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PubMed1978

[Influence of a high fat diet on serum uric acid levels in rats].

In present paper the behaviour of uric acid is investigated in serum from rats fed with a 50% fat containing diet in comparison with 3% fat diet as control group. After feeding high-fat diet 5 resp. 52 weeks the level of uric acid is significantly elevated. In the same diet group heavier animals showed higher uric acid levels than lighter animals. In these experiments the age of animals is without influence of the uric acid level in serum.

Animals↗
PubMed1993

Association of elevated serum uric acid with coronary heart disease in diabetes mellitus.

The relationship between elevated serum uric acid (SUA) and coronary heart disease (CHD) is discussed controversially. In this cross-sectional study, we evaluated the association between hyperuricaemia and small- and large-vessel diseases in diabetic patients by analyzing clinical data of 7847 diabetic patients of both sexes (Type 1 diabetes: n = 3800, Type 2 diabetes: n = 4047). Elevated serum uric acid was defined as concentrations > 7.0 mg/dl in men and > 6.6 mg/dl in women. The prevalence of hyperuricaemia was dependent on age and duration of the disease in Type 1 diabetic patients, whereas in recently diagnosed Type 2 diabetic patients the prevalence of elevated uric acid levels was higher than in patients with long-standing Type 1 diabetes, without any further increase with longer duration of the disease. An elevated uric acid level was also associated with body weight, hypertension and nephropathy in both types of diabetes and in both sexes. In women, hyperuricaemia was correlated with the presence of coronary heart disease both in Type 1 and Type 2 diabetes (p < 0.05). The exclusion of hypertension and nephropathy in the multiple logistic regression had no effect on these associations. However, after adjustment for these two factors a significant correlation between hyperuricaemia and coronary heart disease was also found in Type 2 diabetic men. In addition, increased serum uric acid was associated with gangrene in male Type 2 diabetic patients (p < 0.05). These results suggest that elevated uric acid levels are correlated with the presence of coronary heart disease in female rather than in male diabetic patients, independently of hypertension and nephropathy.

Adolescent↗
PubMed2006

Uric acid reduces brain damage and improves the benefits of rt-PA in a rat model of thromboembolic stroke.

Uric acid is a natural antioxidant that protects the brain in a model of transient focal ischemia in rats. Here we sought to investigate whether uric acid was protective in a model of thromboembolic brain ischemia in rats, and whether the global benefit of recombinant tissue plasminogen activator (rt-PA) was improved by the combined treatment. Adult male Sprague-Dawley rats underwent either ischemia by thromboembolic middle cerebral artery occlusion (MCAO) or sham operation. Uric acid (16 mg/kg) was injected intravenously (i.v.). 20 mins after MCAO, whereas rt-PA (10 mg/kg) was administered i.v. at 3 h. A group of rats received the combined treatment. Rats underwent two neurologic examinations (30 mins and 24 h after MCAO). At 24 h, infarct volume was measured and brain neutrophil infiltration and protein tyrosine nitration were assessed. Treatment with either uric acid or rt-PA reduced infarct volume versus controls (P<0.05). The protective effect against brain ischemia was greater after cotreatment of uric acid with rt-PA (P<0.001), which added further benefit to rt-PA alone (P<0.05). The neurologic score worsened during the first 24 h in treatment controls, whereas it improved in rats receiving uric acid and/or rt-PA. Uric acid strongly reduced ischemia-induced tyrosine nitration, but it was more effective alone than combined with rt-PA, suggesting that reperfusion enhances nitrotyrosine formation. All treatments reduced postischemic brain neutrophil infiltration. These results show that uric acid administered early after thromboembolic stroke is neuroprotective in the rat brain, as it reduces infarct volume, ameliorates the neurologic function, attenuates the inflammatory response, and extends the benefits of rt-PA.

Animals↗
PubMed1981

Interference of levodopa and its metabolites with colorimetry of uric acid.

