Cytidylate cyclase activity in rat brain was determined by EIA and the following results were obtained. 1) Cytidylate cyclase existed in a particulate fraction. 2) Cytidylate cyclase activity in brain was higher than other tissues. 3) The optimal pH of cytidylate cyclase was about 9.5. 4) Cytidylate cyclase activity was dependent on Mn++. 5) Km value of solubilized cytidylate cyclase was 0.0156mM.
Recently, we have developed a method for the determination of uric acid in mammalian tissues by reversed-phase high-performance liquid chromatography with electrochemical detection. In addition, we have achieved to simplify the treatment of mammalian tissues prior to chromatography as well as to shorten the time for uric acid separation by the chromatography. In this article, we demonstrate the effectiveness of the chromatographic method showing some chromatograms of mammalian tissues. The analytical recoveries of uric acid in mammalian tissues were found to be almost 100%. The chromatographic analysis was performed in about 8 min. The assay limit was about 10 pg.
A simple, easy, rapid, accurate, sensitive and selective method for the determination of endogeneous uric acid levels in body fluids such as serum, cerebrospinal fluid, and urine by reversed-phase high-performance liquid chromatography with electrochemical detection has been developed. In this article, the effectiveness of the chromatographic method is described showing some examples. The analytical recoveries of uric acid in body fluids have been found to be almost 100%. Complete separation of uric acid and ascorbic acid in body fluids was achieved in about 2 min by injecting a simply deproteinized body fluid sample onto the reversed-phase column under the present chromatographic conditions. The minimum detectable quantity of uric acid was found to be about 10 pg.
1. A simple and convenient method for the preparation of UA -free and UA-known value control serum by removing UA in a pooled serum with activated charcoal and by dissolved critical amounts of UA in the UA-free serum is described. 2. For the complete removal of UA in a pooled serum with activated charcoal, stirring for 20 minutes at room temperature was needed. Clear UA-free serum like fresh serum was obtained by filtration through "Hyflo Super Cel" filtration aid under redused pressure. 3. The char coal treatment caused a significant change in levels of the following serum components: creatinine, bilirubin, calcium, potassium, and lipids. 4. The powder of the NBS-UA was completely dissolved in the UAfree serum after stirring for 30 to 60 minutes at room temperature. 5. The results of a small survay in Kanto and Tokai area showed that this UA-control materials were very useful aid for UA quality control in routine clinical laboratory.
To elucidate the pathogenesis of hyperuricemia in glycogenosis type VII, we investigated a possible role of altered purine metabolism in exercising muscle in this disorder. Semi-ischemic forearm exercise test wa s performed in unrelated two patients with glycogenosis type VII. Despite of no increases in venous lactate levels, marked elevations of venous ammonia were observed (5.6- and 10.1-fold of control values, respectively), indicating an acceleration of AMP deamination in muscle. This observation suggests that there is an exaggerated degradation of purine nucleotides in exercising muscle and this may contribute to the development of hyperuricemia in glycogenosis type VII.
The study was investigated effects of different kinds of exercise on serum uric acid as the basic research data for preventing athletes and non-athletes from exercised-induced hyperuricemia and carring out exercise treatment for hyperuricemia. The results were summarized as follows: 1) Changes in serum uric acid on different kinds of exercise: On an exhaustive exercise on a bicycle ergometer for 5-10 min, serum uric acid was gradually increased, and reached a peak at 2 hrs after exercise. And then it was gradually decreased until 24 hrs after exercise, but was significantly 9.9% higher at 24 hrs after exercise than before exercise (p<0.001). On a 12 min-run, serum uric acid reached a peak immediatly after ex ercise, and then kept the same level until 2 hrs after exercise. On a 2 hrs running on a treadmill, serum uric acid showed a linear increase, and reached a peak at 45 min during exercise. And then it was the same level until 90 min after exercise. 2) Comparison of the degree of increase in serum uric acid on different kinds of exercise: The degree of increase in serum uric acid against before exercise was the largest (+87.9%, p<0.001) on an exhaustive exercise on a bicycle ergometer in untrained subjects, and was with a range of +9.0 to +34.2% on a 12-min -run, a 2 hrs running on a treadmill and so on. 3) Relationship between exercise in t e nsity and increase inserum uric acid when the amount of exercise was the same: The increase in serum uric acid after exercise was proportional to exercise intensity on 60%, 80%, and 100% V02 max. But serum uric acid was almost unchanged after 40% V02 max exercise, and tended to be decreased after 30% V02 max exercise. 4) The ratio of appearence of exercise-induced hyperuricophenomenon (phenomenon of a temporary high level of serum uric acid over 7 mg/dl after severe exercise): The ratio of appearence of exercise-induced hyperurico-phenomenon was 38.1% (75 out of 197 untrained subjects) at 5,000m run, and 53.3% (16 out of 30 trained subjects) at 12-min-run. 5) Effects of training on the degree of increase in serum uric acid after exercise: After training of walking and jogging for 4 months, the mean distance of 12-min-run was increased (2,444m→2,611m), but the degree of increase in serum uric acid after 12mm-run was decreased (+18.3%→+9.1%) in contrast to before training.
