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PubMed2001

Covalent modification of glassy carbon electrode with glutamic acid for simultaneous determination of uric acid and ascorbic acid.

A novel covalently modified glassy carbon electrode with glutamic acid has been fabricated via an electrochemical oxidation procedure and was applied to the catalytic oxidation of uric acid (UA) and ascorbic acid (AA), reducing the overpotentials by about 0.2 V and 0.3 V, respectively. Based on its strong catalytic function toward the oxidation of UA and AA, the modified electrode resolved the overlapping voltammetric response of UA and AA into two well-defined voltammetric peaks with both cyclic voltammetry (CV) and differential pulse voltammetry (DPV), which can be used for the simultaneous determination of these species in a mixture. The catalytic peak current obtained from DPV was linearly dependent on the UA and AA concentration in the range 2 x 10(-6)-4 x 10(-4) mol L-1 and 1.0 x 10(-6)-4 x 10(-4) mol L-1 with correlation coefficients of 0.996 and 0.997, respectively. The detection limits (3 delta) for UA and AA were 1.1 x 10(-6) mol L-1 and 9.2 x 10(-7) mol L-1, respectively. The modified electrode shows good sensitivity, selectivity and stability, and has been applied to the determination of UA and AA simultaneously in human urine samples with satisfactory results.

Ascorbic Acid↗
PubMed1995

Photoinduction of strand scission in DNA by uric acid and Cu(II)

Uric acid (2,6,8-trioxo purine) is produced in mammalian systems as an end product of purine metabolism and has been proposed as a natural, physiological antioxidant. In the presence of Cu(II) and molecular oxygen, uric acid caused breakage of calf thymus DNA and supercoiled plasmid DNA. Such breakage was considerably enhanced in the presence of visible light. The DNA cleavage did not appear to have any preferred site(s) or sequence(s) for strand scission. Uric acid catalyzed the reduction of Cu(II) to Cu(I), which was shown to be an essential intermediate in the DNA cleavage reaction. Uric acid also reduced oxygen to superoxide, and hydroxyl radicals were formed in the presence of Cu(II). The involvement of active oxygen species in the reaction was established by the inhibition of DNA breakage by known scavengers of oxygen radicals.

Animals↗
PubMed2004

Serum uric acid levels in optic neuritis.

Uric acid, an antioxidant, is reduced in multiple sclerosis (MS). Patients with gout have a reduced incidence of MS. Optic neuritis (ON), often the first manifestation of MS, is not known to be associated with reduced uric acid. Patients with recent onset of ON were investigated to determine whether uric acid levels were reduced at presentation. Twenty-one patients with ON were included, 17 females and 4 males. The mean (SD) serum uric acid in the ON female group was 184.4 ( +/-55.1) micromol/L (range, 116-309 micromol/L), whilst in the control group it was 235.2 (+/- 50.2) micromol/L (range, 172-381 micromol/L). The difference was statistically significant (chi2 = 8.93, P = 0.003). In the small male cohort, mean (SD) serum uric acid was 305 (+/- 52.1) micromol/L, whilst in the control group it was 328 (+/- 80.4) micromol/L. These differences were not statistically significant. Reduced antioxidant reserve is possibly an early pathogenic mechanism in inflammatory demyelination, and raises the possibility that low uric acid levels could be an indicator of disease activity. Since optic neuropathies of other causes were not investigated, future research needs to determine whether low uric acid represents a unique feature of optic neuritis or is seen in other optic neuropathies.

Adult↗
PubMed1987

Effect of isoproterenol on renal uric acid excretion in rats.

Effect of isoproterenol on renal uric acid excretion was examined in oxonate-loaded and oxonate-nonloaded rats, using a clearance technique. Oxonate loading was performed by continuous infusion into the femoral vein. Isoproterenol (50 micrograms/kg, i.v.) induced antidiuresis and hyperuricemia accompanied with decreases in urinary excretion rate of uric acid, uric acid clearance, inulin clearance, and uric acid clearance/inulin clearance ratio in oxonate-nonloaded rats. These effects of isoproterenol were inhibited by propranolol (1 mg/kg, i.v.). Very similar results were obtained in oxonate-loaded rats; i.e., systemic blood pressure decreased synchronously with uric acid excretion by isoproterenol. In contrast, phenylephrine (100 micrograms/kg, i.v.) induced hypertensive, diuretic and slightly uricosuric results. In allopurinol-pretreated and oxonate-loaded rats, isoproterenol also decreased renal uric acid excretion and showed a less potent hyperuricemic effect than that observed in the animals not pretreated with allopurinol. In addition, in rats with ligated renal vessels, the hyperuricemic effect of isoproterenol was completely inhibited by allopurinol. These results suggest that isoproterenol-induced hyperuricemia is related not only to the stimulation of uric acid production, but also to the depression of renal uric acid excretion.

