Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “URIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
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↗
PubMed2005

Free radical scavenging, DNA protection, and inhibition of lipid peroxidation mediated by uric acid.

Uric acid (UA) has been proposed to be the dominant antioxidant in birds. The objective of this study was to investigate the quenching effect of varying concentrations of UA, including those found in avian plasma, on specific reactive oxygen species (ROS) and to determine the ability of UA to protect DNA and cellular membranes from ROS-mediated damage. Hydroxyl (OH) and superoxide (O2-) radicals were detected by electron spin resonance (ESR) and their presence was reduced following addition of UA (p <0.05) in a concentration-dependent manner. UA inhibited hydroxyl-mediated DNA damage, indicated by the presence of more precise, dense bands of lambda Hind III DNA after agarose gel electrophoresis and ethidium bromide staining (p <0.05). Lipid peroxidation of silica-exposed RAW 264.7 cell membranes was diminished (p <0.02) after addition of UA to the cell incubation mixture. These studies demonstrate that UA scavenges hydroxyl and superoxide radicals and protects against DNA damage and lipid peroxidation. These results indicate specific antioxidant protection that UA may afford birds against ROS-mediated damage.

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↗
PubMed1988

The effect of tiaprofenic acid on uric acid excretion in man.

The uricosuric effect of tiaprofenic acid was evaluated in a group of normouricaemic inpatients with various rheumatic disorders. Six patients aged 26 to 60 years were maintained on a standardised low-purine diet and, after a washout period of 72 hours, tiaprofenic acid was administered in 3 oral doses of 300 mg 12-hourly. A normal renal function, as assessed by serum creatinine and creatinine clearance determinations, was considered mandatory for entry into the study. The following parameters were evaluated before and after treatment: haematological values, blood urea nitrogen (BUN), serum and urinary creatine concentrations, serum uric acid concentration and the fractional excretion rate of uric acid. Our preliminary results showed a substantial increase of urinary uric acid excretion in the samples collected after treatment, especially in the first 4 hours.

Adult↗
PubMed1982

[Plasma levels of triglycerides, cholesterol, non-esterified fatty acids and uric acid, during oral glucose load, in subjects with type II diabetes and diminished glucose tolerance].

In order to study triglycerides, cholesterol, FFA and uric acid plasma levels after OGTT, 10 type II diabetics, 8 IGT subjects, 10 controls were studied. A progressive decrease of FFA plasma values in all groups is shown; there is also an increase in triglycerides vs. basal values in all groups, at 240'. In diabetics and IGT groups there are higher cholesterol levels than controls; IGT subjects have the highest uric acid levels, which in all groups decrease at 180' and 240'. We conclude triglycerides, FAA, uric acid are modified, cholesterol levels are unaffected by glucose oral load in all groups.

Blood Glucose↗
PubMed1982

[Effects of acute ingestion of ethanol on several metabolic parameters (blood sugar, triglycerides, non-esterified fatty acids, lactic acid and uric acid) in subjects with type I diabetes mellitus].

7 diabetic type I patients and 17 normal subjects underwent to acute ethanol oral load (0,8 g/Kg), in order to investigate the modifications produced on glucose, triglycerides, FFA, lactate and uric acid plasma values. Our results show basal differences between diabetics and controls in all these parameters; furthermore, acute ethanol ingestion produces no significant variations of blood glucose in both groups, a significant decrease in FFA levels, an increase of triglyceridemic levels, more evident in diabetics and an increase of lactate, earlier in normals. On the other hand, there is no significant modification in uric acid plasma levels in controls, whereas in diabetics there is an increase, probably due to more elevated lactacidemic values in the late phase of the test.

Adolescent↗
PubMed1986

Automated high-performance liquid chromatographic method with column switching for the determination of neurotransmitters and related compounds, ascorbic acid and uric acid in tissue extracts.

