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PubMed1985

Continuous-flow assay for urinary oxalate using immobilised oxalate oxidase.

A continuous-flow assay for measuring oxalate in urine is described. Covalently attached oxalate oxidase (EC 1.2.3.4) is used to oxidize the oxalate anion to carbon dioxide and hydrogen peroxide. The formed hydrogen peroxide is measured colorimetrically (A580) with an established reaction using horseradish peroxidase (EC 1.11.17), 3-methyl-2-benzothiazolinone hydrazone (MBTH) and 3-dimethylaminobenzoic acid (DMAB). Ascorbate interference is eliminated by treating the urine sample with sodium nitrite prior to assaying. The assay is accurate (mean recovery of added oxalate in spiked urine sample is 93 +/- 11%), sensitive (detection limit 1.0 mumol/L), reproducible (within-batch CV 3.5%; between-batch CV 5%) and relatively rapid (15 samples/h). This assay correlates well (R = 0.99) with another established enzymatic method (using oxalate decarboxylase).

Adolescent↗

PubMed1999

Importance of oxalate precursors for oxalate metabolism in rats.

Three metabolic precursors of oxalate were compared after intravenous administration to rats by measuring the urinary excretion of oxalate and related substances using capillary electrophoresis. Urine specimens were collected hourly from eight male Wistar rats (approximately 200 g) in each group. Glyoxylate (2 mg), glycolate (10 mg), and hydroxypyruvate (100 mg) were almost equally oxalogenic based on urinary oxalate excretion, with 22.0, 6.1, and 0.4% of the respective doses being converted into oxalate, 3, 8.9, and 0.2% into glycolate, and 1, 0.1, and 0.003% into glyoxylate. The mean urinary excretion of oxalate peaked between 1 and 2 h, while that of glycolate peaked at 1 h. The baseline urinary excretion of glycolate and glyoxylate was 0.11 to 0.24 micromol/h and 0.0 to 8.3 nmol/h, respectively, and all three agents caused a significant increase of urinary glycolate excretion for 2 to 3 h. Only glyoxylate administration increased urinary glyoxylate excretion at 1 h. Hydroxypyruvate administration significantly increased urinary hydroxypyruvate, glycerate, and citrate excretion at 1 to 2 h. The increase of urinary citrate excretion remains to be explained.

Animals↗

PubMed1979

[Analysis of oxalic acid and oxalates].

It is reported on individual methods for the estimation of the oxalic acid in body fluids, particularly in the urine. The case in question is a survey of the oxalate estimation methods, which, however, has no pretensions to completeness. The at present most actualestimation methods are brought somewhat more in detail. The data are not sufficient for the laboratorytechnical performance of the individual methods, this would transgress the possibilities of the work. However, the original papers are cited which contain all the necessary details. Some technical difficulties and disturbances in the individual estimation methods are also entered. Despite excellent work of several teams the problems of standardization, of the absolutely reliable reference methoda as well as of an objective consideration of advantages and disadvantages of individual, often subjectively judged methods is not yet solved. Comparing these methods, one gets the impression that several reliable methods of the same value are established. It seems that this estimation method brings the greatest progress which will reliably establish so small quantities of oxalate as they are in the blood or in the liquor. By this also the oxalate clearance and the renal oxalate treatment becomes more exactly establishable than up to now.

Carbon Radioisotopes↗

PubMed1983

Determination of urinary oxalate with commercially available oxalate oxidase.

For this direct colorimetry of urinary oxalate, commercially available oxalate oxidase (EC 1.2.3.4) is used. The urine is first diluted, to diminish the effect of interfering substances. Analytical recovery of oxalate from urines with five different oxalate concentrations (0.4 to 2.0 mmol/L) ranged from 92 to 109% (mean 99%). The within-day and between-day precision (CV) of the method for a wide range of oxalate concentrations averaged better than 10%. There is good correlation (r = 0.977) between this enzymatic method (y) and the chemical method of Hodgkinson and Williams (x) [Clin Chim Acta 36: 127-132, 1972], the regression equation being y = 1.014x + 0.061. Urines with added ascorbate give falsely increased results. The proposed method is inexpensive and simple to perform.

Charcoal↗

PubMed1980

Spectrophotometric determination of urinary oxalate with oxalate oxidase prepared from moss.

