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PubMed1990

Action of biologically-relevant oxidizing species upon uric acid. Identification of uric acid oxidation products.

Uric acid is an end-product of purine metabolism in Man, and has been suggested to act as an antioxidant in vivo. Products of attack upon uric acid by various oxidants were measured by high performance liquid chromatography. Hypochlorous acid rapidly oxidized uric acid, forming allantoin, oxonic/oxaluric and parabanic acids, as well as several unidentified products. HOCl could oxidize all these products further. Hydrogen peroxide did not oxidize uric acid at detectable rates, although it rapidly oxidized oxonic acid and slowly oxidized allantoin and parabanic acids. Hydroxyl radicals generated by hypoxanthine/xanthine oxidase or Fe2(+)-EDTA/H2O2 systems also oxidized uric acid to allantoin, oxonic/oxaluric acid and traces of parabanic acid. Addition of ascorbic acid to the Fe2(+)-EDTA/H2O2 system did not increase formation of oxidation products from uric acid, possibly because ascorbic acid can 'repair' the radicals resulting from initial attack of hydroxyl radicals upon uric acid. Mixtures of methaemoglobin or metmyoglobin and H2O2 also oxidized uric acid: allantoin was the major product, but some parabanic and oxonic/oxaluric acids were also produced. Caeruloplasmin did not oxidize uric acid under physiological conditions, although simple copper (Cu2+) ions could, but this was prevented by albumin or histidine. The possibility of using oxidation products of uric acid, such as allantoin, as an index of oxidant generation in vivo in humans is discussed.

Allantoin↗
PubMed1999

Ascorbic acid and uric acid levels in lung cancer patients.

OBJECTIVE: To study any possible association between serum ascorbic acid and uric acid levels with lung cancer. METHOD: Serum ascorbic acid and uric acid levels in lung cancer patients (n = 30) and healthy controls (n = 45) were measured. RESULTS: The mean values for serum ascorbic acid were found to be significantly lower (P< 0.05) in patients (0.112+/-0.020) than in controls (0.394+/-0.029). Serum uric acid levels of patients were also significantly lower than those of controls (P< 0.05). CONCLUSION: There was no association between serum levels of ascorbic acid and uric acid, cholesterol, triglyceride and albumin levels with lung cancer.

Adult↗
PubMed1973

Effect of oestrogen therapy on plasma and urinary levels of uric acid.

Uric acid clearance studies were carried out on a low-purine diet in 22 trans-sexual men before and during oestrogen therapy for this condition (stilboestrol in 21 cases, ethinyloestradiol in one). Plasma uric acid fell in 15 of the subjects and urinary uric acid rose in 17 of 20 subjects in whom satisfactory collections were obtained. These changes are significant and it is suggested that hormonal influences are responsible for the known age and sex differences in plasma uric acid.

Adult↗
PubMed1987

Antiepileptic drugs reduce serum uric acid.

Uric acid examination in 554 epileptic out-patients under long-term anticonvulsant medication revealed significantly lower serum concentrations compared to a group of normal controls. In patients taking enzyme-inducing drugs, uric acid levels were found to be lower than in those under valproate sodium. In addition, uric acid concentrations showed a negative correlation with duration of therapy in epileptic males. At this time, we can only speculate on the mechanism involved in the reduction of uric acid by enzyme-inducing anticonvulsants as well as on the possible implication of this finding in the treatment of hyperuricemia.

Adult↗
PubMed2002

Inhibition of bovine kidney low molecular mass phosphotyrosine protein phosphatase by uric acid.

Uric acid inhibited 50% of the activity of bovine kidney low molecular mass phosphotyrosine protein phosphatase at concentrations of 1.0, 0.4, 1.3, and 0.2 mM, respectively for p-nitrophenyl phosphate (p-NPP), flavine mononucleotide, beta-naphthyl phosphate and tyrosine phosphate (Tyr-P) as substrates. The mixed type inhibition of p-NPP hydrolysis was fully reversible, with Kic and Kiu values of 0.4 and 1.1 mM, respectively; the inhibition by uric acid shifted the pH optimum from 5.0 to 6.5. When Tyr-P was the substrate, competitive inhibition was observed with a Ki value of 0.05 mM. Inhibition studies by uric acid in the presence of thiol compounds, and preincubation studies in the presence of inorganic phosphate suggest that the interaction of uric acid with the enzyme occurred at the active site, but did not involve SH residues, and that the mechanism of inhibition depended on the structure of the substrates.

