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 559 records · Page 31Linked to original sources
PubMed2006

Uric acid inhibits renal proximal tubule cell proliferation via at least two signaling pathways involving PKC, MAPK, cPLA2, and NF-kappaB.

The accumulation of uric acid, an end-product of purine metabolism, is responsible for the many deleterious effects observed in gouty arthritis, including renal injury. Here, we present evidence that under conditions of hyperuricemia (>10(-4) M uric acid) [(3)H]thymidine incorporation into primary renal proximal tubule cells (PTCs) is inhibited, and we delineate the signaling pathways involved. Elevated uric acid was observed to stimulate MAPK phosphorylation. The uric acid induced p38 MAPK phosphorylation was also blocked by H-7 (a PKC inhibitor), indicating that p38 MAPK was a downstream target of PKC. Evidence that cytoplasmic phospholipase A(2) (cPLA(2)) was involved further downstream included 1) the stimulatory effect of uric acid on [(3)H]-labeled arachidonic acid (AA) release; 2) the stimulation of AA release in response to uric acid was blocked by the PKC inhibitor H-7 as well as by the p38 MAPK inhibitor SB 203580; and 3) the uric acid-induced inhibition of [(3)H]thymidine incorporation was prevented by SB 203580, as well as by the cPLA(2) inhibitor arachidonyl trifluoromethyl ketone, and mepacrine (another PLA(2) inhibitor). Evidence of a uric acid-induced activation of NF-kappaB as well as PLA(2) was obtained. Moreover the uric acid-induced inhibition of [(3)H]thymidine incorporation was also blocked by two NF-kappaB inhibitors, pyrrolidine dithiocarbamate and SN 50. However, SN 50 did not block the uric acid induced [(3)H]AA release. Thus the inhibition of [(3)H]thymidine incorporation caused by uric acid can be explained by two distinct mechanisms, the activation of NF-kappaB as well as the activation of PLA(2).

Animals↗
PubMedDate not supplied

[Changes of uric acid levels in rat tissues as a systemic reaction to hyperoxia].

The levels of tissue antioxidant uric acid in relation to chromosomal aberrations and leaving erythrocytic chromatin were determined in the spleen, bone marrow and blood of rats exposed to toxic hyperoxia (0.7 MPa O2, convulsions). Considerable growth of the uric acid levels and the rate of chromosomal aberrations in all tissues was observed within the first hours after treatment. The article discusses mechanisms of uric acid formation, redistribution and disintegration in tissues under extreme conditions. Specificity of the uric acid metabolism in tissues was shown with the help of the correlation analysis of uric acid concentrations. Inverse relationship between uric levels and chromosomal impairments noted in some cases permits to make a supposition about genoprotective properties and adaptogenic role of uric acid during oxidative stress.

Adaptation, Physiological↗
PubMed2005

Serum uric acid levels and leukocyte nitric oxide production in multiple sclerosis patients outside relapses.

BACKGROUND: A number of studies found that patients with multiple sclerosis (MS) have low serum levels of uric acid. It is unclear whether this represents a primary deficit or secondary effect. Uric acid is a scavenger of peroxynitrite, which is the product of nitric oxide (NO) and superoxide. Because peripheral blood leukocyte NO production and NO metabolites in serum are raised in MS patients, associations might be expected between serum uric acid levels and peripheral NO production. METHODS: Serum levels of uric acid and NO production by peripheral blood leukocytes were measured in 60 patients with MS without a relapse in the past 3 months, and 30 age- and sex-matched healthy controls. Uric acid was determined with the uricase PAP method, and NO production was assayed by measuring nitrite concentration in supernatants of lysed leukocytes. RESULTS: Serum uric acid levels were not different between MS patients and controls. Compared to controls, patients with MS had significantly higher peripheral blood leukocytes nitrite concentrations (p<0.001). There was no correlation between leukocyte nitrite concentration and serum uric acid levels. CONCLUSIONS: Our findings suggest that in MS patients there is no primary deficit in serum uric acid. NO production by peripheral blood leukocytes is increased, but there is no association with serum uric acid levels.

Adult↗
PubMed1993

Renal uric acid handling in non-insulin-dependent diabetic patients with elevated glomerular filtration rates.