Reportedly, levodopa (L-DOPA) administration produces spuriously high values for plasma uric acid as measured by the commonly used phosphotungstic acid-hydroxylamine colorimetric method. We confirm this interference, not only by L-DOPA but also by three of its major metabolites: dopamine, 3,4-dihydroxyphenylacetic acid, and 3-methoxy-4-hydroxyphenylacetic acid. However, at therapeutic concentrations in plasma (less than 5 mg/L), the maximum spurious uric acid concentration due to L-DOPA is less than 2 mg/L. Also, at reported peak plasma concentrations of L-DOPA plus three of its major metabolites, the maximum spurious uric acid concentration due to all four compounds combined is less than 8.5 mg/L. Therefore, the hyperuricemia observed with this method in some patients who are chronically receiving L-DOPA cannot be attributed only to interference by L-DOPA and its metabolites in the colorimetric determination of uric acid. Evidently L-DOPA may increase laboratory values for plasma uric acid concentrations, both by pharmacological and chemical mechanisms.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2001

Elevated uric acid increases blood pressure in the rat by a novel crystal-independent mechanism.

An elevation in circulating serum uric acid is strongly associated with the development of hypertension and renal disease, but whether uric acid has a causal role or whether it simply indicates patients at risk for these complications remains controversial. We tested the hypothesis that uric acid may have a causal role in the development of hypertension and renal disease by examining the effects of mild hyperuricemia in rats. Mild hyperuricemia was induced in rats by providing a uricase inhibitor (oxonic acid) in the diet. Hyperuricemic rats developed elevated blood pressure after 3 weeks, whereas control rats remained normotensive. The development of hypertension was prevented by concurrent treatment with either a xanthine oxidase inhibitor (allopurinol) or a uricosuric agent (benziodarone), both of which lowered uric acid levels. Blood pressure could also be lowered by reducing uric acid levels with either allopurinol or oxonic acid withdrawal. A direct relationship was found between blood pressure and uric acid (r=0.75, n=69), with a 10-mm Hg blood pressure increase for each 0.03-mmol/L (0.5-mg/dL) incremental rise in serum uric acid. The kidneys were devoid of urate crystals and were normal by light microscopy. However, immunohistochemical stains documented an ischemic type of injury with collagen deposition, macrophage infiltration, and an increase in tubular expression of osteopontin. Hyperuricemic rats also exhibited an increase in juxtaglomerular renin and a decrease in macula densa neuronal NO synthase. Both the renal injury and hypertension were reduced by treatment with enalapril or L-arginine. In conclusion, mild hyperuricemia causes hypertension and renal injury in the rat via a crystal-independent mechanism, with stimulation of the renin-angiotensin system and inhibition of neuronal NO synthase.

Animals↗
PubMed1999

Regional heterogeneities in the production of uric acid from adenosine in the bivascularly perfused rat liver.

The heterogeneity of the liver parenchyma in relation to uric acid production from adenosine was investigated using the bivascularly perfused rat liver in the anterograde and retrograde modes. Adenosine was infused in livers from fed rats during 20 min at four different concentrations (20, 50, 100 and 200 microM) according to four experimental protocols as follows: (A) anterograde perfusion, with adenosine infusion into the portal vein; (B) anterograde perfusion, with adenosine in the hepatic artery, (C) retrograde perfusion, with adenosine in the hepatic vein; (D) retrograde perfusion, with adenosine in the hepatic artery. With protocols A, B, and D uric acid production from adenosine was always characterized by initial bursts followed by progressive decreases toward smaller steady-states. With protocol C the initial burst was present only when 200 microM adenosine was infused. The initial bursts in uric acid production were accompanied by simultaneous increases in the ratio of uric acid production/adenosine uptake rate. These initial bursts are thus representing increments in the production of uric acid that are not corresponded by similar increments in the metabolic uptake rates of adenosine. Global analysis of uric acid production revealed that the final steady-state rates were approximately equal for all infusion rates with protocols A, B and C, but smaller with protocol D. This difference, however, can be explained in terms of the differences in accessible cellular spaces, which are much smaller when protocol D is employed. When the analysis was performed in terms of the extra amounts of uric acid produced during the infusion of adenosine, where the initial bursts are also taken into account, different dose-response curves were found for each experimental protocol. These differences cannot be explained in terms of the accessible cell spaces and they are likely to reflect regional heterogeneities. From the various dose-response curves and from the known characteristics of the microcirculation of the rat liver it can be concluded that the initial bursts in uric acid production are generated in periportal hepatocytes. The reason for this heterogeneity could be related to the metabolic effects of adenosine, especially to oxygen uptake inhibition, which is likely to produce changes in the ATP/AMP ratios.