Allopurinol↗
PubMed2006

Coronary flow reserve and coronary microvascular functions are strongly related to serum uric acid concentrations in healthy adults.

BACKGROUND: Uric acid is a well known antioxidant; however, the relationship between serum uric acid levels and oxidative stress-caused disorders including cardiovascular diseases is not clear yet. Transthoracic Doppler echocardiographic measurement of coronary flow reserve is a useful tool to investigate coronary flow reserve and coronary microvascular functions. In this study, we investigated the possible association between serum uric acid concentrations and coronary flow reserve in healthy adults. METHODS: One hundred healthy volunteers with normal uric acid levels, between 18 and 55 years of age, were included in this study. The study group was divided into two with regard to the serum uric acid levels. Coronary diastolic peak flow velocities were measured at baseline and after dipyridamole infusion (0.56 mg/kg over 4 min) using echocardiography. RESULTS: Coronary flow reserve and hyperemic mean peak flow velocity were significantly greater in participants with lower serum uric acid concentrations (< or =234 micromol/l for women, < or =302 micromol/l for men) than in those with higher serum uric acid concentrations (>234 micromol/l for women, >302 micromol/l for men) (2.91+/-0.5 vs. 2.47+/-0.5, P<0.001; 66.8+/-11.4 vs. 61.1+/-16.5, P=0.04). The baseline mean peak flow velocity was significantly greater in participants with higher serum uric acid concentrations than in those with lower serum uric acid concentrations (24.7+/-4.1 vs. 23.1+/-2.4, P=0.02). CONCLUSION: Lower serum uric acid concentrations might be regarded as indicative of coronary microvascular and conductance vessel functionality.

Adolescent↗
PubMed1976

Hereditary variation in uric acid transport by avian kidney slices.

Uric acid transport in renal cortical slices from a selected line of hyperuricemic chickens was investigated. Slices from the hyperuricemic (HUA) line accumulated less than half as much uric acid as slices from a control (LUA) line when uric acid in the medium varied from 0.01 to 5 mM. Uric acid uptake by both lines increased as the uric acid concentration in the medium was raised from 0.1 to 0.5 mM, but was markedly inhibited in the HUA line at 3-5 mM. Omission of sodium or potassium from the incubation medium inhibited uric acid uptake by slices from both lines. Ouabain inhibited uric acid uptake in the LUA line. The sodium and potassium requirements for initiation of uric acid uptake were higher, and the potassium requirement for maximal uptake was lower, for slices of the HUA line. No genetic differences in potassium or sodium contents of slices were observed when the potassium content of the incubation medium was altered or when the medium contained ouabain. These studies indicate that hereditary hyperuricemia in chickens may be due to a qualitative change in renal uric acid transport which involves the interaction of cations in the transport process.

Animals↗
PubMed2004

Uric acid promotes tumor immune rejection.

Uric acid released from dying cells has been shown recently to act as a danger signal for the immune system, stimulating dendritic cell maturation and enhancing T-cell responses to foreign antigens. Stimulation of dendritic cell maturation by uric acid has been proposed as a mechanism by which the immune system could generate responses against tumors. We show here that uric acid levels are elevated in tumors undergoing immune rejection and that the inhibition of uric acid production, by systemic administration of allopurinol, or the removal of uric acid, by administration of uricase, delayed tumor immune rejection, whereas subcutaneous administration of crystalline uric acid enhanced the rejection process.

Allopurinol↗
PubMed2005

Genome-wide search for genes affecting serum uric acid levels: the Framingham Heart Study.

