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PubMed1991

Oxalate decarboxylase from Collybia velutipes. Purification, characterization, and cDNA cloning.

The oxalate-degrading enzyme oxalate decarboxylase (EC 4.1.1.2), which is inducible by oxalic acid, was purified to homogeneity from a crude extract of Collybia velutipes, a basidiomycetous fungus. Two forms of the enzyme were resolved on chromatofocusing. The two isozymes were shown to be related by amino acid composition, peptide mapping, and immunological cross-reactivity. Peak A, eluting at pH 3.3, was used for further study; the Km was found to be 4.5 mM, and the Vmax was 166 mumol/min/mg. The subunit molecular mass of the glycosylated enzyme was 64 kDa, whereas the mass of the deglycosylated protein was 55 kDa. The enzyme showed an acidic pl, was very stable over a wide pH range, and was moderately thermostable. The cDNA encoding the enzyme was obtained by immunoscreening a lambda gt11 expression library. In vitro translation of hybrid-selected mRNA gave a 55-kDa protein. Genomic Southern hybridization indicated the oxalate decarboxylase is encoded by a single gene. The cDNA probe hybridized to a single 1.5-kilobase pair species of mRNA. The mRNA was shown to be induced by oxalic acid. A temporal relationship between enzyme activity and mRNA levels was observed, thus suggesting that the expression of oxalate decarboxylase is regulated at the transcriptional level.

Amino Acids↗
PubMed1981

A rapid gas chromatographic procedure for the analysis of oxalate ion in urine.

A specific, precise, rapid and sensitive method for the analysis of oxalic acid in urine is described. This microanalytical procedure can detect concentrations of urinary oxalic acid as low as 4 mg/l with a relative standard deviation of replicates of less than 5% (24-h urine collections). 10% BCl3:2-chloroethanol is used to derivatize 0.1 ml of urine after evaporation to dryness or lyophilization. The bis-2-chloroethyl ester of oxalic acid formed is extracted into ethyl acetate/isopropyl ether (1:3, v/v) and is detected by electron capture gas chromatography at the 50 pg level. The total analysis time for 35 samples in 8 h per GC column. A series of determinations of urinary oxalic acid in 21 kidney stone-forming patients resulted in values ranging from 10.6 to 42.0 mg/24 h with a mean recovery of added oxalic acid of 98.2% (range 84.0-111.3%).

Boranes↗
PubMed1982

The determination of oxalic acid in plasma and urine by means of capillary gas chromatography.

A gas chromatographic procedure for determining oxalate in plasma is described, in which the trimethylsilyl derivative of oxalate is analyzed on a 25-m capillary SE-30 column. In addition the effects of standing of whole blood or plasma and the effect of added glyoxalate on the oxalate concentration were studied. The present method offers good specificity and sensitivity and is easy to perform, in contrast to most methods hitherto described. The normal value of plasma oxalate was found to be 2.8 +/- 1.1 mumol/l (mean +/- 1 SD), which is close to the values obtained with in vivo tracer studies. Plasma oxalate values before and after haemodialysis are presented. By introducing a few minor modifications the method is also applicable to urine samples and in principle it should be possible to determine the glycollic acid concentration as well, both in urine and plasma.

Adolescent↗
PubMed1987

An improved high performance liquid chromatographic method for determining urinary oxalate, making use of an ID-MS reference method.

With the aid of a newly developed isotope dilution mass spectrometric (ID-MS) measurement of urinary oxalate, an existing HPLC method for assaying this substance was investigated. Results obtained with this method were too high, apparently due to a systematic error. Subsequently, this method was improved by additional prepurification in three different ways: (a) precipitation with CaSO4 to Ca-oxalate, (b) adsorption (and subsequent desorption) to columns supplied with a commercial kit for urinary oxalate and (c) the enzymatic destruction of urinary oxalate present. This work demonstrates the successful use of a reference method in improving a newly developed analytical procedure and presents a reliable and reproducible HPLC method for determining urinary oxalate.

Chromatography, High Pressure Liquid↗
PubMed1987

Urinary excretion of orally administered oxalic acid in MYRJ 45-treated NMRI mice.

Polyoxyethylene(8)stearate (MYRJ 45) has been shown to cause bladder tumours in chronic feeding studies. During this study the effects of dietary MYRJ 45 on the urinary excretion of dietary oxalic acid were tested. Male NMRI mice were gradually adapted to 20% MYRJ 45 in their diet. The animals were then dosed, after a 6 h fast, with 2 microCi of [U-14C]oxalic acid either with 1 ml of water or 1 ml of 20% MYRJ 45 in water. The urinary and faecal excretion of the label were determined using the combustion method coupled with liquid scintillation counting. MYRJ 45 was observed to increase significantly the urinary absorption of 14C in male NMRI mice when compared to control mice dosed with oxalic acid and water. The increase was observed both in MYRJ 45-pretreated mice receiving the label with MYRJ 45 or with water and in control mice receiving the label in a 20% MYRJ 45 water solution. The result indicates that dietary MYRJ 45 significantly increases the urinary excretion of dietary oxalic acid in male NMRI mice. This increase may contribute to the bladder tumour formation by facilitating calcium oxalate crystalluria with potential bladder wall irritating effect in mice.