Adenosine↗
PubMed2005

Uric acid: an abettor or protector in calcium oxalate urolithiasis? Biochemical study in stone formers.

BACKGROUND: Free radical induced renal damage leads to crystal retention and formation of large stones. However, the scenario behind uric acid (UA) stone formation is still a mystery, as uric acid, a risk factor of stone formation, seems to be a potent antioxidant that can protect cells from damage by reactive oxygen species. This study was intended to evaluate the role of uric acid in stone formers by assessing the oxidative stress status of the stone patients. METHODS: Determination of urinary stone forming risk factors and oxidative stress factors like plasma lipid peroxidation, protein carbonyls of stone formers and histopathological changes and uric acid deposition in stone patients kidney biopsy were studied. RESULTS: Increased concentrations of urinary uric acid and oxalate in both uric acid as well as calcium oxalate stone formers were observed, whereas calcium is increased in calcium stone formers and not in the uric acid stone patients. Inhibitors such as citrate and glycosaminoglycans (GAGs) were found to be significantly decreased in all the stone patients. Histopathological studies confirmed the deposition of crystals in the damaged tubules and De Galantha staining authenticates that the damage is caused due to uric acid crystals. Increased oxidative stress is dictated by the concentrations of lipid peroxidation and protein carbonyls in stone formers. Moreover, increased activities of urinary marker enzymes substantiate the tubular damage. CONCLUSION: We speculated that uric acid acts as a calculi forming salt rather than an antioxidant and it has no role in preventing oxidative stress pertaining to urolithiasis.

Adult↗
PubMed1990

Determination of serum uric acid by isotope dilution mass spectrometry as a new candidate definitive method.

A new isotope dilution mass spectrometric method for uric acid is described. A known weight of [1,3-15N2]uric acid is added to a known weight of serum, and the mixture is allowed to equillibrate. The serum is put through an anion-exchange resin, and the isolated uric acid is converted to the tetrakis-(tert-butyldlmethylsilyl) derivative of uric acid. For measurement, the derivative is injected into a gas chromatograph interfaced with a low-resolution, magnetic sector mass spectrometer. Isotope ratio measurements are made from the abundances of the [M - tert-butyl]+ ions at m/z 567 and 569. Bias is investigated by measuring the uric acid level in the same samples under different chromatographic conditions and with different ionization techniques. If these confirmatory measurements agree with the principal measurements, we have strong evidence for the absence of measurement bias. Uric acid was determined in three lyophilized human serum pools by this method. For Standard Reference Material (SRM) 909, four sets of six samples each were prepared. For Candidate SRM 909a, which consisted of two pools, each with a different level of uric acid, six sets of two samples of each level were prepared. The coefficient of variation for a single measurement ranged from 0.34% to 0.42%, while the relative standard error of the mean ranged from 0.08% to 0.14%. The results from the confirmatory measurements demonstrated that there was no significant bias in the measurements. The combination of high precision and absence of significant bias in the results qualifies this method as a candidate definitive method as defined by the National Committee for Clinical Laboratory Standards.

Humans↗
PubMed1991

Uric acid content of Drosophila decreases with aging.

Free uric acid concentrations declined with aging in male Oregon R Drosophila melanogaster by 59% or more between 0 and 50 days of adult age. Free xanthine concentrations increased between 0 and 5 days of age and declined by 75% between 5 and 50 days of age. Xanthine oxidase activity was maximal for newly emerged flies and then declined rapidly reaching a minimum at 9 days of age. After 9 days of age xanthine concentrations may be the limiting factor for the production of uric acid by xanthine oxidase in aging fruit flies. Declining uric acid concentrations may represent a loss of antioxidant potential in aging Drosophila.

Aging↗
PubMed1986

Etiopathogenesis of uric acid and ammonium urate uroliths in non-Dalmatian dogs.