Animals↗
PubMed2000

On the mechanism of d-amphetamine-induced changes in glutamate, ascorbic acid and uric acid release in the striatum of freely moving rats.

1. The effects of systemic, intrastriatal or intranigral administration of d-amphetamine on glutamate, aspartate, ascorbic acid (AA), uric acid, dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations in dialysates from the striatum of freely-moving rats were evaluated using microdialysis. 2. d-Amphetamine (2 mg kg-1) given subcutaneously (s.c.) increased DA, AA and uric acid and decreased DOPAC + HVA, glutamate and aspartate dialysate concentrations over a 3 h period after d-amphetamine. 5-HIAA concentrations were unaffected. Individual changes in glutamate and AA dialysate concentrations were negatively correlated. 3. d-Amphetamine (0.2 mM), given intrastriatally, increased DA and decreased DOPAC + HVA and aspartate dialysate concentrations, but failed to change those of glutamate, AA uric acid or 5-HIAA, over a 2 h period after d-amphetamine. Haloperidol (0.1 mM), given intrastriatally, increased aspartate concentrations without affecting those of glutamate or AA. 4. d-Amphetamine (0.2 mM), given intranigrally, increased AA and uric acid dialysate concentrations and decreased those of glutamate, aspartate and DA; DOPAC + HVA and 5-HIAA concentrations were unaffected. 5. These results suggest that d-amphetamine-induced increases in AA and uric acid and decreases in glutamate concentrations are triggered at nigral sites. The changes in aspartate levels may be evoked by at least two mechanisms: striatal (mediated by inhibitory dopaminergic receptors) and nigral (activation of amino acid carrier-mediated uptake).

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Concentration gradients for HVA, 5-HIAA, ascorbic acid, and uric acid in cerebrospinal fluid.

Concentrations of HVA, 5-HIAA, ascorbic acid, and uric acid in the lumbar and cisternal cerebrospinal fluid (CSF) were measured in psychiatric and neurologically impaired patients. The concentration of HVA is 6.1 times and of 5-HIAA 2.7 times higher in cisternal than in lumbar samples, the cisternal level of uric acid is half that of the lumbar region, but no significant differences were found in ascorbic acid concentrations. Correlation between lumbar and cisternal metabolite concentrations is high for 5-HIAA and ascorbic acid, and is less for HVA and uric acid. In cisternal CSF there is a significant correlation between levels of HVA-5-HIAA, 5-HIAA-ascorbic acid, and 5-HIAA-uric acid. These correlations disappear in lumbar CSF. These findings indicate that extrapolations to cisternal neurotransmitter metabolite concentration from lumbar measures are unwarranted for HVA, but not for 5-HIAA.

Adult↗
PubMed1981

Effect of large oral doses of ascorbic acid on uric acid excretion by normal subjects.

The effects of large and oral doses of ascorbic acid on renal clearance and excretion of uric acid were studied in nongouty subjects because ascorbic acid has been reported to increase renal uric acid clearance. Our results indicate that 4 or 12 gm ascorbic acid taken in divided doses had no effect on serum uric acid concentration or uric acid excretion and clearance by the kidney. Reasons for these results, which differ from previous reports, are discussed. We quantitated the magnitude of the interference of ascorbic acid in the measurement of uric acid by the nonspecific methods frequently used, since falsely elevated urine uric acid could lead to misinterpretation of screening tests.

Administration, Oral↗
PubMed1998

Effect of naloxone on morphine-induced changes in striatal dopamine metabolism and glutamate, ascorbic acid and uric acid release in freely moving rats.