1. Hypouricaemia is prevalent in diabetic patients. In most of the studies, the diabetic patients had some degree of diabetic nephropathy as evidenced by a decreased glomerular filtration rate and proteinuria. Therefore we studied renal uric acid handling in a group of type II diabetic patients with elevated glomerular filtration rates. 2. Eighteen type II diabetic patients with normal kidney functions and elevated glomerular filtration rate and a group of 18 healthy, age- and weight-matched control subjects, were studied. Serum fructosamine, creatinine and uric acid levels were determined. Twenty-four hour urine collections were obtained, and microalbumin, glucose, creatinine and uric acid, were measured. 3. The creatinine clearance was higher and the serum uric acid concentration was lower in the diabetic patients (P < 0.05). The 24 h urinary uric acid excretion and filtered uric acid load were similar in both groups. However, the derived parameters of uric acid clearance and fractional excretion were significantly higher in the diabetic patients (P < 0.002 and P < 0.05, respectively). A negative correlation was apparent between serum fructosamine concentration and serum uric acid concentration (r = -0.76). A positive correlation was found between serum fructosamine concentration and fractional uric acid excretion (r = 0.64) and between serum fructosamine concentration and filtered uric acid load (r = 0.66). A positive correlation was found between creatinine clearance and 24 h uric acid excretion (r = 0.61) and between creatinine clearance and filtered uric acid load (r = 0.82).(ABSTRACT TRUNCATED AT 250 WORDS)

Creatinine↗
PubMed1992

User-defined serum aspartate and alanine aminotransferase, cholesterol, triglycerides, urea, and uric acid for the Beckman synchron CX 4/5 using Ames Sera-Pak reagents.

Beckman aspartate aminotransferase (AST), alanine aminotransferase (ALT), cholesterol, triglycerides, urea, and uric acid Liquid Reagents for Synchron CX 4/5 (48, 48, 25, 60, 26, and 30 cents US/test, respectively) are expensive. We have established our own methods for serum AST, ALT, cholesterol, triglycerides, urea, and uric acid (6, 6, 5, 12, 13, and 6 cents US/test, respectively) using Ames Sera-Pak reagents. Linearity of our AST, ALT, cholesterol, triglycerides, urea, and uric acid methods were either similar to or higher than the Beckman methods. The within run and day-to-day run precisions were acceptable. Recovery of our AST, ALT, cholesterol, triglycerides, urea, and uric acid were excellent. Our results for AST, ALT, cholesterol, triglycerides, urea, and uric acid correlated well with the Beckman results. Bilirubin (340.8 mumol/L) did not significantly interfere on our AST, ALT, cholesterol, triglycerides, and urea, while its concentrations of 165.8 mumol/L started giving negative interference on uric acid. Turbidity (2+) did not interfere significantly on our AST and ALT but started giving positive interference on cholesterol, triglycerides, urea, and uric acid. Hemolysis (2+) gave positive interference on our cholesterol, triglycerides, urea, and uric acid. Stability of Ames Sera-Pak working reagents was at least 30 days for AST, ALT, urea, and uric acid and 40 days for cholesterol and triglycerides.

Alanine Transaminase↗
PubMed1991

Effects of phytic acid on the myoglobin-t-butylhydroperoxide-catalysed oxidation of uric acid and peroxidation of erythrocyte membrane lipids.

Phytic acid stimulated the myoglobin-t-butylhydroperoxide (TBHP)-catalysed oxidation of uric acid, but inhibited the peroxidation of erythrocyte membrane lipids induced by the same system. Butylated hydroxytoluene, a free radical chain reaction-terminating antioxidant, also suppressed the myoglobin-TBHP-induced lipid peroxidation. Moreover, phytic acid inhibited the hydroxyl radical-induced degradation of deoxyribose, but the extent of inhibition in this system was reduced by increasing the ferric ion concentration, suggesting that these effects of phytic acid on the myoglobin-TBHP-mediated oxidation are more likely attributable to its metal chelating properties rather than to a free radical scavenging action. The effectiveness of phytic acid, a naturally occurring antioxidant, in the inhibition of both iron- (as previously shown) and myoglobin-dependent lipid peroxidation suggests its possible therapeutic application as a non-toxic antioxidant for ameliorating the extent of oxy-radical-mediated myocardial ischemia/reperfusion damage.

