only 10--15% of the total uptake. The initial rate of uptake was linear over the concentration range 0.04--8 mM urate. Uptake of urage was Na+ gradient independent. It was dependent on external pH and temperature with Q10 near 3. The urate uptake was inhibited reversibly by p-chloromercuribenzoate. Probenecid, ouabain, cyclic adenosine 3',5'--monophosphate, and its dibutyryl derivative had no appreciable effects. Pyrazinoic acid and pyrazinamide stimulated urate uptake. Experiments performed with osmotically shocked vesicles demonstrated that this stimulatory effect resulted from increased binding of urate to the membranes. These results indicate that in several ways urate transport in vesicles resembles that observed with more physiologically intact preparations.

Animals↗
PubMed2004

Hypothesis: Uric acid, nephron number, and the pathogenesis of essential hypertension.

BACKGROUND: Essential hypertension affects more than 25% of the world's population. Genetic, physiologic, and epidemiologic studies provide clues to its origins, but a clear understanding has been elusive. Recent experimental and clinical studies have implicated uric acid in the onset of essential hypertension. METHODS: In a retrospective chart review, we identified 95 children with confirmed, new onset hypertension, and evaluated the cause of hypertension and parental history of hypertension, birth weight, and serum uric acid. In an open-label, cross-over trial we treated 5 children with confirmed essential hypertension with allopurinol as single treatment agent, and screened for change in blood pressure by casual and ambulatory methods. In tissue culture experiments, we evaluated the effect of uric acid on glomerular endothelial cell function. RESULTS: Elevation of serum uric acid is related to the onset of essential hypertension in children, reduced birth weight, and endothelial dysfunction. Normalization of uric acid appears to ameliorate new onset essential hypertension. CONCLUSION: These findings, combined with animal model data, support the hypothesis that uric acid has a key role in the pathogenesis of early onset essential hypertension, and may unify some of the disparate theories of the origins of essential hypertension.

Animals↗
PubMed1990

Uric acid is a major antioxidant in human nasal airway secretions.

Airway mucosal surfaces are potentially subjected to a variety of oxidant stresses. Airway submucosal glands secrete a variety of compounds that may protect the airways from injury. Cholinergically induced nasal submucosal gland secretion has recently been found to contain a low molecular weight nasal antioxidant. In this report, the isolation and identification of this nasal secretory antioxidant are described. Concentrated, cholinergically induced human nasal secretions were fractionated through a 10-kDa sieve and subjected to DEAE anion-exchange chromatography. Fractions containing antioxidant activity were subjected to gel filtration with Bio-Gel P-2 gel (resolution range, 200-2000 Da). The resultant antioxidant fractions were then desalted by gel filtration over the same column equilibrated in HPLC-grade water, yielding only a single peak with antioxidant activity. The absorption spectrum of the purified antioxidant revealed peaks at 238 and 292 nm at pH 7. These peaks shifted to 230 and 280 nm in 0.1 M HCl and 226 and 296 nm in 0.1 M NaOH. Sodium borohydride reduction of the antioxidant had no effect on the UV absorption, whereas platinum-catalyzed hydrogenation ablated all absorption peaks. Uric acid had identical absorption peaks and showed the same chromatographic behavior as the nasal antioxidant activity on both gel filtration and DEAE columns. Uricase (which degrades uric acid) metabolized both uric acid and the purified antioxidant. Uric acid was shown to have antioxidant activity at concentrations greater than 1.5 microM. These data indicate that nasal secretions contain uric acid that serves as an antioxidant.

Antioxidants↗
PubMed2002

Relative associations of fitness and fatness to fibrinogen, white blood cell count, uric acid and metabolic syndrome.

OBJECTIVE: To examine the relation between fitness and fibrinogen, white blood cell count, uric acid and metabolic syndrome across levels of adiposity in apparently healthy, nonsmoking men. DESIGN: Cross-sectional study of 4057 men from the Aerobics Center Longitudinal Study examining the age-adjusted resting levels and risk of having a clinically significant elevation of fibrinogen, white blood cell count, uric acid and metabolic syndrome score across nine fitness-body fatness combinations. Fitness categories (low fitness, moderately fit or high fitness) were based on a maximal treadmill test. Body mass index (BMI) <25.0 was classified as normal weight, BMI > or = 25.0 but <30.0 as overweight and BMI > or = 30.0 as obese. RESULTS: Fitness (inversely) and BMI (directly) were independently related to the age-adjusted values of all four variables (P for trend P<0.0001 for each). For all four variables, the greatest age-adjusted risk of having a clinically relevant value was found in the low fitness-obese category and the lowest age-adjusted risk was found in the high fitness-normal weight group. CONCLUSION: Fibrinogen, white blood cells, uric acid and metabolic syndrome score are independently related to both fitness (inversely) and fatness (directly). Within levels of fatness, risk for significant elevations in fibrinogen, white blood cells, uric acid and metabolic syndrome score is lower for the higher fitness groups.

Adipose Tissue↗