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PubMedDate not supplied

Release of uric acid from perfused rat heart.

The release of purine compounds from the perfused rat heart under basal conditions was determined by high pressure liquid chromatography. Uric acid resulted the major degradative released into the perfusate. Lower levels of hypoxanthine, xanthine and inosine were found. The uric acid concentration showing that the rat heart is able to catabolize the purine compounds up to uric acid. No leakage of catabolic enzymes was observed and thereby the breakdown of the released nucleosides and bases proved to be intracellular. This heart ability was confirmed by the analysis of the degradation products of AMP added to the perfusion medium in the recirculating system. AMP was sequentially broken down to adenosine, then to inosine, hypoxanthine and xanthine and finally to uric acid that as end product accumulated in the perfusate.

Adenosine Monophosphate↗
PubMed2000

Urate oxidase electrode based on dissolved oxygen probe for urine uric acid determination.

A biosensor for the specific determination of uric acid in urine was developed using urate oxidase (EC 1.7.3.3) in combination with a dissolved oxygen probe. Urate oxidase was immobilized with gelatin by means of glutaraldehyde and fixed on a pretreated teflon membrane to serve as enzyme electrode. The electrode response was maximum when 50 mM glycine buffer was used at pH 9.2 and 35 degrees C. The enzyme electrode response depends linearly on uric acid concentration between 5-40 microM with a response time of 5 min. The enzyme electrode is stable for more than 2 weeks and during this period over 35 assays were performed.

Biosensing Techniques↗
PubMedDate not supplied

Relationships between serum uric acid and lipids in healthy subjects.

BACKGROUND: Raised serum uric acid (SUA) levels are associated with conditions at high risk for coronary heart disease. SUA levels can be partly modified by the diet, but little is known about the association of SUA with several dietary factors, particularly the quality of ingested lipids. METHODS: The associations between SUA levels and biological and dietary factors were investigated in a sample of 90 healthy subjects (45 males and 45 females; ages 55.6 +/- 18 years) living in Nove, a village near Vicenza (Veneto Region, northern Italy). A careful selection of subjects to exclude those with chronic or acute disease (influencing SUA directly or indirectly through their pharmacological treatments) was obtained with the collaboration of three general practitioners operating in Nove. RESULTS: SUA was higher among men than among women and higher among postmenopausal women than among women of child-bearing age (P < 0.01). Stepwise multiple linear regression analysis of the population as a whole showed that serum triglycerides and total RBC omega-6 PUFA were significant and independent predictors of a consistent proportion of serum uric acid variability (R = 0.59; R2 = 0.332; P < 0.001). Taking men and postmenopausal women together, the result was the same. CONCLUSIONS: Triglycerides and SUA are related even in the normal population and not only in "Syndrome X." Dietary enrichment with omega-6 PUFA might be useful for the negative modulation of SUA.

Adult↗
PubMed1975

Plasma uric acid concentration related to the urinary excretion of aldosterone and of electrolytes in normal subjects.

1. The relations between the concentration of plasma uric acid and urinary excretion of aldosterone, sodium and potassium, were studied in ten healthy males on a diet containing 160 mmol of sodium and 90 mmol of potassium per day. 2. Plasma uric acid correlated positively with aldosterone excretion and this correlation was statistically independent of sodium and potassium excretion. 3. Plasma uric acid correlated positively with potassium excretion and negatively with the urinary sodium/potassium ratio. There was no significant simple correlation with sodium excretion but the partial correlation of plasma uric acid and sodium excretion was negative and significant when excretion of aldosterone and potassium were held constant.

Adult↗
PubMed2004

[Uric acid and multiple sclerosis].

Multiple Sclerosis (MS) is a chronic inflammatory disease of the central nervous system. Its etiology is not known, but it is well established that auto-reactive T-cells and monocytes play an important pathogenetic role. Experimental allergic encephalomyelitis (EAE) of mice serves as disease model for MS. In both EAE and MS inflammatory cells produce nitric oxide and its oxidizing congeners such as peroxynitrite. Peroxynitrite and other reactive nitrogen oxide species exert a toxic effect on neurons, axons and glia cells and enhance apoptosis. In addition, they increase the blood-CNS-barrier permeability and can therefore promote invasion of inflammatory cells into the CNS. On the other hand, uric acid, a peroxynitrite scavenger inhibits blood-CNS-barrier permeability changes, CNS inflammation and tissue damage in EAE. Epidemiological studies have shown that MS and gout are almost mutually exclusive diseases. Uric acid levels in MS patients are lower than in controls and in patients with active disease lower than in MS patients in remission. Inosine, a uric acid precursor, can be used to raise uric acid levels in serum and may provide some benefit in MS patients. A small study of ten patients with progressive MS has demonstrated some improved function in three of them and no sign of progression or relapse in the other. However, this study does not justify a recommendation for use of inosine in MS patients yet. At present, uric acid can solely be regarded as a marker of disease activity in MS. In addition, the current knowledge of uric acid and MS supports hypotheses which predict a positive effect of radical scavengers in MS.