Erythrocyte Membrane↗
PubMed2006

Uric acid and hypertension.

Epidemiologic studies published during the past 3 years support the possible role of uric acid in the onset of essential hypertension. Data from several large, longitudinal cardiovascular disease studies indicate that elevated serum uric acid is a predictor of incident hypertension and blood pressure progression. In a pediatric study, more than 90% of children with essential hypertension have serum uric acid levels above 5.5 mg/dL. During the same period, laboratory studies have provided compelling mechanistic evidence to explain the clinical observations. Uric acid causes hypertension in a rat model through the activation of the renin-angiotensin system, downregulation of nitric oxide, and induction of endothelial dysfunction and vascular smooth muscle proliferation. Ongoing clinical trials will elucidate the role of uric acid in human hypertension and will determine whether control of uric acid may be a new way to prevent or treat essential hypertension.

Animals↗
PubMed2006

Serum uric acid predicts incident hypertension in a biethnic cohort: the atherosclerosis risk in communities study.

Serum uric acid has been positively associated with incident hypertension, but previous studies have had limited ability to explore this relationship across sex and ethnic strata. We sought to evaluate this association in a biethnic cohort of middle-aged men and women. Participants in the Atherosclerosis Risk in Communities (ARIC) study who were free of hypertension at baseline (N=9104) were evaluated for hypertension at 3-year intervals over 4 examinations. Adjusted Cox proportional hazards models evaluated risk of incident hypertension or progression of blood category for each SD higher baseline serum uric acid. At baseline, the mean age was 53.3 years (range: 45 to 64 years), with a mean (SD) systolic blood pressure of 113.8 (12.2) mm Hg, mean diastolic blood pressure of 70.2 (8.6) mm Hg, and mean serum uric acid of 5.7 (1.4). Higher serum uric acid was associated with greater risk of hypertension in the overall cohort (hazard ratio for each SD of higher uric acid [95% CI]: 1.10 [1.04 to 1.15]) and in subgroup analyses (black men: 1.32 [1.14 to 1.54]; black women: 1.16 [1.03 to 1.31]; white men: 1.01 [0.94 to 1.09]; white women: 1.04 [0.96 to 1.11]), after adjustment for age, baseline blood pressure, body mass index, renal function, diabetes, and smoking. The pattern was similar when modeling blood pressure progression (overall: 1.10 [1.05 to 1.14]; black men: 1.26 [1.11 to 1.42]; black women: 1.18 [1.06 to 1.31]; white men: 1.05 [0.99 to 1.11]; white women: 1.05 [1.00 to 1.12]). In conclusion, serum uric acid was positively associated with incident hypertension over 9 years of follow-up, and this relationship was stronger in blacks than in whites. More research is warranted concerning the physiological and clinical consequences of hyperuricemia, especially in blacks.

Black or African American↗
PubMed2005

Protective effect of urate oxidase on uric acid induced-monocyte apoptosis.

Uremic patients have a higher risk of infection and malignancy than normal subjects. Previous studies have deomonstrated that monocytes isolated from uremic patients display an increased apoptosis rate compared to normal subjects; furthermore uremic plasma can increase apoptosis rates on U937, a human monocytic cell line. In several pathological conditions, precipitation of uric acid crystals can lead to renal insufficiency or acute renal failure by different mechanisms. In recent studies uric acid has been shown to induce inflammatory response from monocytes and it has been suggested to be involved in cell dysfunction. Rasburicase is a new recombinant urate oxidase developed to prevent and treat hyperuricaemia in patients with cancer or renal failure; it degrades uric acid to allantoin, a less toxic and more soluble product. In the present study, we aimed at determining whether uric acid may be a factor affecting U937 apoptosis, and whether urate oxidase may reduces or even prevent uric acid induced cell apoptosis. Hoechst staining and internucleosome ledder fragmentation of DNA showed that uric acid increased the percentage of apoptotic cells comparing to the control and that when the U937 cells were incubated with uric acid and urate oxidase the percentage of apoptosis significantly decreased (from 43+/-7% to 19+/- 3%, p<0.05). Also, the activity of caspase-8 and caspase-3 showed the same trend (caspase 3: from 2.7+/-0.53 to 1.6+/-0.42; caspase-8: from 2.2+/-0.43 to 1.3+/-0.57). A reduction of intracellular reduced glutathione (GSH) concentration was found in uric acid treated cells while the addition of urate oxidase in the uric acid incubated cells decreased the GSH extrusion. The concentration of TNF-alpha was increased in the sample incubated with uric acid comparing to the control. Uric acid is an inducer of apoptosis on U937 cell line, and therefore it may be a component of the mosaic of uremic toxins both in acute and chronic renal disease. We can hypothesize that uric acid might be directly involved in the apoptotic process trough the activation of both death receptor and mitochondrial-mediated pathways. We have, also, demonstrated that urate oxidase is able to prevent at least in part, the effect of uric acid on U937 apoptosis. This effect might be a result of different mechanisms of action.