The etiopathogenesis of uric acid, sodium acid urate, and ammonium acid urate uroliths in non-Dalmatian dogs appears to be a complex phenomenon. It may involve one or more pathologic and/or physiologic processes acting independently or in concert to increase urinary concentration of lithogenic substances that result in initiation, growth, and retention of urate uroliths. Increased urine uric acid concentration and/or urinary excretion of uric acid appear to be primary predisposing factors in urate lithogenesis. Specific disorders resulting in hyperuricuria may involve abnormalities of increased synthesis, diminished biodegradation, and/or enhance excretion of uric acid. In addition, ammonium ion, hydrogen ion, and other organic and inorganic urine constituents appear to have major influences on urate urolith formation. Unfortunately, many specific disorders of uric acid metabolism and other factors promoting or inhibiting urate urolith formation remain poorly characterized in the majority of non-Dalmatian dogs with urate urolithiasis. Growing awareness of the significance of urate uroliths in non-Dalmatian dogs should encourage further investigation into the identification, characterization, and quantitation of parameters influencing urate lithogenesis. Results of such studies are required for development of practical and effective strategies for treatment and prevention of canine urate urolithiasis.

Animals↗
PubMed2002

Serum uric acid as an independent predictor of mortality in patients with angiographically proven coronary artery disease.

It is a matter of controversy as to whether uric acid is an independent predictor of mortality in patients with coronary artery disease (CAD) or whether it represents only an indirect marker of adverse outcome by reflecting the association between uric acid and other cardiovascular risk factors. Therefore, we studied the influence of uric acid levels on mortality in patients with CAD. In 1,017 patients with angiographically proven CAD, classic risk factors and uric acid levels were determined at enrollment. A follow-up over a median of 2.2 years (maximum 3.1) was performed. Death from all causes was defined as an end point of the study. In CAD patients with uric acid levels <303 micromol/L (5.1 mg/dl) (lowest quartile) compared with those with uric acid levels >433 micromol/L (7.1 mg/dl) (highest quartile), the mortality rate increased from 3.4% to 17.1% (fivefold increase). After adjustment for age, both sexes demonstrated an increased risk for death with increasing uric acid levels (female patients: hazard ratio [HR] 1.30, 95% confidence intervals [CI] 1.14 to 1.49, p < or = 0.001; male patients: HR 1.39 [95% CI 1.21 to 1.59], p < or = 0.001). In multivariate Cox regression analysis performed with 12 variables that influence overall mortality-including diuretic use-elevated levels of uric acid demonstrated an independent, significant positive relation to overall mortality (HR 1.23 [95% CI 1.11 to 1.36], p <0.001) in patients with CAD. Thus, uric acid is an independent predictor of mortality in patients with CAD.

Adult↗
PubMed1982

Critical evaluation of serum uric acid levels in acute myocardial infarction.

Serial measurements of serum uric acid were performed on patients suffering from acute myocardial infarction. Nearly 80 percent of the cases demonstrated a fall in uric acid concentrations during the first two days of hospitalization and a subsequent return to initial levels within six to eight days. There was a relationship between the decrease in uric acid levels and the serum lactate dehydrogenase activity. No evidence could be found that male patients were hyperuricemic as compared to control subjects. However, female patients between 40 and 60 years of age demonstrated significantly higher uric acid levels than healthy women of corresponding ages, even after adjustment for diuretic use.

Aged↗
PubMed1986

Interorgan metabolism of amino acids, glucose, lactate, glycerol and uric acid in the domestic fowl (Gallus domesticus).

Arterial--venous differences for metabolites across liver, kidney and hindquarters were measured in fed or starved, artificially ventilated chickens. The results indicate that the liver takes up amino acids under both conditions. Urate and glucose are released by the liver in both the fed and the starved state. Lactate and amino acids are extracted from blood by the kidneys, and this increases in the starved chicken. Urate is removed from the circulation by the kidney in the fed and starved state and excreted. In the fed bird there is no significant arteriovenous difference of glucose across the kidney, but in the starved state the kidney releases glucose into the circulation. The hindquarters take up glucose in the fed but not in the starved state. The branched-chain amino acids valine and leucine were taken up by the hindquarters in the fed, but not the starved, chicken. Glycerol is released by the hindquarter of fed and starved chickens. In the starved state, alanine and glutamine represent 57% of the amino acids released by the hindquarter. Lactate is released by the hindquarter of starved chickens and represents the major gluconeogenic carbon source released by the hindquarter and taken up by kidney and liver. Although the liver is the major gluconeogenic organ in the starved chicken, the kidney accounts for approx. 30% of the glucose produced.