Effects of dietary sodium and potassium on serum uric acid concentration (S-UA) and urinary uric acid excretion (UUA) in Japanese young women were studied in this paper. Subjects (n=4, female, l9yrs) were fed w ith low sodium (Na), potassium (K) diet for four days, thereafter fed with relatively higher Na, K diet for successive four days. S-UA was determined at first, fourth and eighth experimental days. UUA and urinary electrolytes excretion were measured throughout experiment. S-UA was decreased, while urine volume (UV), urinary Na (UNa), K (UK) excretion, UUA and urinary creatinine excretion (UCr) were increased, accompanied with the increase in dietary electrolytes intake. Urinary uric acid concentration was significantly correlated to urinary creatinine concentration (r=0.88), K concentration (r=0.71), (Na+K) concentration (r=0.49) and Na/K ratio (r=-0.43). Urinary uric acid excretion was correlated to UUA/UCr(r=0.59), UCr (r=0.56) and UK (r=0.45). These results sugge s ted that uric acid metabolism was influenced by dietary electrolytes levels. And it was also suggested that renal uric acid handling was partly correlated to urinary sodium and potassium excretions. A possible roles of electrolytes on dietary treatment for hyperuricemia were discussed.
To investigate the presence of hyperuricemia in 94 patients with solid malignant tumors, serum uric acid (SUA) were measured and the following results were obtained. 1. The mean SUA levels in patient s with liver cancer were highest. 2. Hyperuricemia with the SUA over 6.5 mg/dl and over 7.5 mg/dl were found in 19% and 7.5% of them respectively. Hypouricem ia with the SUA below 2.5 mg/dl was found in 7.4%. 3. There were no significant differences between the mean SUA levels in solid malignant patients with metastases and in those without metastases and also the mean SUA levels in patients with serum CEA over 5.0 ng/ml were not statistically significant compared to those with serum CEA below 5.0 ng/ml. 4. There were not characteristic clinical pictures in patients with hyperuricemia or hypouricemia.
Pre and postoperative values of serum uric acid and 24 hr urinary excretion of uric acid were measured in 29 patients with primary hyperparathyroidism. Serum uric acid levels were 6.0 ± 1.0 mg/dl and 6.0 ± 0.6 mg/dl in males, and 5.7 ± 0.8 mg/dl and 5.3 ± 0.1 mg/dl in females, respectively pre and postoperatively. No significant change was observed. Positive correlation (p<0.01) was found between the ratios of Ca/Creatinine and Uric Acid/Creatinine before but not after operation. Serum uric acid levels increased on first to third days after operation and returned normal within a week. Under low calcium diet for five days, serum uric acid levels were elevated. These findings suggest that primary hyperparathyroidism has some influences on uric acid metabolism.
Acute arthritis of gout frequentry associates with the elevation of erythrocyte sedimentation rate (ESR) and acute phase reactant; including c-reactive protein (CRP), α1-acid glycoprotein, α1-antitrypsin, seromucoid, α1-macroglobulin and α2-macroglobulin. Recently, among the acute phase reactants acid soluble proteins (ASP), which are solublized in 6M perchloric acid solution, are utilized widely as a routine laboratory examination. In this study we evaluated the serum levels of A SP in 88 samples gathered from 54 patients with primary gout. Serum levels of ASP from gouty patients were higher than those of normal individuals. More prominent elevation of serum ASP was observed at the time of acute gouty attacks. When serially assayed, changes of the serum level of ASP well correlated with the times of acute gouty attacks. Some patients with gouty attacks showed only the elevation of serum ASP without elevation of ESR and CRP. Serum levels of ASP did not correlate with levels of ESR and CRP at the time of acute gouty attacks. From these findings we concluded that serum levels of ASP were a useful index for acute gouty attacks.
Some studies on the cerebrospinal fluid (CSF) uric acid in patients with various neurological diseases were reported in the literature. In this study we discussed the clinical value of the sequential measurement of the CSF uric acid and CSF cells in patients with postoperative acute meningitis. CSF was investigated for uric acid and cells in 9 cases with postoperative meningitis and 4 cases without that. The results as follows, 1) The CSF uric acid level was increased markedly in direct proportion to neutrophilia in the CSF. 2) Seven cases of the 9 with postoperative meningitis had biphasic pattern patteronf the CSF uric acid level. 3) Four cases without postoperative meningitis had reduced progressively the CSF uric acid level and then they were nor m alized until the fourth day after operation.
Many epidemiological and clinical studies in recent years have confirmed a positive correlation between the serum urate concentration and body weight. The aim of the present study was to determine whether weight reduction in obese people had any effect on the urate metabolism. Twenty-two massively o bese subjects, eight men (183 ± 30% of ideal body weight) and fourteen women (170 ± 21% of ideal body weight), were hospitalized and treated with low-calorie diets (800 - 1,000 kcal) for intensive weight reduction, and an exercise therapy (walking and bicycle ergometer) was added to this regime afterwards. We examined serum levels of uric acid, creatinine, lipids and lipoproteins as well as urinary urate and creatinine excretions, and then calculated urate clearance (CUA) to creatinine clearance (CCR) ratio. Urinary urate excretions were not increased, but rather reduced. CUA/CCR ratios (%) were significantly lower in both sexes (3.3 ± 1.2% in male and 5.1 ± 3.3% in female, respectively) than control subjects. These data suggest that hyperuricemia in massively obese people is mainly due to an impaired renal clearance ratio of uric acid rather than overproduction. During weight reduction by a low-calorie diet, serum levels of cholesterol and triglyceride fell gradually except for HDL-cholesterol. Serum urate levels were also reduced during weight reduction, while CUA/CCR ratios gradually rose up to almost normal levels. This increase of CUA/CCR ratio was also maintained after the exercise therapy. The mechanism of the imp r ovement in urate metabolism during weight reduction is yet unclear, but a reduced intake of total calorie or purine nucleotides might be a possible mechanism.