Serum uric acid levels are associated with hypertension, cardiovascular disease, and renal disease. Uric acid has been shown to be heritable; however, genome-wide linkage analyses have not been reported. Genome-wide multipoint variance components linkage analyses with 401 markers spaced at approximately 10 centimorgan (cM) were conducted on 1258 subjects of the Framingham Heart Study, using the average of two serum uric acid measurements obtained in examinations 1 and 2 around 1971 and 1979. Covariates in fully adjusted model included sex, age, body mass index (BMI), serum creatinine, alcohol consumption, diabetes, diuretic treatment, and triglycerides. To investigate possible pleiotropic effects between uric acid and covariates that may have a genetic component, bivariate linkage analyses of uric acid with BMI, triglycerides, and glucose were conducted at the uric acid linkage regions. The heritability of uric acid was 0.63. The highest multipoint log-of-the-odds (LOD) score was 3.3 at 50 cM on chromosome 15 for age-sex-adjusted uric acid, but decreased to 1.5 after multivariable adjustment. Additional evidence of linkage was seen on chromosomes 2 (LOD score 1.1 at 4 cM) and 8 (LOD score 1.7 at 6 cM) for multivariable-adjusted uric acid. Pleiotropic effects were only found between uric acid and glucose and BMI at chromosomes 8 and 15 linkage locations, respectively. We have identified several novel loci linked to uric acid. We found possible pleiotropic effects between uric acid and BMI and glucose. Further research is necessary to identify the genes involved in uric acid metabolism and their roles in hypertension, cardiovascular disease, and renal disease.

Adult↗
PubMed1978

Quantitation of renal uric acid synthesis in the chicken.

The contribution of uric acid synthesized in the kidney (nephrogenic uric acid) to the total uric acid excreted in the urine was studied in the chicken by use of the isotope-dilution technique. In the non-fasted chicken the urine-to-plasma specific activity ratio (SAR) of [14C]uric acid was 0.83, suggesting that a minimum of 17% of the uric acid excreted in the urine is synthesized in the kidney. During allopurinol infusion into the renal portal circulation of one kidney the SAR increased to 0.99, indicating that the renal synthesis of uric acid was almost completely inhibited and that the SAR is a valid indicator of the contribution of nephrogenic uric acid excreted into the urine without first entering the circulation. Chickens fasted for 18 h showed a lower rate of renal synthesis of uric acid. Hypoxanthine infusion into the systemic circulation increased the rate of renal synthesis of uric acid in both fasted and nonfasted chickens, suggesting that circulating precursor levels may in part regulate the renal synthesis of uric acid.

Animals↗
PubMed2002

Uric acid and cardiovascular risk.

Uric acid has long been associated with cardiovascular disease. Most epidemiological evidence suggests a significant, graded, independent and specific association between the level of serum uric acid and cardiovascular morbidity and mortality. This is particularly robust among persons at high cardiovascular risk, including those with hypertension, diabetes and congestive heart failure. Although several potential mechanisms have been identified to explain this association, as yet there is no evidence that uric acid bears a causal or reversible relationship to vascular disease.

Animals↗
PubMed2006

Simultaneous electrochemical determination of uric acid and ascorbic acid on a glassy carbon electrode modified with cobalt(II) tetrakisphenylporphyrin.

A cobalt(II) tetrakisphenylporphyrin (Co(II)TPP) film modified glassy carbon electrode (Co(II)TPP-GCE) was prepared by just coating Co(II)TPP solution on the surface of the electrode. It can be used for the simultaneous determination of ascorbic acid and uric acid. The anodic peaks of AA and UA can be separated well. Owing to the strongly hydrophobic property of porphyrin, the modified electrode has good stability and long life. The linear range for UA and AA were 2.0 x 10(-6)-1.0 x 10(-4) M and 9.0 x 10(-6)-2.0 x 10(-3) M with detection limits of 5.0 x 10(-7) and 5.0 x 10(-6) M, respectively. Furthermore, metalloporphyrins of other kinds were also used to construct modified electrodes. Their performances were inferior compared with that of the Co(II)TPP modified electrode.

Ascorbic Acid↗
PubMed2003

[Role of uric acid in cardiovascular diseases].

Uric acid has been suggested as a risk factor in cardiovascular disease since the beginning of the twentieth century. While some clinical evidence have found a significant, specific and independent association between the uric acid serum level and cardiovascular morbidity and mortality, others came to an opposite conclusion. Hyperuricemia commonly coexists with hyperlipidaemia, hypertension, diabetes, obesity and others cardiovascular risk factors. This strong association makes the the role of risk factors difficult to separate out. Thus, the role of uric acid as an independent risk marker remains an open question.

Biomarkers↗
PubMed1997

Nitrogen dioxide depletes uric acid and ascorbic acid but not glutathione from lung lining fluid.