Biomarkers↗
PubMed2005

[Uric acid--more deleterious than we thought?].

BACKGROUND: Hyperuricaemia is associated with reduced renal function and increased cardiovascular risk. It is still disputed, however, whether hyperuricaemia is an independent cardiovascular risk factor or just a marker of increased cardiovascular risk. MATERIAL AND METHODS: A review of the literature based on Medline is presented and data from the LIFE (Losartan Intervention For Endpoint reduction in hypertension) study discussed in relation to the association between uric acid and cardiovascular events. RESULTS: Epidemiological data have shown an independent relationship between serum uric acid and cardiovascular risk, at least in women. In LIFE, uric acid at baseline corresponded positively with cardiovascular risk in women, though not in men. Differences in serum uric acid during the study could statistically explain 29% of the reduction in cardiovascular events in the losartan group compared to atenolol. INTERPRETATION: These findings support the hypothesis that uric acid is an independent cardiovascular risk factor. Further studies are warranted.

Angiotensin II Type 1 Receptor Blockers↗
PubMed1989

Red blood cell sodium-lithium countertransport, blood pressure, and uric acid metabolism in untreated healthy men.

The relationship of red blood cell (RBC) Na/Li countertransport to the renal handling of lithium and uric acid was investigated in a sample of 176 untreated men. Subjects in the upper quintile of the Na/Li countertransport distribution (n = 40), compared to those in the two lower quintiles (n = 72), had higher serum uric acid levels (0.34 +/- 0.06 v 0.29 +/- 0.05 mmol/L, P less than 0.001) and systolic blood pressure (131 +/- 19 v 123 +/- 16 mm Hg, P less than 0.02) and slightly lower fractional excretion of uric acid (7.5 +/- 1.5 v 8.4 +/- 2.6%, P less than 0.08). The lithium fractional excretion was not significantly related to either blood pressure or RBC Na/Li countertransport. The altered uric acid metabolism in individuals with high RBC Na/Li countertransport could be the expression of an abnormality of renal tubular function.

Biological Transport↗
PubMed2004

Uric acid correlates with the severity of histopathological parameters in IgA nephropathy.

BACKGROUND: Immunoglobulin-A nephropathy (IgAN) is the most common chronic glomerulonephritis worldwide. Many clinical and histopathological risk factors for progression have been found previously. Recently, metabolic risk factors, such as hyperuricaemia and hypertriglyceridaemia, also have been associated with the progression of IgAN. METHODS: In the present study we correlated clinical and metabolic risk factors with histopathological parameters in 202 patients with IgAN. Morphological changes in glomerular, tubulointerstitial and vascular tissue were semiquantitatively graded into three classes. Mesangial proliferation activity and the amount of inflammatory cells were also evaluated by immunohistochemical staining of Ki-67 (MIB-1), CD45 (LCA) and CD68 stainings. Serum uric acid, triglycerides and cholesterol, urine protein excretion (UPE), blood pressure and body mass index (BMI) were measured. Smoking habits and occurrence of diabetes mellitus also were evaluated. The independent role of serum uric acid in the development of renal morphological changes was evaluated in multivariate analysis. RESULTS: Serum uric acid and UPE level correlated with several histological parameters. Uric acid level showed the strongest correlation with tubulointerstitial changes and UPE with glomerulosclerosis. The level of serum triglycerides correlated with interstitial fibrosis and hyaline arteriolosclerosis. Blood pressure correlated with hyaline arteriolosclerosis, glomerulosclerosis and tubulointerstitial changes. BMI and diabetes mellitus correlated with both tubulointerstitial and vascular changes. We found no significant correlations between histopathological parameters and smoking habits or serum cholesterol level. Serum uric acid had independent associations with the presence of tubular atrophy and interstitial fibrosis and inflammation. CONCLUSIONS: We conclude that many metabolic factors are univariately associated with renal morphological findings in IgAN. These same factors are central in the metabolic or insulin resistance syndrome and may have a pathogenetic role in the progression of IgAN. Serum uric acid may have an independent role in development of tubulointerstitial lesions as well as being associated with inflammation in renal tissue of patients with IgAN.

Adolescent↗
PubMed2004

[Relationships among urine pH, serum uric acid and pyuria in hospitalized elderly patients].