Recent findings have shown that systemic morphine increases extracellular dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), ascorbic acid (AA) and uric acid concentrations in the striatum of freely moving rats. The morphine-induced increase in DA oxidative metabolism is highly correlated with that of xanthine. In the present study, we evaluated the effects of subcutaneous (s.c.) naloxone (1 mg/kg) on morphine-induced changes in DA, DOPAC, HVA, 5-hydroxyindoleacetic acid (5-HIAA), AA, uric acid and glutamate in the striatum of freely moving rats using microdialysis. Dialysates were assayed by high performance liquid chromatography with electrochemical detection or (glutamate) ultraviolet detection. Morphine (5-20 mg/kg) given s.c. increased DA, DOPAC+HVA, 5-HIAA, AA and uric acid and decreased glutamate dialysate concentrations over a 3 h period after morphine. Morphine (1 mM), given intrastriatally, did not affect all the above parameters, with the exception of an early short-lasting decrease in AA concentration. Naloxone antagonised all morphine-induced changes with the exception of AA increase and glutamate decrease in dialysate concentrations. Systemic or intrastrial (0.2-2 mM) naloxone increased AA and decreased glutamate dialysate concentrations. When given intranigrally, morphine (1 mM) increased DOPAC+HVA, AA and uric acid and decreased glutamate dialysate concentrations over a 2 h period after morphine; DA and 5-HIAA concentrations were unaffected. These results suggest that: (i) morphine increases striatal DA release and 5-hydroxytryptamine oxidative metabolism by a micro-opioid receptor-mediated mechanism mainly at extranigrostriatal sites; (ii) morphine increases DA and xanthine oxidative metabolism and affects glutamate and AA release by a micro-opioid receptor mediated mechanism acting also at nigral sites; and (iii) a micro-opioid receptor-mediated mechanism tonically controls at striatal sites extracellular AA and glutamate concentrations.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Possibilities and limitations in miniaturized sensor design for uric acid.

Uric acid (UA) has been under intensive investigation by electrochemists owing to its important role as a metabolite in biological fluids. One of the major problems in biological determinations of uric acid comes from electrochemical interferences such as ascorbic acid (AA), which has a similar oxidation potential, E1/2 approximately 200 mV versus SCE, at graphite electrodes, and is present at high concentrations in biological systems. UA undergoes a 2 H+, 2 e- oxidation in aqueous buffers. The oxidation product, a diimine, is an unstable intermediate with a half-life of less than 22 ms. A follow-up hydration reaction converts the diimine to an imine alcohol. Results of previous work show that UA weakly adsorbs and undergoes a fast electron transfer reaction, ks = 54 s-1, at carbon fiber electrodes. These characteristics make UA an excellent candidate for fast scan voltammetric (FSV) determinations. This paper presents the results of FSV at bare carbon fiber electrodes. The results show good selectivity and sensitivity in the determination of low concentrations of UA in the presence of high concentrations of AA. By increasing the scan rate above 500 V s-1, voltammograms of UA in the presence of AA can be resolved because of the kinetic differences in the response of the two anions, without the need for a permselective film on the electrode. Results are also presented that demonstrate an effective way to reach a stable background current at bare carbon fiber electrodes, which is required in FSV because the signal from the analyte is smaller than the electrochemical signal from the background current. Signal-to-noise ratios at bare carbon fiber electrodes in FSV are improved, because the high temporal resolution in fast scan methods allows the acquisition of a large number of scans that can be signal averaged in a short period of time. In addition, large signals can be measured because the voltammetric peak current increases with increase in scan rate.

Electrochemistry↗
PubMed1990

The effects of haloperidol and amphetamine on ascorbic acid and uric acid in caudate and nucleus accumbens of rats as measured by voltammetry in vivo.

The ability of haloperidol (0.1 mg/kg) to reduce the amphetamine-induced (2 and 5 mg/kg) increase in ascorbic and uric acid in anterior caudate and in nucleus accumbens was tested using voltammetry in vivo. In both areas, haloperidol reduced the amphetamine-induced increase in uric acid. In both areas, haloperidol only marginally affected the amphetamine-induced increase in ascorbic acid. Amphetamine-induced increases in uric acid were more nearly dose-related than changes in ascorbic acid. Of the two compounds, uric acid seems more likely to be associated with dopamine.

Amphetamine↗
PubMedDate not supplied

[Effect of ascorbic acid on uric acid formation in men and animals].