Animals↗
PubMed2004

Oxalic acid alters intracellular calcium in endothelial cells.

Patients with chronic renal failure (CRF) who undergo hemodialysis experience accelerated atherosclerosis and premature death. While the cause of uremic atherogenesis is unknown, we reported that uremic levels of oxalate, an excretory metabolite, severely inhibit proliferation and migration of human endothelial cells (EC) without affecting other cell types. Since the physical, cellular and molecular events of endothelial injury are clearly established as key factors in the development of plaque, and since inhibition of proliferation and migration would enhance endothelial injury, we have proposed that oxalate is an atherogenic toxin of uremia. In the current study, we used in situ cell counting and total DNA measurement to show that the inhibitory effect of oxalate on proliferation is exclusive to endothelial cells among human cell lines tested (endothelial cells, fibroblasts, aortic smooth muscle cells (SMC), glioblastoma and embryonic kidney cells). Using the fluorescent calcium indicators fura-2 and fluo-3, we correlated the inhibition of proliferation with a prolonged elevation in intracellular free calcium levels. We also demonstrated that all cells tested internalize 14C-oxalic acid. We conclude that plasma oxalate exerts its atherogenic effects by elevating intracellular calcium exclusively in endothelial cells and preventing re-endothelialization.

Biological Transport, Active↗
PubMed2002

Effects of 5 different diets on urinary risk factors for calcium oxalate kidney stone formation: evidence of different renal handling mechanisms in different race groups.

PURPOSE: Since the incidence of renal calculi in the South African black population is extremely rare while in white subjects it occurs at the same rate as elsewhere in the western world, we investigated the possibility that different renal handling mechanisms in response to different dietary challenges might occur in the 2 race groups. MATERIALS AND METHODS: We administered 5 different dietary protocols, including low calcium, high oxalate, vitamin C, high salt and lacto-vegetarian, to 10 healthy male subjects from each race group. We collected 24-hour urine at baseline and after 4 days on the prescribed diet which were analyzed for biochemical and physicochemical risk factors. Dietary intake was controlled throughout the experimental period. A 24-hour dietary recall questionnaire was recorded at baseline and analyzed using food composition tables. Statistical analysis of variance was performed on all the data. RESULTS: The low calcium diet caused statistically significant changes only in black subjects, which consisted of urinary oxalate increase (0.17 to 0.23 mmol./24 hours, p = 0.01), relative supersaturation of calcium oxalate decrease (1.88 to 0.97, p = 0.03) and relative supersaturation of brushite increase (0.85 to 1.69, p = 0.03). The high oxalate diet caused statistically significant changes in both race groups but these changes were different in the 2 groups. In white subjects urinary pH increased (6.24 to 6.62, p = 0.01), potassium excretion increased (40.01 to 73.49, p = 0.01) and relative supersaturation of brushite increased (1.34 to 2.12, p = 0.05). In black subjects urinary citrate increased (1.94 to 2.99 mmol./24 hours, p = 0.01). Clinically unimportant changes occurred in both race groups after the other 3 diets. CONCLUSIONS: Renal handling of dietary calcium and oxalate in South African black and white subjects is different and may explain the different stone incidence in the 2 race groups.

Adolescent↗
PubMed1984

Effect of orchiectomy and ovariectomy on oxalate production, transport and excretion in rats.

The role of sex hormones on oxalate synthesis by liver, transport by renal cortical mitochondria and urinary excretion was studied in adult male and female Sprague-Dawley rats. Orchiectomy decreased the hepatic synthesis of oxalate whereas ovariectomy increased it by 10 per cent. Castration inhibited oxalate transport by the renal mitochondria uncompetitively in both sexes. Urinary levels of oxalate were unaffected after orchiectomy whereas ovariectomy resulted in an initial elevation in the urinary oxalate levels which returned to control values by 21 days. The results are discussed in light of recent data.

Animals↗
PubMed1983

Effect of calcium restriction on renal excretion of oxalate and the probability of stones in the various pathophysiological groups with calcium stones.