Apoptosis↗
PubMed1989

Effects of traxanox sodium on blood pressure and serum uric acid in hypertensive patients: a preliminary study.

The effects of chronic administration of traxanox sodium (traxanox) on blood pressure and serum uric acid level were investigated in 15 patients who had mild to moderate hypertension. Traxanox or its placebo was orally administered in a single-blind protocol. Blood pressure was significantly reduced from baseline after treatment with traxanox. The serum uric acid level after drug administration was significantly lower than with placebo whereas urinary uric acid excretion was significantly greater and uric acid clearance tended to be greater. These results indicate that chronic administration of traxanox reduces serum uric acid level as well as blood pressure in patients with mild to moderate hypertension. This reduction in serum uric acid is due in part to a traxanox-induced elevation of urinary uric acid excretion.

Adult↗
PubMed2000

Influence of purine intake on uric acid excretion in infants fed soy infant formulas.

OBJECTIVE: These studies tested the hypothesis that increasing intake of purines, delivered as RNA from soy protein-based infant formula, would increase urinary uric acid excretion in infants. METHODS: Study One examined the influence of feeding on serum uric acid in a total of 178 infants from four separate trials with infants fed commercial and experimental soy-based and milk-based infant formulas or human milk. Studies Two and Three compared the effect of a standard purine soy formula (STD Purine; 180 mg purines/L from RNA) and a reduced purine soy formula (Reduced Purine; 65 mg purines/L; 26 mg/L from RNA and 39 mg/L from ribonucleotides) on urinary uric acid excretion in infants. In Study Two, 11 infants ranging in age from 16 to 128 days of age were fed both formulas in a random crossover design. Complete 72-hour urine collections were done at the end of each 11-day feeding period. Urinary uric acid excretion was expressed as mmol/day. In Study Three, 33 infants were enrolled before eight days of age and randomized to one of the formulas one week later. Spot urine samples were collected at 28 and/or 56 days of age and urinary uric acid concentration was expressed as mmol/mmol creatinine. RESULTS: In Study One, each of the feedings resulted in mean serum uric acid levels within normal reference ranges. Soy formula led to higher serum uric acid levels than human milk, and human milk to levels indistinguishable from cow milk-based formulas. In Study Two, infants excreted significantly more uric acid in the urine when fed the STD Purine formula compared to the Reduced Purine formula (0.86+/-.04 vs. 0.57+/-.04 mmol/d) (p = 0.006). In Study Three, infants fed the STD Purine formula had a significantly higher concentration of uric acid in their urine compared to those fed the Reduced Purine formula (2.1+/-0.2 vs. 1.4+/-0.1 mmol uric acid/mmol creatinine) (p = 0.0001). CONCLUSION: These data indicate that healthy infants can digest RNA and subsequently absorb the liberated purine ribonucleotides as determined by urinary uric acid concentration.

Cross-Over Studies↗
PubMed1999

Serum uric acid and risk for cardiovascular disease and death: the Framingham Heart Study.