An automated high-performance liquid chromatographic method with electrochemical and fluorimetric detection and on-line data evaluation is described for the simultaneous measurement of indoleaminergic and catecholaminergic neurotransmitters, some of their metabolites and precursors and ascorbic and uric acids. Deproteinized tissue extracts from the central nervous system or peripheral organs are injected without prior purification (recovery greater than 90%). A switching system enables the compounds to be passed as necessary through one, two or three reversed-phase columns, which are then eluted simultaneously (analysis time 25 min). Fifty samples per day can be analysed with a precision of 95% for neurotransmitters and about 90% for ascorbic and uric acids.

Animals↗
PubMed1991

Further investigations into the relationship between the dopaminergic system, ascorbic acid and uric acid in the rat striatum.

Levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), ascorbic acid (AA), dehydroascorbic acid (DHAA), and uric acid were determined in the rat striatum following single apomorphine (1 mg/kg), scopolamine (0.6 mg/kg), pilocarpine (4 mg/kg), or pilocarpine + scopolamine (4 and 0.6 mg/kg, respectively) injections. The decrease in DOPAC levels and in the DOPAC/DA ratio, induced by the pharmacological manipulation, was linearly correlated with the increase in DHAA levels (r = -0.9060, P less than 0.05) and with the increase in the DHAA/AA ratio (r = -0.9004, P less than 0.05), respectively. It is concluded that dopaminergic activation or cholinergic inhibition both increase striatal AA oxidation, which is correlated with a decrease in DA turnover.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

Analysis of creatinine, vanilmandelic acid, homovanillic acid and uric acid in urine by micellar electrokinetic chromatography.

A simultaneous determination of vanilmandelic acid, homovanillic acid, creatinine and uric acid using capillary electrophoresis was investigated. The optimum conditions of buffer concentration, pH and surfactant concentration were studied, and high resolution was obtained using a 30 mM phosphate buffer (pH 7.0) containing 150 mM sodium dodecyl sulfate. The detection was by UV absorbance at 245 nm and the column was a fused-silica capillary of 67 cm x 75 microm I.D.. The determination of these metabolites in human urine was completed within 15 min without any interferences.

Buffers↗
PubMed1987

Effects of haloperidol on amphetamine-induced increases in ascorbic acid and uric acid as determined by voltammetry in vivo.

Amphetamine produces dramatic changes in extracellular ascorbic acid (AA) and uric acid (UA) in rat caudate; the origin of extracellular AA and UA is being widely investigated. In this study, linear sweep voltammetry with carbon paste electrodes was used to monitor extracellular AA and UA levels in conscious behaving rats. Amphetamine (2 and 4 mg/kg) produced a dose-related increase in UA; the increase in AA was very similar at both doses. Haloperidol (0.2 mg/kg) blocked the amphetamine-induced increase in UA but reduced the AA increase only by about 20%. Thus the amphetamine-induced increase in AA is only partly dependent on dopamine (DA) receptor stimulation whereas the amphetamine-induced increase in UA is completely dependent upon DA receptor stimulation.

Animals↗
PubMed1991

Relationship between resistance to insulin-mediated glucose uptake, urinary uric acid clearance, and plasma uric acid concentration.

OBJECTIVE: To define the relationship, if any, between insulin-mediated glucose disposal and serum uric acid. DESIGN: Cross-sectional study of healthy volunteers. SETTING: General Clinical Research Center, Stanford (Calif) University Medical Center. PARTICIPANTS: Thirty-six presumably healthy individuals, nondiabetic, without a history of gout. MEASUREMENTS: Obesity (overall and regional), plasma glucose and insulin responses to a 75-g oral glucose load, fasting uric acid concentrations, plasma triglyceride and high-density lipoprotein-cholesterol concentrations, systolic and diastolic blood pressure, insulin-mediated glucose disposal, and urinary uric acid clearance. RESULTS: Magnitude of insulin resistance and serum uric acid concentration were significantly related (r = .69; P less than .001), and the relationship persisted when differences in age, sex, overall obesity, and abdominal obesity were taken into account (r = .57; P less than .001). Insulin resistance was also inversely related to urinary uric acid clearance (r = -.49; P less than .002), and, in addition, urinary uric acid clearance was inversely related to serum uric acid concentration (r = -.61; P less than .001). CONCLUSIONS: Urinary uric acid clearance appears to decrease in proportion to increases in insulin resistance in normal volunteers, leading to an increase in serum uric acid concentration. Thus, it appears that modulation of serum uric concentration by insulin resistance is exerted at the level of the kidney.