The effect of the level of ascorbic acid on the formation of uric acid in the animals and human organisms has been learned. Activation of the hydroxylation of adenyl purins and uric acid by ascorbic acid has been found. A hypothesis was made about the activation of formation of glucocorticoids by ascorbic acid. Glucocorticoids, perhaps, lower the level of uric acid. Hypothesis was confirmed by experiments.

Adenine↗
PubMed1988

[Effect of acetylsalicylic acid on uric acid metabolism in patients with rheumatism].

Concentrations of uric acid (UA) in the blood, saliva, circadian urine and serum xanthinoxidase activity were studied in 150 rheumatic fever patients during acetylsalicylic acid (ASA) therapy. UA concentrations were also studied in the organs (myocardium, mitral cusp, liver and kidneys) of the dead. Low salicylemia in nonreactive rheumatic fever and therapeutic salicylemia in recurrent rheumatic carditis produced a normalizing effect on uric acid metabolism but in limited renal and salivary gland excretory capacity ASA therapy aggravated uric acid metabolic disorder.

Adult↗
PubMed1986

Azlocillin and serum uric acid.

Uric acid levels in serum were observed to fall significantly in a group of 23 patients with cerebrovascular disease receiving azlocillin and vasodilators. Our findings suggest that the hypouricemic effect of azlocillin is dose-dependent and can be demonstrated mainly after the first 24 h of treatment.

Azlocillin↗
PubMed1993

Towards the physiological function of uric acid.

Uric acid, or more correctly (at physiological pH values), its monoanion urate, is traditionally considered to be a metabolically inert end-product of purine metabolism in man, without any physiological value. However, this ubiquitous compound has proven to be a selective antioxidant, capable especially of reaction with hydroxyl radicals and hypochlorous acid, itself being converted to innocuous products (allantoin, allantoate, glyoxylate, urea, oxalate). There is now evidence for such processes not only in vitro and in isolated organs, but also in the human lung in vivo. Urate may also serve as an oxidisable cosubstrate for the enzyme cyclooxygenase. As shown for the coronary system, a major site of production of urate is the microvascular endothelium, and there is generally a net release of urate from the human myocardium in vivo. In isolated organ preparations, urate protects against reperfusion damage induced by activated granulocytes, cells known to produce a variety of radicals and oxidants. Intriguingly, urate prevents oxidative inactivation of endothelial enzymes (cyclooxygenase, angiotensin converting enzyme) and preserves the ability of the endothelium to mediate vascular dilatation in the face of oxidative stress, suggesting a particular relationship between the site of urate formation and the need for a biologically potent radical scavenger and antioxidant.

Animals↗
PubMed1977

The effect of ascorbic acid on uric acid excretion with a commentary on the renal handling of ascorbic acid.

Under spontaneous conditions in man and dog, very little ascorbic acid is excreted in urine. Ascorbic acid clearance (C ascorbic acid) is promptly augmented when plasma ascorbic acid is increased by intravenous injection. No net tubular secretion of ascorbic acid is demonstrable in either man or dog when plasma ascorbic acid is elevated to levels as high as 12 mg/100 ml in man, and 28 mg/100 ml in the dog. Nevertheless, both in men and the Dalmatian dog, when the glomerular filtration rate (GFR) is decreased, excreted ascorbic acid in relation to the amount filtered is exaggerated so that C ascorbic acid:GFR approaches unity. It is possible that secreted ascorbic acid is masked under ordinary circumstances, with a more significant contribution of secreted ascorbic acid to total urinary ascorbic acid becoming apparent under conditions of low GFR. In man, when the plasma ascorbic acid level is raised to above 6 mg/100 ml, C urate:GFR rises from control value of 0.081 +/- 0.020, to 0.116 +/- 0.026. In both mongrel and Dalmatian dogs an effect of ascorbic acid on urate excretion is not conclusively shown. The uricosuric effect of ascorbic acid in man may be due to competition with uric acid for renal tubular reabsorptive transport. The difference in the metabolism of ascorbic acid in the dog as compared to man may help account for the inconsistent effect of ascorbic acid on uric acid excretion in the dog.

Aged↗