To identify risk factors of urinary tract infection (UTI) in geriatric patients, the levels of serum uric acid, serum creatinine, and urine pH were compared between pyuria-positive and -negative patients in a geriatric ward. The level of serum uric acid was higher with lower urine pH level in the pyuria-negative patients than in positive patients. The level of serum creatinine was relatively higher in the pyuria-negative patients than in the positive patients. Even after matching for serum creatinine, serum uric acid was significantly higher in the pyuria-negative male patients. The results in the present study proposed an interesting hypothesis about backgrounds for UTI in geriatric patients. The relationships among serum uric acid, serum creatinine, urine pH, and pyuria should be examined further in a larger population and in experimental studies.

Aged↗
PubMed1980

[Longitudinal study of uric acid changes in a constant group from 1968-78].

From 1968 to 1978 in 195 test persons (53 males, 142 females) the longitudinal behaviour of the serum uric acid was examined by regular estimation. Independent on age, sex and body weight the concentration of uric acid significantly increased in the course of 10 years. As causes are discussed influences of nutrition, problems of physical and mental activity, therapeutic measures and medicaments as well as hormonal change. Change of the relative weight and level of uric acid did not correlate together. Developmental tendency of serum cholesterol and uric acid showed a negative correlation in younger men and a positive one in older men.

Adult↗
PubMed2001

[Distribution and correlation of uric acid with classic cardiovascular risk factors in an adult population in Campania. VIP project data].

BACKGROUND: The aim of this study was to correlate uric acid levels with the classic cardiovascular risk factors in an adult population in Campania. METHODS: The following parameters were assessed in the study population (600 men and 600 women) aged between 25-74 years old, subdivided into 5 age groups (25-34, 35-44, 45-54, 55-64, 65-74): ECG, arterial pressure and body mass index (obtained by dividing weight in kg by height in metres squared). A blood sample was also taken to evaluate uric and other biochemical variables including: total cholesterol, HDL, L DI, glycemia, triglycerides, red and white blood cells, C3, fibrinogen, platelets and insulin serum levels. RESULTS: The results confirmed the positive correlation between uric acid and red and white blood cells in males, and between uric and the following variables in females: cholesterol, C3, LDL, systolic blood pressure, diastolic blood pressure, triglycerides, white blood cells, BMI and fibrinogen. When the correlation was performed in the entire population, uric acid correlated with triglycerides and red and white blood cells. Multivariate analysis for the entire population showed a strong correlation between uric acid, triglycerides and white blood cells. CONCLUSIONS: This study confirms the data reported in the literature and highlights the correlation between uric and the classic cardiovascular risk factors. This association is more evident in females.

Adult↗
PubMed1990

Changes in plasma concentration of hypoxanthine and uric acid in man with short-distance running at various intensities.

The relationship between running intensity and the accumulation of hypoxanthine and uric acid in plasma was studied in four well-trained runners. The runners each performed several 800-m runs at different velocities, each run being performed on separate days. Venous blood samples were collected before and at regular intervals after the runs. The concentration of hypoxanthine and uric acid was determined with high performance liquid chromatography (HPLC) in plasma extracts. A marked increase in the plasma concentration of both hypoxanthine and uric acid occurred simultaneously at intensities corresponding to 110, 108, 115 and 107% of VO2max for subject a, b, c and d, respectively. The sudden sharp increase in plasma concentration of hypoxanthine and uric acid may indicate that at a certain level of running intensity ATP catabolism exceeds the rate of ATP regeneration from the normal metabolic pathways.

Adolescent↗
PubMed1999

Serum uric acid concentration and thyroid-stimulating-hormone (TSH): results of screening for hyperuricaemia in 2359 consecutive patients with various degrees of thyroid dysfunction.

Serum uric acid concentration (sUA) and hyperthyroidism have been reported to positively correlate with each other. Furthermore, epidemiological data indicate that uric acid may be an independent risk factor for hypertension-associated morbidity and mortality. To evaluate whether screening for hyperuricaemia might be worthwhile in patients with hyperthyroidism we determined serum concentrations of uric acid in 2359 consecutive patients (1939 female, 420 male; age: 48 +/- 17 years, mean +/- SD) with various degrees of thyroid dysfunction (hyperthyroidism: n = 242; subclinical hyperthyroidism: n = 143, hypothyroidism: n = 71, subclinical hypothyroidism: n = 212) and in 1688 euthyroid subjects. No association (r = 0.03) between sUA and total T4/TSH was detected. The significant difference (p < 0.05) in serum uric acid between hyperthyroid (4.8 +/- 1.32 mg/dl) and euthyroid (4.5 +/- 1.32 mg/dl) patients was of no clinical significance. We conclude that routine determination of sUA in hyperthyroid patients is not warranted.