A novel spectrophotometric enzymic procedure for estimating oxalic acid in urine is described. Oxalate oxidase, prepared from moss species, converts oxalic acid to hydrogen peroxide and carbon dioxide. Hydrogen peroxide is determined enzymatically with horseradish peroxidase, by oxidative coupling of 3-methyl-2-benzothiazolinone hydrazone with N,N-dimethylaniline; the resulting indamine due is determined spectrophotometrically at 595 nm. Interfering substances are removed by adsorption to ion-exchange resins and oxidation with charcoal, thus avoiding oxalate recovery problems accompanying oxalate isolation. The procedure is rapid, sensitive, linear, and precise. Results agreed well with those obtained with a widely used chemical technique.

Adult↗

PubMed1993

Enzyme electrode based on oxalate oxidase immobilized in gelatin for specific determination of oxalate.

A biosensor for the specific determination of oxalate was developed using oxalate oxidase (EC 1.2.3.4) from barley (Hordeum vulgare) seedling roots in combination with a dissolved oxygen probe. Oxalate oxidase immobilized with gelatin using glutaraldehyde and fixed on pretreated teflon membrane served as an enzyme electrode. The electrode response was maximum when 50 mM succinate buffer was used at pH 3.2 and 35 degrees C. The biosensor response depends linearly on oxalate concentration between 5 x 10(-6)-2 x 10(-4) M with response time 30 sec and substrate specificity of the oxalate oxidase electrode of 100%. The sensor is stable for more than 3 months during which time more than 400 assays can be performed.

Biosensing Techniques↗

PubMed1998

Determination of plasma oxalate with chloride ion insensitive oxalate oxidase.

A simple colorimetric method has been developed for determination of oxalate in plasma using a C1-insensitive oxalate oxidase purified from grain sorghum leaves. The ultrafiltered plasma collected in 3.5 N HC1 was pretreated with NaNO2 to avoid possible interference by ascorbate. The minimum detection limit of the method is 0.225 mg/l. The % recovery of the added oxalate was 91.5 +/- 5.0 (mean +/- S.D., n = 15). The coefficient of variation within and between batch were < 3 and < 5 respectively. The mean plasma oxalate concentration in healthy subjects was 0.29 mg/l. The method has the advantage over other enzymic methods that it doesn't require the removal of C1- prior to oxalate assay.

Adult↗

PubMed1981

[14C]Oxalate absorption by normal persons, calcium oxalate stone formers, and patients with surgically disturbed intestinal function.

Intestinal absorption of oxalate can be judged from the urinary excretion of orally administered [14C]oxalate. Fifteen normal subjects, 21 patients with "idiopathic" calcium oxalate stone disease and a high oxalate excretion, four patients operated with ileocecal resection, and seven patients operated with jejunoileal bypass were so investigated. We saw no significant difference in the amount of isotope excreted by normal subjects and idiopathic stone formers; 13.6% (SD 5.9%) and 14.4% (SD 6.5%), respectively, of the administered dose was accounted for in the urine. The patients with resection or bypass showed a quite different pattern of isotope excretion, and 18.3% (SD 7.0%) and 36.8% (SD 14.0%), respectively, of the isotope was accounted for in the urine.

Calcium Oxalate↗

PubMed1987

The role of oxalate and calcium oxalate activity and formation product ratio in patients with renal stones before and during treatment.

The participation of oxalate in nephrolithiasis was evaluated in 202 stone patients. The activity product and formation product ratios of calcium oxalate were substantially altered in the stone population. Treatment with thiazide derivatives and/or allopurinol was able to decrease urine oxalate and normalize the activity product and formation product ratios. Stone activity decreased in the stone population after treatment. Our data suggest that oxalate may have a critical role in nephrolithiasis activity.

Allopurinol↗

PubMed1994

Influence of various calcium intakes on calcium-oxalate crystalluria in rats on sodium-oxalate diet.

Forty adult male Wistar rats were placed in metabolic cages on a Ca-deficient diet (0.1%) for 7 days and then on a Ca-deficient, Na-oxalate (NaOx) enriched diet (20 mg/100 g) for another 14 days. The animals were subdivided into three groups receiving three different types of mineral water: group I (n = 13), Badoit (Ca 222 mg/l); group II (n = 14), Contrexéville (Ca 467 mg/l); and group III (n = 13), Evian (Ca 78 mg/l). Another series of 25 rats (group I, n = 9; group II, n = 8; group III, n = 8) underwent the same study protocol, except that they received a normal Ca diet (1%). On the low-Ca diet, urinary Ca-Ox monohydrate (COM) crystals were observed only under the Na-Ox diet, with a mean crystal number significantly greater in group III (16.7 +/- 4.5 crystals/mm3) than in group I or II rats (2.5 +/- 1.5 or 4.1 +/- 1.5 crystals/mm3, respectively). Urinary Ca concentrations decreased in all groups (P < 0.001) under the Na-Ox diet, while urinary oxalate concentrations increased in all groups (P < 0.001). On the normal Ca diet, COM crystal excretion was observed only with the Na-Ox-enriched diet, but in this case feeding the Na-Ox diet did not modify urinary oxalate excretion. Ca/Ox ratio was significantly lower under 0.1% Ca diet than under normal Ca diet, related with the type and the number of crystals observed, demonstrating that assessment of crystalluria can provide an index of disease severity. Moreover, the hardness of the drinking water influences urinary COM crystal excretion only under a low-Ca, oxalate-rich diet, suggesting that the total calcium intake rather than the water calcium content is an important factor in the occurrence of Ca-Ox nephrolithiasis.