Amino Acids↗
PubMed2004

Serum uric acid and risk of death from cancer, cardiovascular disease or all causes in men.

OBJECTIVE: Although many epidemiological studies have suggested that increased serum uric acid levels are a risk factor for mortality, this relationship remains uncertain. This cohort study examined the effects of serum uric acid level on death from cancer, atherosclerotic cardiovascular disease (ASCVD) or all causes in men. METHOD: A 9-year, prospective cohort study was carried out with 22698 Korean men, aged 30 to 77 years, who received health insurance from the National Health Insurance Corporation and who underwent biennial, secondary medical evaluations in 1992-1996. The main outcome measures were death from cancer, ASCVD or all causes, compared by quintiles of serum uric acid level. At baseline, the mean (SD) level of serum uric acid was 354.4 (98.1) micromol/l. RESULTS: During 199746 person-years of follow-up, there were 387 cancer deaths, 323 ASCVD (99 ischaemic heart disease, 192 stroke) deaths and 1625 all-cause deaths. In multivariate Cox proportional hazards models, having controlled for age, current smoking, diabetes, hypertension and hypercholesterolaemia, uric acid levels were not associated with mortality from cancer, ASCVD or all causes. However, for those with diabetes, uric acid levels were associated with mortality from all causes even after full adjustment of the covariates. When the interaction term was included in the multivariate model, there was significant interactive effect of uric acid with diabetes (RR=1.26, 95% confidence interval 1.02-1.55) on the risk of all cause of death, whereas the effects of uric acid itself did not attain significance. CONCLUSION: These findings indicate that uric acid level is not an independent risk factor for death from cancer, ASCVD or all causes.

Adult↗
PubMedDate not supplied

Uric acid permeability coefficient in the rat papillary collecting duct.

1. While it is believed that the mammalian distal nephron is not involved in uric acid transport, this has not been directly evaluated. Nevertheless, some studies are consistent with significant distal nephron transport. 2. As uric acid transport in man may be similar to the rat, undirectional uric acid permeability was evaluated by perfusion of the isolated rat papillary collecting duct. 3. Uric acid permeability was 0.61 +/- 0.04 micron/s, which was similar to sodium permeability (0.66 +/- 0.05 micron/s) but was less than chloride permeability (0.93 +/- 0.07 micron/s) and markedly less than water permeability (4.81 +/- 0.21 micron/s). Uric acid permeability was not changed following the addition of a maximal antidiuretic concentration of arginine vasopressin (200 microU/mL), nor was it changed by altering the uric acid concentration in the perfusate and bath. 4. These results demonstrate that the papillary collecting duct is permeable to uric acid. The coefficient of transport is sufficiently low and insensitive to arginine vasopressin and uric acid concentrations to suggest that any transport that occurs is probably passive and only of minor physiological significance.

Animals↗
PubMed1975

[Uric acid as electronic acceptor of chicken liver's XDH (author's transl)].

Uric acid seems to act as an electronic acceptor in the dehydrogenation of hypoxanthine catalyzed by chicken liver's xanthinedehydrogenase (XDH). Oxidation was observed in crude homogenates under anaerobic conditions, although dialyzed homogenates or purified hepatic XDH also induce a similar action either in aerobic or anaerobic conditions. The reaction pH optimum is about 6.0. Xanthine appears to be the only inhibited product of the reaction when its concentration is greater than 1 X 10(-4) M. When hypoxanthine and uric acid concentrations exceed 2 X 10(-3) M and 1 X 10(-4) M, respectively, they induce inhibition by substrate. Purine is a fairly good substrate of XDH when uric acid acts as acceptor. Allopurinol inhibits hypoxanthine oxidation by uric acid in the presence of XDH. XDH also catalyzes the dismutation of xanthine to hypoxanthine and uric acid.

Animals↗