To evaluate the adequacy of simple calcium restriction for patients with idiopathic calcium stones the effect of 5 days of calcium restriction without oxalate restriction on renal excretion of calcium and oxalate, and the corresponding probability of stones were assessed in 50 controls and 48 patients. Renal excretion of calcium decreased and that of oxalate increased significantly in all groups but the importance of the changes was critically dependent upon the underlying pathophysiological condition. The probability of stones decreased only in patients with absorptive hypercalciuria type II owing to the usual excessive calcium intake and increased in those with absorptive hypercalciuria type I and renal hypercalciuria, which are associated with true hyperabsorption of calcium and represent the 2 forms of idiopathic hypercalciuria. We believe that simple calcium restriction is beneficial for patients with idiopathic calculi only when the hypercalciuria is caused by exaggerated intake of calcium, since it increases the probability of stones in patients with idiopathic hypercalciuria. Calcium restriction always is associated with an increase in oxalate excretion, suggesting that simultaneous oxalate restriction should be added in all cases to decrease the probability of stones.

Adult↗
PubMed1991

Diet and hyperoxaluria in the syndrome of idiopathic calcium oxalate urolithiasis.

Hyperoxaluria is an important risk factor in patients who form calcium oxalate stones within the urinary tract. It occurs in patients with primary hyperoxaluria, enteric hyperoxaluria, and the syndrome of idiopathic calcium oxalate urolithiasis. In the latter condition, the specific causes of the hyperoxaluria are not well defined. Diet and the availability of calcium and oxalate from the diet within the intestine are important factors in the hyperoxaluria that is present in some of these patients with idiopathic calcium oxalate urolithiasis. Other abnormalities in endogenous metabolism or transport of oxalate may play a role in the hyperoxaluria in some of these patients.

Calcium↗
PubMed1998

Simultaneous determination of oxalate, citrate and sulfate in children's plasma with ion chromatography.

To improve our understanding of both diagnosis and treatment of diseases of oxalate metabolism, we first set out to establish a new ion-chromatographic method to determine normal plasma levels of oxalate, citrate and sulfate from single plasma samples. In 50 infants and children (23 girls, 27 boys, aged 0.2 to 17 years) with normal renal function, blood was drawn in Li-heparin tubes, placed on ice and preserved immediately with 40 microliters M HCl/ml plasma in two ultracentrifugation steps. For measurement, plasma was injected onto an ion chromatography system with NaOH as the mobile phase, and then run as a linear gradient from 5 mM to 52.5 mM over 21 minutes. Analysis yielded measurable and reproducible oxalate (6.43 +/- 1.06 microM/liter), citrate (79.3 +/- 27.4 microM/liter) and sulfate (235.0 +/- 85.3 microM/liter) levels, without any age and gender specific differences. The least detectable plasma oxalate level was < 0.3 microM with a high reliability and reproducibility (coefficient of variance 1.95 to 4.75%). In conclusion, we established a reproducible, precise method to determine the relevant plasma anions involved in mineral metabolism, which heretofore have not been easily measurable. Studies of diseases of oxalate and citrate metabolism are ongoing on the basis of the normal plasma values achieved in this study.

Adolescent↗
PubMed2004

Gut-inhabiting bacterium Oxalobacter formigenes: role in calcium oxalate urolithiasis.

Oxalate plays a crucial role in the formation of most renal stones. Oxalate is a common constituent of most diets and a byproduct of metabolism, and if it is not sufficiently degraded, it may accumulate. In humans, gut bacteria degrade 70 to 100 mg of oxalate per day. Oxalobacter formigenes is a gram-negative, obligately anaerobic, rod-shaped bacterium with an absolute requirement for oxalate. Although not present in the gut at birth, it quickly colonizes most children, and there is epidemiologic evidence that its absence is a risk factor in calcium oxalate stone formation. We review the metabolism, genetics, and identification of this organism and its possible therapeutic role in recurrent stone-forming patients.

Animals↗
PubMed1983

Calcium oxalate urinary calculi: clinical and chemical aspects.

In 117 male patients with proven calcium oxalate renal calculi, adults of all ages were affected. There was a low incidence of urinary tract obstruction and infection and a high incidence of recurrence and bilateral disease. The group of patients could not be characterized as to a specific abnormality of blood or urine. There were no differences between all patients, a subset with multiple stones and normals with regard to the mean urinary excretions of calcium, magnesium and oxalic acid. There were no differences between the frequency distribution of patients with high excretions of both calcium and oxalic acid or low excretions of both calcium and oxalic acid. Mean supersaturation ratios and the frequency distribution of supersaturation ratios in 31 stone patients were the same as in 32 normal men. The data suggest that the difference between calcium oxalate stone patients and normals lies in the process of initiation.

Adult↗
PubMed1987

Urinary oxalate levels are not affected by dietary purine intake or allopurinol.