Adult↗
PubMed2003

Uric acid or 1-methyl uric acid in the urinary bladder increases serum glucose, insulin, true triglyceride, and total cholesterol levels in Wistar rats.

In animals deprived of food for a long period, a drop in the fat mass below 5% of the total body mass results in an increase in blood glucocorticoids and uric acid levels, followed by foraging activity. Since the glucocorticoids increase the uric acid excretion, an increase in the level of uric acid in the bladder urine could be the signal for this feeding behaviour and subsequent fat storage. Accumulation of fat is associated with hyperglycaemia, hyperinsulinaemia, hyperlipidaemia, and hypercholesterolaemia as seen in the metabolic syndrome or hibernation. It is hypothesized that uric acid or its structurally related compound, 1-methyl uric acid (one of the metabolites of the methyl xanthines namely caffeine, theophylline, and theobromine present in coffee, tea, cocoa, and some drugs), can act on the urinary bladder mucosa and increases the blood glucose, insulin, triglyceride, and cholesterol levels. In rats, perfusion of the urinary bladder with saturated aqueous solution of uric acid or 1-methyl uric acid results in a significant increase in the serum levels of glucose, insulin, true triglyceride, and total cholesterol in comparison with perfusion of the bladder with distilled water at 20, 40, and 80 min. The uric acid or the 1-methyl uric acid acts on the urinary bladder mucosa and increases the serum glucose, insulin, true triglyceride, and total cholesterol levels.

Administration, Intravesical↗
PubMed1989

Effects of diltiazem on plasma uric acid level and renal uric acid excretion in rats.

The effects of diltiazem on plasma uric acid level (PUA) and renal uric acid excretion were investigated in oxonate-loaded rats. Diltiazem (0.5 mg/kg, i.v.) decreased PUA without producing uricosuria, and it decreased fractional excretion of uric acid and renal blood flow. The present results suggest that diltiazem produces hypouricemia not accompanied by uricosuria, probably by affecting uric acid metabolism, and it may also cause an alteration in the renal handling of uric acid partly due to changes in renal hemodynamics.

Animals↗
PubMed2005

Immobilization of DNA on carbon fiber microelectrodes by using overoxidized polypyrrole template for selective detection of dopamine and epinephrine in the presence of high concentrations of ascorbic acid and uric acid.

The overoxidized polypyrrole (PPyox) film as a template for DNA immobilization has been demonstrated in this paper. The DNA molecules inserted into the micropores of the ultrathin PPyox matrix under the driving forces of an electric field and were firmly immobilized on the carbon fiber electrode (CFE). Such a DNA-PPyox biocomposite layer exhibited more effective rejection of anionic ascorbate (AA) and uric acid (UA) and more preferential collection of the cationic dopamine (DA) and epinephrine (EP) than pure PPyox and DNA coatings. The DPV peak currents increased linearly with increasing DA and EP concentrations in the range of 3.0 x 10(-7) to 1.0 x 10(-5) M and 5.0 x 10(-7) to 2.0 x 10(-5) M with the lowest detected concentrations of 8.0 x 10(-8) M and 6.0 x 10(-8) M, respectively. The electrochemical signal of AA could be totally suppressed under a concentration of 20 mM and beyond this concentration, the overlapped responses of AA, DA/EP and UA could be resolved into three well-defined voltammetric peaks. The selectivity factors k(DA/AA) and k(EP/AA) were about 5000 and 2000 for an equal concentration in the presence of 0.5 mM UA. The properties of the biocomposite film have been characterized by atomic force microscopy and electrochemical investigations.

Ascorbic Acid↗