BACKGROUND: Hyperuricemia is associated with risk for cardiovascular disease and death. However, the role of uric acid independent of established risk factors is uncertain. OBJECTIVE: To examine the relation of serum uric acid level to incident coronary heart disease, death from cardiovascular disease, and death from all causes. DESIGN: Community-based, prospective observational study. SETTING: Framingham, Massachusetts. PATIENTS: 6763 Framingham Heart Study participants (mean age, 47 years). MEASUREMENTS: Serum uricacid level at baseline (1971 to 1976); event rates per 1000 person-years by sex-specific uric acid quintile. RESULTS: During 117,376 person-years of follow-up, 617 coronary heart disease events, 429 cardiovascular disease deaths, and 1460 deaths from all causes occurred. In men, after adjustment for age, elevated serum uric acid level was not associated with increased risk for an adverse outcome. In women, after adjustment for age, uric acid level was predictive of coronary heart disease (P = 0.002), death from cardiovascular disease (P = 0.009), and death from all causes (P = 0.03). After additional adjustment for cardiovascular disease risk factors, uric acid level was no longer associated with coronary heart disease, death from cardiovascular disease, or death from all causes. In a stepwise Cox model, diuretic use was identified as the covariate responsible for rendering serum uric acid a statistically nonsignificant predictor of outcomes. CONCLUSIONS: These findings indicate that uric acid does not have a causal role in the development of coronary heart disease, death from cardiovascular disease, or death from all causes. Any apparent association with these outcomes is probably due to the association of uric acid level with other risk factors.

Age Distribution↗
PubMed1981

Effects of two diphosphonates (EHDP and Cl2MDP) on serum uric acid in pagetic patients.

The effects on serum uric acid (SUA) of two diphosphonates (EHDP at 5 and 20 mg/kg/day and Cl2MDP at 400 and 1600 mg/day) were studied in 49 pagetic patients treated for 6 months. Patients were divided into two groups: group I, initially normouricemic (SUA less than 385 mumol/l); group II, initially hyperuricemic (SUA greater than or equal to 385 mumol/l). SUA was significantly decreased (P less than 0.01) after 6 months of diphosphonate therapy in all group II patients. However, 3 months after withdrawal of therapy, SUA returned to values not significantly different from those initially recorded in this group. SUA did not change during or after treatment in the group I patients. Groups I and II could not be differentiated on the basis of initial serum alkaline phosphatase or urinary hydroxyproline values. In response to therapy, both groups showed the same reduction in these parameters. These results suggest that diphosphonates have no effect at a single level in uric acid metabolism. They certainly reduce the part of the urate pool coming from the nucleic acids of the increased bone cell population by reducing the number of osteoclasts and osteoblasts, which is extremely high in pagetic bone. They also must act on uric acid metabolism through other mechanisms which need to be investigated in further studies.

Adult↗
PubMed1976

Alpha-methyldopa interference with the phosphotungstate uric acid test.

The effect of alpha-methyldopa on the phosphotungstate method of uric acid analysis was tested using a group of 17 hypertensive patients being treated with only this drug for their elevated blood pressure. The uric acid values of these patients tested by the phosphotungstate method showed no significant difference from the uricase test values, when compared to a control population of 32 normotensive patients tested in the same manner. The proposed interference was further tested by in vitro studies. Both uricase and phosphotungstate analysis of uric acid was performed on serum containing various dilutions of alpha-methyldopa. The concentration of alpha-methyldopa required to clinically affect the uric acid level, whereby a false positive result occurred, was 60 mug/ml. The mean plasma aplha-methyldopa concentration in the study group, however, was found to be only 2.03 mug/ml. The postulated interference of therapeutic levels of alpha-methyldopa on the phosphotungstate uric acid method was invalid.

Adult↗
PubMed1981

Long-term follow-up of incorporation of 15N from glycine into uric acid in gout.

The incorporation of 15N-glycine into urinary uric acid was studied in three gouty patients, repeating a study carried out 13 to 27 years ago. The 15N incorporation attained a lower maximum and declined less rapidly in the repeat study in all three patients. The cumulative 15N incorporation into uric acid was reduced to one half of that determined previously. Similarly, urinary uric acid excretion was less, along with a lower uric acid nitrogen to total nitrogen ratio. The data indicate changes in the nature of the metabolic aberrations, which are apparently related to long-term drug therapy, changes in lifestyle, aging and associated medical complications.

Adult↗
PubMed2005

Uric acid causes vascular smooth muscle cell proliferation by entering cells via a functional urate transporter.