Female↗
PubMed1976

Uric acid catabolism in the woolly monkey.

The degradation and excretion of 2-14C-uric acid were examined in three adult woolly monkeys (Lagothrix lagothrichia) to determine the basis for the relatively high serum and urinary uric acid concentrations previously reported in this species. Like man and the great apes which lack uricase, but in distinction to most other mammals, these animals converted very little urate to allantoin. Uric acid turnover, as has been reported for other New World monkeys, was several times that of normal man. Renal urate excretion as well as disposition by extrarenal mechanisms may protect Lagothrix vrom hyperuricemia. The capacity to convert urate to allantoin appears to have been lost late in the evolution of New World monkeys. The woolly monkey deserves further study as a primate model for investigations of enzyme replacement strategies.

Animals↗
PubMed1993

Effect of uric acid on plasma levels of 1,25(OH)2D in renal failure.

Previous studies from these laboratories have demonstrated that uremic biologic fluids contain substances that suppress 1,25(OH)2D metabolism. Among these substances, it was found that uric acid suppresses 1 alpha-hydroxylase activity and synthesis of 1,25(OH)2D in rats. In this study, the effect of uric acid on plasma concentrations of 1,25(OH)2D in patients with renal failure was examined. Nine patients with stable chronic renal failure (serum creatinine, 1.9 to 6.4 mg/dL) were studied. None of the patients received vitamin D supplementation. Plasma concentrations of Ca, P, parathyroid hormone, creatinine, uric acid, 1,25(OH)2D, and 25(OH)D were measured before and 1 wk after the patients received allopurinol, 300 mg daily. Plasma creatinine, Ca, P, parathyroid hormone, and 25(OH)D did not change before or after allopurinol treatment. However, plasma uric acid decreased significantly from 7.3 +/- 0.4 to 4.0 +/- 0.4 mg/dL (P < 0.01) and plasma concentration of 1,25(OH)2D rose from 30.8 +/- 2.7 to 38.2 +/- 4.8 pg/mL (P < 0.01) after the ingestion of allopurinol. Allopurinol itself did not appear to directly enhance 1 alpha-hydroxylase activity in rats. It was concluded that a short-term administration of allopurinol suppresses plasmic uric acid and increases plasma 1,25(OH)2D in patients with chronic mild to moderate renal failure.

Adult↗
PubMed1989

Acute renal failure due to uric acid nephropathy in a patient with renal hypouricemia.

This report is about a 23-year-old man who required hemodialysis in connection with an acute renal failure resulting from uric acid nephropathy without hyperuricemia. After recovering renal function he showed extreme hypouricemia (0.1-0.3 mg/dl) and elevated uric acid clearance (100-300 ml/min). The fractional excretion of uric acid (Cua/Ccr) could be suppressed by oral pyrazinamide and enhanced by probenecid. As no other renal tubular or metabolic abnormalities were detected, it is suggested that a markedly increased renal tubular urate secretion was responsible for the hypouricemia and also for the rare side-effect of an uric acid nephropathy in this patient.

Acute Kidney Injury↗
PubMed1989

Uric acid as radical scavenger and antioxidant in the heart.

Uric acid (UA) is released from the heart of many species, including man, and its site of formation has been shown to be the microvascular endothelium. Since UA reacts with oxygen radicals in vitro, experiments were conducted on guinea pig hearts perfused with Krebs-Henseleit buffer (KHB) to evaluate whether the formation of UA could afford protection from damage by radicals and oxidants. The following results were obtained: (1) Upon addition of the hydroxyl radical scavenger DMSO to the perfusate, the coronary rate of release of endogenous uric acid was increased relative to the precursor purines. (2) UA was degraded during passage through the coronary system and also in KHB in vitro after addition of substances generating hydroxyl radicals or hypochlorite. Superoxide (O2-) radicals did not seem to react directly with UA, though UA concentration-dependently quenched the chemiluminescence generated from luminol in the presence of O2- and OH radicals. (3) Coronary dilation by acetylcholine (Ach) and sub-microM concentrations of adenosine, induced by both via endothelial mechanisms, was attenuated after prolonged inhibition of endothelial UA formation by allopurinol. Furthermore, the effect of Ach but not of adenosine proved acutely sensitive to methylene blue and O2-, substances known to inactivate EDRF. This finding suggests involvement of EDRF in Ach-mediated, but not in adenosine-induced dilatation of the intact coronary system. Exogenously applied UA prevented the impairment of vascular responses to Ach and adenosine caused by allopurinol, and to Ach upon generation of O2-. (4) Hearts performed more pressure-volume work and exhibited greater functional stability when perfused with KHB supplemented with UA in a physiological concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