Animals↗

PubMed2001

Biosynthesis of L-ascorbic acid and conversion of carbons 1 and 2 of L-ascorbic acid to oxalic acid occurs within individual calcium oxalate crystal idioblasts.

L-Ascorbic acid (AsA) and its metabolic precursors give rise to oxalic acid (OxA) found in calcium oxalate crystals in specialized crystal idioblast cells in plants; however, it is not known if AsA and OxA are synthesized within the crystal idioblast cell or transported in from surrounding mesophyll cells. Isolated developing crystal idioblasts from Pistia stratiotes were used to study the pathway of OxA biosynthesis and to determine if idioblasts contain the entire path and are essentially independent in OxA synthesis. Idioblasts were supplied with various (14)C-labeled compounds and examined by micro-autoradiography for incorporation of (14)C into calcium oxalate crystals. [(14)C]OxA gave heavy labeling of crystals, indicating the isolated idioblasts are functional in crystal formation. Incubation with [1-(14)C]AsA also gave heavy labeling of crystals, whereas [6-(14)C]AsA gave no labeling. Labeled precursors of AsA (L-[1-(14)C]galactose; D-[1-(14)C]mannose) also resulted in crystal labeling, as did the ascorbic acid analog, D-[1-(14)C]erythorbic acid. Intensity of labeling of isolated idioblasts followed the pattern OxA > AsA (erythorbic acid) > L-galactose > D-mannose. Our results demonstrate that P. stratiotes crystal idioblasts synthesize the OxA used for crystal formation, the OxA is derived from the number 1 and 2 carbons of AsA, and the proposed pathway of ascorbic acid synthesis via D-mannose and L-galactose is operational in individual P. stratiotes crystal idioblasts. These results are discussed with respect to fine control of calcium oxalate precipitation and the concept of crystal idioblasts as independent physiological compartments.

Araceae↗

PubMed2000

Nephrolithiasis: a consequence of renal epithelial cell exposure to oxalate and calcium oxalate crystals.

PURPOSE: Formation of calcium oxalate (CaOx) kidney stones was investigated using three approaches. MATERIALS AND METHODS: Pathogenesis of crystalluria and crystal deposition in the kidneys was examined in vivo by inducing hyperoxaluria in rats. Cultures of LLC-PK1 and MDCK cells were exposed to oxalate (Ox) and CaOx crystals to examine the effect on cells in various sections of the renal tubules. The nucleation potential of various substrates was examined by incubating them in metastable solutions of CaOx. RESULTS: Calcium oxalate crystals and nonphysiologic levels of Ox were injurious to renal epithelial cells. To combat these nephrotoxins, renal epithelial cells produce a variety of macromolecules such as bikunin and osteopontin, which are modulators of crystallization and may also be involved in crystal attachment to the cells. Sustained hyperoxaluria in association with CaOx crystals induced apoptosis as well as necrosis. Cellular degradation products induced heterogeneous nucleation of crystals at lower and physiologic levels of oxalate. They also promoted aggregation. CONCLUSIONS: Crystals begin to form in earlier segments of the nephron with a chance to grow and be retained in the collecting ducts after aggregation with other large crystals. Crystal deposits in the collecting ducts near the papillary surface, when exposed to the renal pelvic urine, become nidi for the development of kidney stones.

Animals↗

PubMed1987

Sensitivity of the direct oxalate oxidase assay of urinary oxalate improved.

The direct colorimetric method for urinary oxalate has been modified to improve its sensitivity. Oxalate is precipitated overnight with calcium chloride and ethanol, the precipitate is redissolved, and the oxalate is measured by use of oxalate oxidase (EC 1.2.3.4), methylbenzothiazolinone hydrazone, and dimethylaniline. The color developed is more intense, analytical recovery averages 102%, and the overall imprecision is less than 5%. To assess the accuracy of the method, we used a gas-chromatography comparison method and control sera. Interference from ascorbate is negligible. The modified method retains its simplicity and is less expensive.