BACKGROUND: Soluble uric acid stimulates vascular smooth muscle cell (VSMC) proliferation by activating mitogen-activated protein kinases, and stimulating COX-2 and PDGF synthesis. The mechanism by which uric acid enters the VSMC is not known. We hypothesized that uric acid enters via transporters similar to that observed in the kidney. METHODS: We studied the uptake of uric acid into rat VSMC under polarized and depolarized conditions and in the presence of organic anion transport (OAT) inhibitors (probenecid and benzbromarone) or p-aminohippurate (PAH). We also examined the ability of probenecid to inhibit uric acid-induced VSMC proliferation and monocyte chemoattractant protein-1 (MCP-1) synthesis. RESULTS: (14)C-Urate uptake was shown in VSMC and was enhanced under depolarized conditions. (14)C-Uric acid uptake was inhibited by probenecid and benzbromarone, as well as by unlabelled urate and PAH. Probenecid blocked VSMC proliferation and MCP-1 expression in response to uric acid. VSMC did not express rOAT1-3, rOAT-5 or URAT-1 mRNA by PCR, but did express the voltage-sensitive transporter (UAT) by both PCR and RNase protection assay. CONCLUSIONS: Urate enters VSMC by both voltage-sensitive and OAT pathways, and the uptake, cell proliferation and MCP-1 expression can be blocked by OAT inhibitors. The specific transporter(s) responsible for the urate uptake remains to be determined.

Animals↗
PubMed1982

Effect of L-dopa on renal handling of uric acid.

Several reports have indicated that L-dopa may cause hyperuricemia and gout. The reports of hyperuricemia have generally been explained on the basis that L-dopa is known to produce a false hyperuricemia by interfering in the colorimetric analysis of uric acid. Our studies of the interference of L-dopa in the analysis of uric acid revealed that the false elevation of uric acid produced by therapeutic plasma concentrations of L-dopa is minor. The present studies used the Sperber in vivo chicken technique to determine whether L-dopa interferes with the renal excretion of uric acid. We found that a 440 mg/kg dose of L-dopa given by stomach tube results in a 30% decrease in the renal tubular excretory transport of [14C]uric acid. L-Dopa infused along with [14C]uric acid into the renal portal circulation also decreases the excretory transport of [14C]uric acid. In addition, i.v. L-dopa at 8.5 or 11.6 mumol/min/leg causes an increase in plasma urate of 26 or 45%, respectively. During infusion of L-[14C]dopa into the peritubular circulation, the 14C-label was excreted into the urine at a rate equivalent to 35% that of simultaneously infused p-aminohippuric acid or [3H] tetraethylammonium. The excretory transport of 14C-label was inhibited by probenecid. Because the renal tubular excretory transport of uric acid in chickens has many similarities to that of man, the results suggest that inhibition of uric acid excretory transport may be one of the effects of L-dopa, or its metabolites, in man.

Animals↗
PubMed2004

[Effect of optimum jogging in a hot environment on uric acid metabolism].

OBJECTIVES: The purpose of this study was to estimate the effect of optimum jogging in a hot environment on uric acid metabolism. METHODS: Six male subjects performed jogging at each optimum speed. The distance of jogging was 8000 m (400 m track x 20 laps). Each jogging was performed twice, once in the summer season (Sept.) and once in the winter season (March). Blood samples were collected before and at 0, 1, 2, 3, 5 and 24 h after each jogging. Urine was also collected before (after 60 min at rest) and from the onset of jogging until 24 h after. RESULTS: The wet bulb globe temperature (W.B.G.T.) during jogging ranged from 24.9 to 27.8 degrees C in the summer and from 5.9 to 11.4 degrees C in the winter. There was no difference in the duration of each jogging between summer and winter. However, the heart rate (H.R.) during jogging in the summer was higher than that in the winter. Serum uric acid at each rest ranged from, on average, 6.2 to 6.4 (mg/dl). After jogging in the summer, serum uric acid rose significantly (p < 0.05) and the increase was maintained until 5 h after. Exercise-induced hyperuricemia (above 7.5 mg/dl of serum uric acid) was shown in 3 out of all the subjects. In contrast, serum uric acid in the winter showed no significant change throughout protocol. There was no difference in the change in clearance of uric acid during each protocol between summer and winter. Urinary uric acid excretion at 24 h after, between summer and winter, showed similar levels. The rate of urinary oxypurine excretion (xanthine + hypoxanthine) in summer was higher than that in winter at 1 h and 2 h. CONCLUSIONS: These results suggest that not only jogging but also a hot environment affects uric acid metabolism, especially the increase of purine nucleotide degradation.

Adult↗