The aim of this study was to determine the kinetics of the reactions between the gaseous free-radical pollutant, nitrogen dioxide (NO2), and the water-soluble antioxidants present in respiratory tract lining fluid (RTLF). Samples of RTLF, recovered from 12 subjects (mean age 54.1+/-16.3 years; eight male, four female) as bronchoalveolar lavage (BAL) fluid were exposed ex vivo to NO2 [50-1000 parts per billion (ppb)] for 4 h. For comparison, similar exposures were carried out with single and composite solutions with relevant RTLF antioxidant concentrations. Ascorbic acid (AA), uric acid (UA), GSH depletion, and GSSG and malondialdehyde (MDA) formation were determined with time. In the three models, UA and AA were consumed in a time- and NO2-concentration-related fashion. In addition, their rate of depletion correlated positively with their initial concentration (UA, r=0.92, P<0.05; AA, r=0.94, P<0.05). Little difference was found between the rate of loss of AA (2.2+/-0. 2; 1.9+/-0.5; 1.4+/-0.3 nmol.l-1.h-1.ppb-1), and that of UA (2.4+/-0. 2; 2.1+/-0.6; 1.3+/-0.2 nmol.l-1.h-1.ppb-1) in the three RTLF models examined (single, composite, BAL fluid respectively). GSH loss from BAL fluid (0.2+/-0.1) was significantly less than that seen in either single (1.4+/-0.3) or composite (1.2+/-0.5 nmol.l-1.h-1. ppb-1) antioxidant solutions. In all cases, GSH consumption was significantly less than AA or UA. As model complexity increased, the rate of individual antioxidant loss decreased, such that in BAL fluid, AA, UA and GSH consumption rates were significantly less (P<0. 05) than in the pure or composite antioxidant mixtures. In BAL fluid, little GSSG production was observed at any NO2 concentration. MDA concentration, determined as a measure of lipid peroxidation, did not change following exposure to 50, 150 or 400 ppb NO2, but increased MDA was seen in BAL fluid from 8/12 subjects following exposure to 1000 ppb NO2 for 1 h or more. In conclusion, NO2, at environmentally relevant concentrations, depletes BAL fluid of the antioxidant defences, UA and AA, but not GSH.

Antioxidants↗
PubMed1983

Trends in serum uric acid levels 1961--1980.

Uric acid levels of adult male volunteers in a longitudinal study of human aging rose steadily between 1961 and 1978. In the 1,141 men with 3 serial physical examinations, who developed no diseases and who took no drugs known to affect uric acid levels, levels rose from means below 5.5 mg/dl in 1961--1963 to means above 6.5 mg/dl in 1975--1978. The best predictor of a longitudinal increase in uric acid level was a gain in weight, but this, and other significant predictors, explained only a small portion of the increase in this population. Preliminary data available from a fourth examination indicate that the rising trend has leveled off.

Adult↗
PubMed1978

Serum uric acid in Jordanian Arabs.

Serum uric acid was measured in 96 male and 140 female healthy Jordanian Arabs. Values obtained for serum uric acid were slightly higher than those previously reported by workers from other parts of Arabia, but comparable to those reported from the United States and United Kingdom. The frequency histograms for serum uric acid in both males and females do not appear to be normally distributed. A hint of bimodality is evident in both sets of data, being more evident in males than in females. A significant positive correlation was seen when, uric acid was compared with ponderal index (P less than 0.05) and total body surface area in both males and females (P less than 0.001). No significant correlation was observed when, uric acid was compared with either age, height or body weight in both sexes.

Adolescent↗
PubMed1979

Increased serum concentrations of lactic, pyruvic and uric acid and bilibubin after postoperative xylitol infusion.

Xylitol has been suggested as a more advantageous calory source for intravenous administration than glucose in certain clinical situation, but the general suitability of intravenous xylitol infusion has not been confirmed. Thirty-middle-aged women were infused with 100 g of xylitol as postoperative fluid therapy after gynaecological laparotomy and general anaesthesia. Another 10 women received 50 g of glucose in a similar manner and served as a reference group. Infusion of xylitol both at the rate of 0.25 g/kg/h (1000 ml 10% xylitol in approx. 8 h) and 0.5 g/kg/h (1000 ml 10% xylitol in approx. 4 h) caused a distinct increase in the serum concentrations of lactic acid, pyruvic acid, and uric acid; such an increase was not seen with glucose infusion. The faster infusion of xylitol also distinctly increased serum bilirubin concentrations. Because of the possibility of lactic acidosis and urate deposits in kidneys, infusion of 100 g or more of xylitol at a rate of 0.25 g/kg/h or faster is not safe for postoperative fluid therapy in routine clinical work.

Anesthesia, General↗