We showed previously that ingestion of a non-specific high purine diet by healthy subjects increased not only urinary uric acid levels but urinary oxalate as well. Both increments were reduced significantly during concomitant allopurinol therapy. The present study was undertaken to investigate these findings in more detail under carefully controlled dietary conditions where a single specific purine, guanosine, was used as an additive and several different methods for oxalate determination (GLC, HPLC, isotacophoresis) were compared with the enzymatic method used previously. Results obtained by two direct techniques of oxalate determination showed no significant alteration in oxalate levels during any dietary regime, suggesting that the earlier results derived from problems inherent in the experimental design and methodology employed. The study confirmed that one of the beneficial effects of allopurinol was to reduce dietary purine absorption. The results may thus provide a logical explanation for the reduced incidence of urolithiasis during allopurinol therapy in some idiopathic oxalate stone formers addicted to purine-rich foods and beverages.

Adult↗
PubMed1996

Generation of a proton motive force by the anaerobic oxalate-degrading bacterium Oxalobacter formigenes.

The generation of transmembrane ion gradients by Oxalobacter formigenes cells metabolizing oxalate was studied. The magnitudes of both the transmembrane electrical potential (delta psi) and the pH gradient (internal alkaline) decreased with increasing external pH; quantitatively, the delta psi was the most important component of the proton motive force. As the extracellular pH of metabolizing cells was increased, intracellular pH increased and remained alkaline relative to the external pH, indicating that O. formigenes possesses a limited capacity to regulate internal pH. The generation of a delta psi by concentrated suspensions of O. formigenes cells was inhibited by the K+ ionophore valinomycin and the protonophore carbonyl cyanide-m-chlorophenylhydrazone, but not by the Na+ ionophore monensin. The H+ ATPase inhibitor N,N'-dicyclohexyl-carbodiimide inhibited oxalate catabolism but did not dissipate the delta psi. The results support the concept that energy from oxalate metabolism by O. formigenes is conserved not as a sodium ion gradient but rather, at least partially, as a transmembrane hydrogen ion gradient produced during the electrogenic exchange of substrate (oxalate) and product (formate) and from internal proton consumption during oxalate decarboxylation.

Biodegradation, Environmental↗
PubMed1983

Prevalence of hyperoxaluria in idiopathic calcium oxalate kidney stone disease.

Urinary excretion of oxalate, calcium and urate has been investigated in 88 patients affected by idiopathic calcium oxalate stone disease and in 20 normal subjects. Of these ions, only oxalate was found significantly higher in stone formers. Defining hyperoxaluria as urinary oxalate excretion greater than 2 SD above normal, 50% of stone-forming people were found to be hyperoxaluric. When stone formers were classified in normo- and hyperoxaluric, the prevalence of hypercalciuria, hyperuricuria, family history of stone disease and recurrencies in stone formation was the same in both groups. It is concluded that hyperoxaluria is a frequent finding in finding in idiopathic calcium oxalate renal stone disease.

Adult↗
PubMed1994

Oxalic acid in saliva, teeth and tooth tartar.

Oxalic acid was determined in human saliva, teeth, tartar, and in animal teeth. Saliva from dentally healthy male subjects contained 0.10 +/- 0.09 mmol/l (n = 41) and those of dentally healthy female subjects 0.18 +/- 0.17 mmol/l (n = 40). Oxalic acid in tartar from 16 patients was 3.3 +/- 1.2 mmol/kg tartar. In human teeth, oxalic acid was 1.0 +/- 0.3 mmol/kg in milk teeth (n = 12) and 0.9 +/- 0.6 mmol/kg in permanent teeth (n = 60). Human teeth were sorted into age groups and into molars, incisors and premolars. In animal teeth, oxalic acid content varied widely. The formed calcium oxalate is proposed to be a 'physiological' protective mechanism for teeth.

Adolescent↗
PubMed2005

Role of the organic matter in calcium oxalate lithiasis.

Urine contains variable amounts of organic matter derived from cell degradation. The cellular detritus is composed by membranous and cytosolic glycoproteins, etc. The aim of this paper was to study the role of organic matter in calcium oxalate crystal development and to evaluate the action of some crystallization inhibitors on this process. Crystallization studies were carried out on urine in stagnant urine as well as under flow conditions, in presence and absence of cellular debris. Low amounts of cellular debris (when batch conditions were used), exhibited some inhibitory activity on heterogeneous nucleation of calcium oxalate monohydrate crystals, probably due to glycoproteins. Increasing amounts of cellular debris, however, promoted the nucleation of calcium oxalate monohydrate crystals. When cellular debris was retained in a cavity with a urine flow, this organic matter effectively induced the development of primary aggregates of calcium oxalate monohydrate crystals (crystallization range 2.8 mg/h per mg of organic matter). Presence of crystallization inhibitors prevented or minimized crystal development. These findings show that cell debris provides the necessary elements for the development of oxalate crystals and that this process can be effectively inhibited by presence of crystallization inhibitors.

Animals↗