Calcium Chloride↗

PubMed1984

[Respective effect of calcium and oxalate on calcium oxalate crystallization in the urine].

Our aim is to determine the respective role of calcium (Ca) and of oxalate (ox) in the formation of calcium oxalate (Caox) crystals. Two urine samples are mixed after increasing either the calcium concentration (Ca) in one sample or the oxalate concentration (ox) in the other. The crystals formed are identified by their habits or by x-ray. Similarly, urine from 37 hypercalciuric stone-formers is analysed. Caox crystallizes at an oversaturation beta greater than or equal to 13,5, critical beta. An almost linear relationship exists between beta and (ox), the critical beta being obtained at an (ox) approximately 0,26 mmol/l. No simple relationship links beta and (Ca). These results point out the predominant role of oxalate in the formation of Caox crystals.

Adult↗

PubMed2000

Nucleation and aggregation of calcium oxalate in whole urine; spectrophotometric sedimentation analysis: a new approach to study the aggregation of calcium oxalate dihydrate.

Spectrophotometric and scanning electron microscopic (SEM) studies of oxalate-induced crystallization have been performed in whole urine with and without continuous magnetic stirring and before and after millipore filtration of urine. With continuous stirring, preferential nucleation was observed and this followed second order kinetics. Important crystal aggregation only occurred after an oxalate load above 1 mmol/l and without stirring. Under these conditions and at an ionic calcium concentration of 2 mmol/l, single crystals and aggregates of calcium oxalate dihydrate and monohydrate of well defined sizes were produced. Single dehydrates, their aggregates and the other particles could be distinguished by their significantly different sedimentation rates. From sedimentation curves an aggregation ratio for calcium oxalate dihydrate (aggregated/total dihydrate particles) was extrapolated. Millipore filtration removing important urinary macromolecules increased this aggregation ratio as well as the size of the aggregates on SEM pictures.

Calcium Oxalate↗

PubMed1989

A simple, rapid assay for plasma oxalate in uraemic patients using oxalate oxidase, which is free from vitamin C interference.

An enzymatic assay for the determination of oxalate in plasma was developed which is specific, simple, rapid and requires no specialised equipment; interference from vitamin C was removed by incubation of acidified plasma ultrafiltrate with ascorbate oxidase prior to oxalate estimation. Recoveries were 93 +/- 11% and the inter-batch coefficient of variation for 31 determinations at an oxalate level of 24 mumol/l was 10%. The assay is linear up to 300 mumol/l with a detection limit of 2 mumol/l. The reference range, based on results from 25 healthy volunteers, was defined as less than 2-5 mumol/l which is similar to levels established for the in vivo isotope dilution technique. The assay has an added advantage over the latter method, which requires a urine collection, in that it can be applied to plasma from anuric patients. A linear correlation (r = 0.68, p less than 0.001) was found between plasma oxalate and serum creatinine in individuals with varying degrees of renal failure.

Ascorbic Acid↗

PubMed2005

Catalytic kinetic spectrophotometry for the determination of trace amount of oxalic acid in biological samples with oxalic acid-rhodamine B-potassium dichromate system.

A new catalytic kinetic spectrophotometric method was proposed for determining trace oxalic acid based on the catalytic effect of oxalate on the oxidation of potassium dichromate with rhodamin B in 0.10 M of sulfuric acid. Good linearity is obtained over the concentration range 0.40-6.0 microg/mL of oxalic acid. After the reactions of the catalytic and non-catalytic systems were terminated by using 2.00 mL of 4 M sodium hydroxide solution, they can be stable for 3 h at room temperature. The apparent activation energy of the catalytic reaction is 12.44 kJ/mol. The effect of 50 coexisting substances was observed. The method was used to determine trace oxalic acid in tea, spinach and urine samples with satisfactory results.

Catalysis↗

PubMed2001

Improved determination of urinary oxalate with alkylamine glass bound barley oxalate oxidase.

The measurement of oxalate in urine was improved by employing barley oxalate oxidase immobilized on alkylamine glass beads affixed in a glass beaker. The minimum detection limit was 3.6 mg l(-1) urine. The recovery of added oxalate was 88.9+/-9.2%. Within- and between-assay coefficients of variation (CV) were <4.0 and <9.4%, respectively. The urinary oxalate values were obtained by a commercial kit method and the present method showed a good correlation (0.999). The method is free from tedious handling of glass beads and Cl- interference.

Adult↗